The Differentiation Between Benign and Malignant Hiperthrophy Prostate Informations










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Benign prostatic hyperplasia


Benign prostatic hyperplasia
Classification and external resources

Diagram illustrating normal prostate (left) and benign prostatic hyperplasia (right).
ICD-10 N40
ICD-9 600
DiseasesDB 10797
eMedicine med/1919
MeSH D011470

Benign prostatic hyperplasia (BPH) also known as benign prostatic hypertrophy (technically a misnomer), benign enlargement of the prostate (BEP), and adenofibromyomatous hyperplasia, refers to the increase in size of the prostate.

Properly, BPH involves hyperplasia rather than hypertrophy, but the nomenclature is often interchangeable, even amongst urologists.[1] It involves hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra, which interferes with the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary tract infections, and urinary retention. Although prostate specific antigen levels may be elevated in these patients because of increased organ volume and inflammation due to urinary tract infections, BPH is not considered to be a premalignant lesion.

Adenomatous prostatic growth is believed to begin at approximately age 30 years. An estimated 50% of men have histologic evidence of BPH by age 50 years and 75% by age 80 years. In 40-50% of these patients, BPH becomes clinically significant.[2]


Signs and symptoms

Benign prostatic hyperplasia symptoms are classified as storage or voiding.

Storage symptoms include urinary frequency, urgency (compelling need to void that cannot be deferred), urgency incontinence, and voiding at night (nocturia).

Voiding symptoms include urinary stream, hesitancy (needing to wait for the stream to begin), intermittency (when the stream starts and stops intermittently), straining to void, and dribbling. Pain and dysuria are usually not present. These storage and voiding symptoms are evaluated using the International Prostate Symptom Score (IPSS) questionnaire, designed to assess the severity of BPH.[3]

BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in stasis of bacteria in the bladder residue and an increased risk of urinary tract infection. Urinary bladder stones are formed from the crystallization of salts in the residual urine. Urinary retention, termed acute or chronic, is another form of progression. Acute urinary retention is the inability to void, while in chronic urinary retention the residual urinary volume gradually increases, and the bladder distends. Some patients that suffer from chronic urinary retention may eventually progress to renal failure, a condition termed obstructive uropathy.


A study published in 2008 in the journal of andrology “Andrologia”[4] reports on a newly discovered venous route by which free (active) testosterone reaches the prostate in extremely high concentrations, promoting the accelerated proliferation of prostate cells, leading to the gland’s enlargement. The study (conducted by two Israeli doctors: Dr. Yigal Gat and Dr. Menachem Goren) suggests that BPH is caused by malfunction of the valves in the internal spermatic veins manifesting as varicocele, a phenomenon which has been shown to increase rapidly with age,[5][6] roughly equal to 10-15% each decade of life. The 6- to 8-fold elevated hydrostatic pressure then leads to retrograde venous drainage, allowing free communication with the prostatic circulation. Having measured a concentration of free testosterone of some 130-fold above serum level in the internal spermatic vein (the testes being the main source and the blood being undiluted in systemic circulation), the authors conclude that the elevated venous pressure causes hypertrophy and exposure to high concentrations of free testosterone causes hyperplasia in the prostate. The study also proposes a treatment method (Gat–Goren Technique) similar to that used in treating varicocele, which restores normal pressure in the venous drainage system, effectively reducing the volume of the prostate and clinical manifestation of BPH.

Most experts consider androgens (testosterone and related hormones) to play a permissive role. This means that androgens have to be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by the fact that castrated boys do not develop BPH when they age. On the other hand, administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms.[citation needed] Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. This enzyme is localized principally in the stromal cells; hence, those cells are the main site for the synthesis of DHT.

DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is 10 times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5α-reductase is given to men with this condition. Therapy with 5α-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and, in many cases, BPH symptoms.[citation needed]

Testosterone promotes prostate cell proliferation,[7] but relatively low levels of serum testosterone are found in patients with BPH.[8][9] One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in the prostate.[10]

While there is some evidence that estrogen may play a role in the etiology of BPH, this effect appears to be mediated mainly through local conversion of estrogen to androgens in the prostate tissue rather than a direct effect of estrogen itself.[11] In canine in vivo studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate.[12] Studies looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have generally shown none.[9][13]

On a microscopic level, BPH can be seen in the vast majority of men as they age, in particular over the age of 70 years, around the world. However, rates of clinically significant, symptomatic BPH vary dramatically depending on lifestyle. Men that lead a western lifestyle have a much higher incidence of symptomatic BPH than men that lead a traditional or rural lifestyle. This is confirmed by research in China showing that men in rural areas have very low rates of clinical BPH, while men living in cities adopting a western lifestyle have a skyrocketing incidence of this condition, though it is still below rates seen in the West.

Much work remains to be done to completely clarify the causes of BPH.


Urinary bladder (black butterfly-like shape) and hyperplastic prostate (BPH) visualized by sonography

Micrograph showing nodular hyperplasia (left off center) of the prostate from a transurethral resection of the prostate (TURP). H&E stain.

Microscopic examination of different types of prostate tissues (stained with immunohistochemical techniques): A. Normal (non-neoplastic) prostatic tissue (NNT). B. Benign prostatic hyperplasia. C. High-grade prostatic intraepithelial neoplasia (PIN). D. Prostatic adenocarcinoma (PCA).

Prostate with a large median lobe bulging upwards. A metal instrument is placed in the urethra (which passes through the prostate). This specimen was almost 7 centimeters long with a volume of about 60 cubic centimetres on transrectal ultrasound and was removed during a Hryntschak procedure or transvesical prostatectomy (removal of the prostate through the bladder) for benign prostatic hyperplasia.

Rectal examination (palpation of the prostate through the rectum) may reveal a markedly enlarged prostate, usually affecting the middle lobe.

Often, blood tests are performed to rule out prostatic malignancy: Elevated prostate specific antigen (PSA) levels needs further investigations such as reinterpretation of PSA results, in terms of PSA density and PSA free percentage, rectal examination and transrectal ultrasonography. These combined measures can provide early detection.

Ultrasound examination of the testicles, prostate, and kidneys is often performed, again to rule out malignancy and hydronephrosis.

Screening and diagnostic procedures for BPH are similar to those used for prostate cancer. Some signs to look for include:[14]

  • Weak urinary stream
  • Prolonged emptying of the bladder
  • Abdominal straining
  • Hesitancy
  • Irregular need to urinate
  • Incomplete bladder emptying
  • Post-urination dribble
  • Irritation during urination
  • Frequent urination
  • Nocturia (need to urinate during the night)
  • Urgency
  • Incontinence (involuntary leakage of urine)
  • Bladder pain
  • Dysuria (painful urination)
  • Problems in ejaculation



Patients should decrease fluid intake before bedtime, moderate the consumption of alcohol and caffeine-containing products, and follow timed voiding schedules.


The two main medications for management of BPH are alpha blockers and 5α-reductase inhibitors.

  • The 5α-reductase inhibitors finasteride[23] and dutasteride[24] are another treatment option. These medications inhibit 5a-reductase, which in turn inhibits production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years.[25] When used together with alpha blockers, a reduction of BPH progression to acute urinary retention and surgery has been noted in patients with larger prostates.[26] Side effects include decreased libido and ejaculatory or erectile dysfunction.[23]

Antimuscarinics such as tolterodine may also be used, especially in combination with alpha blockers.[27] They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control symptoms of an overactive bladder.[citation needed]

Sildenafil citrate shows some symptomatic relief, suggesting a possible common etiology with erectile dysfunction.[28]

 Herbal remedies

People often seek herbal remedies for BPH.[29] Several are approved in European countries, but none in the USA. Saw palmetto extract from Serenoa repens is one of the most extensively studied. It showed promise in early studies,[30] though later trials of higher methodological quality indicated no difference from placebo.[31][32][33] There are no known negative effects of saw palmetto, so if taking the supplement relieves symptoms, there is no harm in taking it. The quality of saw palmetto products varies.[34]

Other herbal medicines that have research support in systematic reviews include beta-sitosterol[35] from Hypoxis rooperi (African star grass) and pygeum (extracted from the bark of Prunus africana),[36] while there is less substantial support for the efficacy of pumpkin seed (Cucurbita pepo) and stinging nettle (Urtica dioica) root.[37] There is weak evidence that pollen extracts frp, rye grass (Secale cereale) may also correlate with modest symptomatic relief.[38]

Minimally invasive therapies

Medication is often prescribed as the first treatment option, there are many patients who do not achieve success with this line of treatment. Those patients may not achieve sustained improvement in symptoms or they may stop taking the medication because of side-effects.[39] There are options for treatment in a urologist’s office before proceeding to surgery. The two most common types of office-based therapies are transurethral microwave thermotherapy (TUMT) and transurethral needle ablation (TUNA). Both of these procedures rely on delivering enough energy to create sufficient heat to cause cell death (necrosis) in the prostate. The goal of the therapies is to cause enough necrosis so that, when the dead tissue is reabsorbed by the body, the prostate shrinks, relieving the obstruction of the urethra. These procedures are typically performed with local anesthesia, and the patient returns home the same day. Some urologists have studied and published long-term data on the outcomes of these procedures, with data out to five years. The most recent American Urological Association (AUA) Guidelines for the Treatment of BPH in 2003 lists minimally invasive therapies including TUMT and TUNA as acceptable alternatives for certain patients with BPH.[40]

Transurethral microwave therapy (TUMT) was originally approved by the FDA in 1996, with the first generation system by EDAP Technomed. Since 1996, other companies have received FDA approval for TUMT devices, including Urologix, Dornier, Thermatrix, Celsion, and Prostalund. Multiple clinical studies have been published on TUMT. The general principle underlying all the devices is that a microwave antenna that resides in a urethral catheter is placed in the intraprostatic area of the urethra. The catheter is connected to a control box outside of the patient’s body and is energized to emit microwave radiation into the prostate to heat the tissue and cause necrosis. It is a one-time treatment that takes approximately 30 minutes to 1 hour, depending on the system used. It takes approximately 4 to 6 weeks for the damaged tissue to be reabsorbed into the patient’s body. Some of the devices incorporate circulating coolant through the treatment area with the intent of preserving the urethra while the microwave energy heats the prostatic tissue surrounding the urethra.

Transurethral needle ablation (TUNA) operates with a different type of energy, radio frequency (RF) energy, but is designed along the same premise as TUMT devices, that the heat the device generates will cause necrosis of the prostatic tissue and shrink the prostate. The TUNA device is inserted into the urethra using a rigid scope much like a cystoscope. The energy is delivered into the prostate using two needles that emerge from the sides of the device, through the urethral wall and into the prostate. The needle-based ablation devices are very effective at heating a localized area to a high enough temperature to cause necrosis. The treatment is typically performed in one session, but may require multiple sticks of the needles depending on the size of the prostate.


If medical treatment fails, and the patient elects not to try office-based therapies or the physician determines the patient is a better candidate for transurethral resection of prostate (TURP), surgery may need to be performed. In general, TURP is still considered the gold standard of prostate interventions for patients that require a procedure. This involves removing (part of) the prostate through the urethra. There are also a number of new methods for reducing the size of an enlarged prostate, some of which have not been around long enough to fully establish their safety or side-effects. These include various methods to destroy or remove part of the excess tissue while trying to avoid damaging what remains. Transurethral electrovaporization of the prostate (TVP), laser TURP, visual laser ablation (VLAP), ethanol injection, and others are studied as alternatives.

Newer techniques involving lasers in urology have emerged in the last 5–10 years, starting with the VLAP technique involving the Nd:YAG laser with contact on the prostatic tissue. A similar technology called Photoselective Vaporization of the Prostate (PVP) with the GreenLight (KTP) laser have emerged very recently. This procedure involves a high-power 80-watt KTP laser with a 550-micrometre laser fiber inserted into the prostate. This fiber has an internal reflection with a 70-degree deflecting angle. It is used to vaporize the tissue to the prostatic capsule. KTP lasers target haemoglobin as the chromophore and typically have a penetration depth of 2.0 mm (four times deeper than holmium).

Another procedure termed Holmium Laser Ablation of the Prostate (HoLAP) has also been gaining acceptance around the world. Like KTP, the delivery device for HoLAP procedures is a 550 um disposable side-firing fiber that directs the beam from a high-power 100-watt laser at a 70-degree angle from the fiber axis. The holmium wavelength is 2,140 nm, which falls within the infrared portion of the spectrum and is invisible to the naked eye. Whereas KTP relies on haemoglobin as a chromophore, water within the target tissue is the chromophore for Holmium lasers. The penetration depth of Holmium lasers is <0.5 mm, avoiding complications associated with tissue necrosis often found with the deeper penetration and lower peak powers of KTP.

HoLEP, Holmium Laser Enucleation of the Prostate, is another Holmium laser procedure reported to carry fewer risks compared with either TURP or open prostatectomy.[41] HoLEP is largely similar to the HoLAP procedure; the main difference is that this procedure is typically performed on larger prostates. Instead of ablating the tissue, the laser cuts a portion of the prostate, which is then cut into smaller pieces and flushed with irrigation fluid. As with the HoLAP procedure, there is little bleeding during or after the procedure.

Both wavelengths, KTP and Holmium, ablate approximately one to two grams of tissue per minute.

Post surgery care often involves placement of a Foley catheter or a temporary prostatic stent to permit healing and allow urine to drain from the bladder.


Disability-adjusted life year for benign prostatic hyperplasia per 100,000 inhabitants in 2004.[42]

  no data
  less than 20
  more than 100

The prostate gets larger in most men as they get older, and, overall, 45% of men over the age of 46 can expect to suffer from the symptoms of BPH if they survive 30 years. Incidence rates increase from 3 cases per 1000 man-years at age 45–49 years, to 38 cases per 1000 man-years by the age of 75–79 years. Whereas the prevalence rate is 2.7% for men aged 45–49, it increases to 24% by the age of 80 years.[43]

For some men, the symptoms may be severe enough to require treatment

indonesia version



Hiperplasia prostat jinak
Hiperplasia prostat jinak
Klasifikasi dan sumber daya eksternal

Diagram yang menggambarkan prostat normal (kiri) dan benign prostatic hyperplasia (kanan).
ICD-10 N40
ICD-9 600
DiseasesDB 10797
eMedicine med/1919
MESH D011470

Benign prostatic hyperplasia (BPH) juga dikenal sebagai benign prostatic hypertrophy (secara teknis keliru), pembesaran prostat jinak dari (BEP), dan hiperplasia adenofibromyomatous, mengacu pada peningkatan ukuran prostat.

Benar, BPH melibatkan hiperplasia daripada hipertrofi, namun nomenklatur sering dipertukarkan, bahkan di antara urolog [1]. Ini melibatkan hiperplasia sel stroma dan epitel prostat, menghasilkan pembentukan besar, nodul cukup diskrit di wilayah periuretra prostat . Jika sudah cukup besar, nodul kompres kanal uretra menyebabkan obstruksi parsial, atau kadang-kadang hampir lengkap, dari uretra, yang mengganggu aliran normal urin. Ini menyebabkan gejala keraguan kencing, sering buang air kecil, disuria (kencing terasa sakit), peningkatan risiko infeksi saluran kemih, dan retensi urin. Meskipun kadar antigen prostat spesifik dapat meningkat pada pasien ini karena volume organ meningkat dan peradangan akibat infeksi saluran kemih, BPH tidak dianggap sebagai lesi premalignant.

Pertumbuhan prostat adenomatosa diyakini akan dimulai pada sekitar usia 30 tahun. Diperkirakan 50% pria memiliki bukti histologis BPH pada usia 50 tahun dan 75% pada usia 80 tahun. Dalam 40-50% dari pasien tersebut, BPH menjadi klinis signifikan. [2]

1 Tanda dan gejala
2 Penyebab
3 Diagnosis
4 Manajemen
4.1 Gaya Hidup
4.2 Obat-obatan
4.3 obat herbal
4.4 terapi invasif minimal
4,5 Bedah
5 Epidemiologi
6 Lihat juga
7 Bacaan lebih lanjut
8 Referensi
9 Pranala luar

Tanda dan gejala
Gejala jinak prostatic hyperplasia diklasifikasikan sebagai penyimpanan atau berkemih.

Gejala Penyimpanan termasuk frekuensi kencing, urgensi (kebutuhan mendesak untuk kekosongan yang tidak dapat ditangguhkan), inkontinensia urgensi, dan berkemih pada malam hari (nokturia).

Gejala berkemih termasuk aliran kemih, hesitansi (perlu menunggu aliran untuk mulai), intermittency (ketika sungai mulai dan berhenti sebentar-sebentar), berusaha untuk membatalkan, dan dribbling. Nyeri dan disuria biasanya tidak hadir. Gejala-gejala penyimpanan dan berkemih dievaluasi menggunakan Prostat Internasional Skor Gejala (IPSS) kuesioner, yang dirancang untuk menilai keparahan BPH [3].

BPH dapat menjadi penyakit yang progresif, terutama jika tidak diobati. Lengkap membatalkan hasil dalam stasis bakteri dalam kandung kemih dan residu peningkatan risiko infeksi saluran kemih. Batu kandung kemih yang terbentuk dari kristalisasi garam dalam urin residual. Retensi urin, disebut akut atau kronis, adalah bentuk lain dari kemajuan. Retensi urin akut adalah ketidakmampuan untuk membatalkan, sementara di retensi urin kronis volume residu urin secara bertahap meningkat, dan kandung kemih mengalami distensi. Beberapa pasien yang menderita retensi urin kronis pada akhirnya dapat berkembang menjadi gagal ginjal, kondisi disebut uropati obstruktif.

Sebuah studi yang diterbitkan pada tahun 2008 dalam jurnal andrologi “Andrologia” [4] laporan pada rute vena yang baru ditemukan oleh yang bebas (aktif) testosteron mencapai prostat dalam konsentrasi yang sangat tinggi, mempromosikan proliferasi dipercepat sel prostat, yang menyebabkan kelenjar itu pembesaran. Penelitian (yang dilakukan oleh dua dokter-dokter Israel: Dr Yigal Gat dan Dr Menachem Goren) menunjukkan bahwa BPH disebabkan oleh kerusakan katup dalam vena spermatika internal yang mewujudkan sebagai varikokel, sebuah fenomena yang telah terbukti meningkatkan cepat dengan usia, [5] [6] kurang lebih sama dengan 10-15% setiap dekade kehidupan. The 6 – untuk tekanan hidrostatik meningkat 8 kali lipat kemudian menyebabkan drainase vena retrograde, yang memungkinkan komunikasi bebas dengan sirkulasi prostat. Setelah mengukur konsentrasi testosteron bebas dari beberapa tingkat 130 kali lipat serum di atas dalam vena spermatika internal (testis menjadi sumber utama dan darah yang murni dalam sirkulasi sistemik), penulis menyimpulkan bahwa tekanan vena meningkat menyebabkan hipertrofi dan paparan konsentrasi tinggi menyebabkan hiperplasia testosteron bebas dalam prostat. Penelitian ini juga mengusulkan metode pengobatan (Gat-Goren Teknik) mirip dengan yang digunakan dalam mengobati varikokel, yang mengembalikan tekanan normal dalam sistem drainase vena, efektif mengurangi volume prostat dan manifestasi klinis BPH.

Kebanyakan ahli menganggap androgen (testosteron dan hormon terkait) untuk memainkan peran permisif. Ini berarti bahwa androgen harus hadir untuk BPH terjadi, tetapi tidak selalu secara langsung menyebabkan kondisi tersebut. Hal ini didukung oleh fakta bahwa anak laki-laki dikebiri tidak mengembangkan BPH ketika mereka usia. Di sisi lain, pemberian testosteron eksogen tidak terkait dengan peningkatan yang signifikan pada risiko gejala BPH. [Kutipan diperlukan] dihidrotestosteron (DHT), suatu metabolit testosteron, adalah mediator kritis pertumbuhan prostat. DHT disintesis dalam prostat dari beredar testosteron oleh aksi dari enzim 5α-reduktase, tipe 2. Enzim ini lokal terutama di sel-sel stroma, maka, sel-sel adalah situs utama untuk sintesis DHT.

DHT dapat bertindak dalam mode autokrin pada sel stroma atau dalam mode parakrin dengan menyebarkan ke dalam sel epitel di dekatnya. Dalam kedua jenis sel, DHT berikatan dengan reseptor androgen sinyal nuklir dan transkripsi faktor pertumbuhan yang mitogenik ke sel epitel dan stroma. DHT adalah 10 kali lebih kuat daripada testosteron karena berdisosiasi dari reseptor androgen lebih lambat. Pentingnya DHT dalam menyebabkan hiperplasia nodular didukung oleh pengamatan klinis di mana suatu inhibitor 5α-reduktase diberikan kepada laki-laki dengan kondisi ini. Terapi dengan inhibitor 5α-reduktase nyata mengurangi isi DHT prostat dan, pada gilirannya, mengurangi volume prostat dan, dalam banyak kasus, gejala BPH. [Kutipan diperlukan]

Testosteron meningkatkan proliferasi sel prostat, [7] tetapi tingkat yang relatif rendah testosteron serum yang ditemukan pada pasien dengan BPH [8]. [9] Salah satu penelitian kecil telah menunjukkan bahwa pengebirian medis menurunkan kadar hormon serum dan prostat tidak merata, memiliki efek kurang pada tingkat testosteron dan dihidrotestosteron dalam prostat [10].

Sementara ada beberapa bukti bahwa estrogen mungkin memainkan peran dalam etiologi BPH, efek ini tampaknya dimediasi terutama melalui konversi lokal estrogen terhadap androgen dalam jaringan prostat ketimbang efek langsung dari estrogen itu sendiri [11]. Pada anjing di vivo pengebirian, yang secara signifikan mengurangi tingkat androgen tetapi tingkat estrogen tidak berubah, menyebabkan atrofi signifikan dari prostat. [12] Studi mencari korelasi antara hiperplasia prostat dan tingkat estrogen serum pada manusia umumnya menunjukkan tidak ada. [9] [13]

Pada tingkat mikroskopis, BPH dapat dilihat di sebagian besar laki-laki dengan bertambahnya usia mereka, khususnya di atas usia 70 tahun, di seluruh dunia. Namun, tingkat signifikan secara klinis, gejala BPH bervariasi secara dramatis tergantung pada gaya hidup. Pria yang menjalani gaya hidup Barat memiliki insiden yang lebih tinggi BPH gejala dibandingkan laki-laki yang menjalani gaya hidup tradisional atau pedesaan. Hal ini dikonfirmasi oleh penelitian di Cina menunjukkan bahwa laki-laki di daerah pedesaan memiliki tingkat yang sangat rendah klinis BPH, sedangkan pria yang tinggal di kota mengadopsi gaya hidup barat memiliki insiden meroket kondisi ini, meskipun masih di bawah tingkat yang terlihat di Barat.

Masih banyak pekerjaan yang harus dilakukan untuk benar-benar mengklarifikasi penyebab BPH.


Kandung kemih (hitam kupu-kupu seperti bentuk) dan hiperplastik prostat (BPH) divisualisasikan dengan sonografi

Mikrograf menunjukkan hiperplasia nodular (kiri dari pusat) dari prostat dari reseksi transurethral dari prostat (TURP). H & E noda.

Pemeriksaan mikroskopik dari berbagai jenis jaringan prostat (diwarnai dengan teknik imunohistokimia): A. Normal (non-neoplastik) jaringan prostat (NNT). B. jinak prostat hiperplasia. C. neoplasia intraepitel kelas tinggi prostat (PIN). D. adenokarsinoma prostat (PCA).

Prostat dengan lobus median besar menggembung ke atas. Sebuah instrumen logam ditempatkan di uretra (yang melewati prostat). Spesimen ini hampir 7 cm panjang dengan volume sekitar 60 sentimeter kubik pada USG transrectal dan telah dihapus selama prosedur Hryntschak atau prostatektomi transvesical (pengangkatan prostat melalui kandung kemih) untuk hiperplasia prostat jinak.

Pemeriksaan rektal (palpasi prostat melalui dubur) dapat mengungkapkan sebuah prostat yang membesar nyata, biasanya mempengaruhi lobus tengah.

Seringkali, tes darah dilakukan untuk menyingkirkan keganasan prostat: Peningkatan antigen prostat spesifik (PSA) tingkat kebutuhan penyelidikan lebih lanjut seperti reinterpretasi hasil PSA, dalam hal kepadatan PSA dan persentase PSA bebas, pemeriksaan dubur dan ultrasonografi transrectal. Langkah-langkah ini dikombinasikan dapat memberikan deteksi dini.

USG pemeriksaan testis, prostat, dan ginjal sering dilakukan, sekali lagi untuk menyingkirkan keganasan dan hidronefrosis.

Skrining dan diagnostik prosedur untuk BPH mirip dengan yang digunakan untuk kanker prostat. Beberapa tanda-tanda untuk mencari mencakup: [14]

Lemahnya aliran kemih
Berkepanjangan pengosongan kandung kemih
Abdomen tegang
Tidak teratur perlu buang air kecil
Mengosongkan kandung kemih tidak lengkap
Pasca-buang air kecil menggiring bola
Iritasi saat buang air kecil
Sering buang air kecil
Nokturia (perlu buang air kecil pada malam hari)
Inkontinensia (kebocoran urin involunter)
Nyeri kandung kemih
Disuria (nyeri buang air kecil)
Masalah ejakulasi
Gaya hidup
Pasien harus mengurangi asupan cairan sebelum tidur, sedang konsumsi alkohol dan kafein mengandung produk, dan mengikuti jadwal berkemih waktunya.

Dua obat utama untuk manajemen BPH adalah alpha blockers dan 5α-reduktase inhibitor.

Alpha blocker (teknis α1-adrenergik antagonis reseptor) adalah pilihan yang paling umum untuk terapi awal di Amerika Serikat [15] [16] dan Eropa [17] Alpha blocker digunakan untuk BPH termasuk doxazosin, [18]. Terazosin, alfuzosin, [19 ] [20] tamsulosin, dan silodosin. Semua lima sama-sama efektif tetapi memiliki profil efek samping yang sedikit berbeda. [21] Obat-obatan yang lebih tua phenoxybenzamine dan prazosin tidak dianjurkan [22]. Alpha blocker rileks otot polos di prostat dan leher kandung kemih, sehingga mengurangi penyumbatan aliran urin. Efek samping yang umum dari alpha blockers termasuk hipotensi ortostatik, perubahan ejakulasi, hidung tersumbat, dan kelemahan. [Kutipan diperlukan]
Para 5α-reduktase inhibitor finasterida [23] dan dutasteride [24] adalah pilihan lain pengobatan. Obat-obat ini menghambat 5a-reduktase, yang pada gilirannya menghambat produksi DHT, hormon yang bertanggung jawab untuk memperbesar prostat. Efek mungkin memakan waktu lebih lama untuk muncul dari alpha blockers, tetapi mereka bertahan selama bertahun-tahun. [25] Ketika digunakan bersama dengan alpha blockers, penurunan perkembangan BPH untuk retensi urin akut dan pembedahan telah dicatat pada pasien dengan prostat yang lebih besar. [26] Efek samping termasuk penurunan libido dan ejakulasi atau disfungsi ereksi. [23]
Antimuscarinics seperti tolterodine juga dapat digunakan, terutama dalam kombinasi dengan alpha blockers [27]. Mereka bertindak dengan mengurangi efek asetilkolin pada otot polos kandung kemih, sehingga membantu mengendalikan gejala dari kandung kemih terlalu aktif. [Kutipan diperlukan]

Sildenafil sitrat menunjukkan beberapa bantuan gejala, menunjukkan etiologi umum mungkin dengan disfungsi ereksi. [28]

 Obat herbal
Orang sering mencari obat herbal untuk BPH [29]. Beberapa disetujui di negara-negara Eropa, tetapi tidak ada di Amerika Serikat. Saw palmetto ekstrak dari Serenoa repens adalah salah satu yang paling ekstensif dipelajari. Ini menunjukkan janji dalam studi awal, [30] meskipun percobaan kemudian kualitas metodologi yang lebih tinggi menunjukkan tidak ada perbedaan dari plasebo. [31] [32] [33] Tidak ada efek negatif diketahui saw palmetto, jadi jika mengambil suplemen mengurangi gejala, tidak ada salahnya dalam mengambil itu. Kualitas produk saw palmetto bervariasi [34].

Obat herbal lain yang memiliki dukungan penelitian di review sistematis termasuk beta-sitosterol [35] dari Hypoxis rooperi (Afrika rumput bintang) dan pygeum (diekstraksi dari kulit Prunus africana), [36] sementara ada kurang mendukung substansial untuk keberhasilan biji labu (Cucurbita pepo) dan jelatang menyengat (urtika dioica) akar. [37] Ada bukti lemah bahwa ekstrak serbuk sari FRP, rye rumput (Secale cereale) juga dapat berhubungan dengan bantuan gejala yang sederhana. [38]

Terapi minimal invasif
Obat ini sering diresepkan sebagai pilihan pengobatan pertama, ada banyak pasien yang tidak mencapai sukses dengan lini pengobatan. Pasien tidak dapat mencapai perbaikan berkelanjutan dalam gejala atau mereka mungkin berhenti minum obat karena efek samping [39]. Ada pilihan untuk pengobatan di kantor seorang urolog sebelum melanjutkan ke operasi. Dua jenis yang paling umum dari terapi kantor berbasis microwave transurethral thermotherapy (TUMT) dan ablasi jarum transurethral (TUNA). Kedua prosedur ini mengandalkan memberikan energi yang cukup untuk menciptakan panas yang cukup untuk menyebabkan kematian sel (nekrosis) dalam prostat. Tujuan dari terapi adalah untuk menyebabkan nekrosis cukup sehingga, ketika jaringan mati adalah diserap kembali oleh tubuh, menyusut prostat, menghilangkan obstruksi uretra. Prosedur ini biasanya dilakukan dengan anestesi lokal, dan pasien kembali pulang hari yang sama. Beberapa urolog telah mempelajari dan menerbitkan data jangka panjang pada hasil dari prosedur ini, dengan data keluar untuk lima tahun. Amerika paling baru Urological Association (AUA) Pedoman Pengobatan BPH pada tahun 2003 daftar terapi minimal invasif termasuk TUMT dan TUNA sebagai alternatif diterima untuk pasien tertentu dengan BPH. [40]

Terapi microwave transurethral (TUMT) awalnya disetujui oleh FDA pada tahun 1996, dengan sistem generasi pertama oleh EDAP Technomed. Sejak tahun 1996, perusahaan lain telah menerima persetujuan FDA untuk perangkat TUMT, termasuk Urologix, Dornier, Thermatrix, Celsion, dan Prostalund. Beberapa studi klinis telah dipublikasikan pada TUMT. Prinsip umum yang mendasari semua perangkat adalah bahwa antena microwave yang berada dalam sebuah kateter uretra ditempatkan di daerah intraprostatic uretra. Kateter terhubung ke kotak kontrol di luar tubuh pasien dan energi untuk memancarkan radiasi gelombang mikro ke dalam prostat untuk memanaskan jaringan dan nekrosis menyebabkan. Ini adalah pengobatan satu-waktu yang berlangsung sekitar 30 menit sampai 1 jam, tergantung pada sistem yang digunakan. Dibutuhkan sekitar 4 sampai 6 minggu untuk jaringan yang rusak diserap kembali ke dalam tubuh pasien. Beberapa perangkat menggabungkan beredar pendingin melalui area pengobatan dengan maksud melestarikan uretra sedangkan energi microwave memanaskan jaringan prostat di sekitarnya uretra.

Ablasi jarum transurethral (TUNA) beroperasi dengan berbagai jenis energi, energi frekuensi radio (RF), tetapi dirancang sepanjang premis yang sama sebagai perangkat TUMT, bahwa panas perangkat akan menyebabkan nekrosis menghasilkan dari jaringan prostat dan mengecilkan prostat. Perangkat TUNA dimasukkan ke dalam uretra menggunakan lingkup kaku seperti sebuah cystoscope. Energi diserahkan ke prostat menggunakan dua jarum yang muncul dari sisi perangkat, melalui dinding uretra dan masuk ke prostat. Jarum perangkat berbasis ablasi sangat efektif pada area lokal pemanasan dengan suhu yang cukup tinggi untuk menyebabkan nekrosis. Pengobatan ini biasanya dilakukan dalam satu sesi, tapi mungkin membutuhkan beberapa batang jarum tergantung pada ukuran prostat.

Jika perawatan medis gagal, dan pasien memilih untuk tidak mencoba kantor berbasis terapi atau dokter menentukan pasien adalah kandidat yang lebih baik untuk reseksi transurethral dari prostat (TURP), pembedahan mungkin perlu dilakukan. Secara umum, TURP masih dianggap standar emas intervensi prostat bagi pasien yang memerlukan prosedur. Hal ini melibatkan menghapus (bagian dari) prostat melalui uretra. Ada juga sejumlah metode baru untuk mengurangi ukuran pembesaran prostat, beberapa yang belum cukup lama untuk sepenuhnya membangun keselamatan mereka atau efek samping. Ini meliputi berbagai metode untuk menghancurkan atau menghapus bagian dari jaringan yang berlebihan ketika mencoba untuk menghindari kerusakan apa yang tersisa. Electrovaporization transurethral dari prostat (TVP), laser TURP, visual ablasi laser (VLAP), injeksi etanol, dan lain-lain dipelajari sebagai alternatif.

Teknik-teknik baru melibatkan laser dalam urologi telah muncul dalam 5-10 tahun terakhir, mulai dengan teknik VLAP melibatkan Nd: YAG laser dengan kontak pada jaringan prostat. Sebuah teknologi serupa yang disebut Penguapan Photoselective dari Prostat (PVT) dengan Greenlight tersebut (KTP) laser telah muncul baru-baru ini. Prosedur ini melibatkan daya tinggi-80-watt KTP laser dengan laser serat 550-micrometre dimasukkan ke dalam prostat. Serat ini memiliki refleksi internal dengan sudut 70 derajat membelokkan. Hal ini digunakan untuk menguapkan jaringan untuk kapsul prostat. KTP laser sasaran hemoglobin sebagai kromofor dan biasanya memiliki kedalaman penetrasi 2,0 mm (empat kali lebih dalam dari holmium).

Prosedur lain disebut Laser Ablation holmium Prostat (HOLAP) juga telah mendapatkan penerimaan di seluruh dunia. Seperti KTP, perangkat pengiriman untuk HOLAP prosedur adalah 550 mm pakai sisi-menembak serat yang mengarahkan balok dari daya tinggi-100-watt laser pada sudut 70 derajat dari sumbu serat. Panjang gelombang adalah 2.140 nm holmium, yang jatuh dalam bagian inframerah dari spektrum dan tidak terlihat dengan mata telanjang. Sedangkan KTP bergantung pada hemoglobin sebagai air, kromofor dalam jaringan target adalah kromofor untuk laser holmium. Kedalaman penetrasi holmium laser adalah <0,5 mm, menghindari komplikasi yang terkait dengan nekrosis jaringan sering ditemukan dengan penetrasi lebih dalam dan kekuatan puncak yang lebih rendah dari KTP.

HoLEP, holmium enukleasi Laser Prostat, adalah suatu prosedur holmium laser yang dilaporkan membawa risiko lebih sedikit dibandingkan dengan TURP baik atau prostatektomi terbuka [41] HoLEP sebagian besar serupa dengan prosedur HOLAP;. Perbedaan utama adalah bahwa prosedur ini biasanya dilakukan pada lebih besar prostat. Alih-alih terablasi jaringan, laser memotong sebagian dari prostat, yang kemudian dipotong-potong kecil dan memerah dengan cairan irigasi. Seperti prosedur HOLAP, ada sedikit perdarahan selama atau setelah prosedur.

Kedua panjang gelombang, KTP dan holmium, mengikis sekitar satu hingga dua gram jaringan per menit.

Perawatan pasca operasi sering melibatkan penempatan kateter Foley atau stent prostat sementara untuk memungkinkan penyembuhan dan memungkinkan urin mengalir dari kandung kemih.


Cacat-tahun hidup disesuaikan untuk benign prostatic hyperplasia per 100.000 penduduk pada tahun 2004. [42]

  tidak ada data
  kurang dari 20
  lebih dari 100
Prostat semakin besar pada kebanyakan pria ketika usia mereka bertambah, dan, secara keseluruhan, 45% pria di atas usia 46 dapat mengharapkan untuk menderita gejala BPH jika mereka bertahan hidup 30 tahun. Tingkat insiden meningkat dari 3 kasus per 1000 orang-tahun pada usia 45-49 tahun, menjadi 38 kasus per 1000 orang-tahun pada usia 75-79 tahun. Sedangkan angka prevalensi 2,7% untuk laki-laki berusia 45-49, itu meningkat menjadi 24% pada usia 80 tahun [43].

Bagi sebagian pria, gejala dapat cukup parah untuk memerlukan perawatan





Prostate cancer

Prostate Cancer
Classification and external resources

Micrograph of prostate adenocarcinoma, acinar type, the most common type of prostate cancer. Gleason pattern 4. Needle biopsy. H&E stain.
ICD-10 C61
ICD-9 185
OMIM 176807
DiseasesDB 10780
MedlinePlus 000380
eMedicine radio/574
MeSH D011471

Prostate cancer is a form of cancer that develops in the prostate, a gland in the male reproductive system. Most prostate cancers are slow growing; however, there are cases of aggressive prostate cancers.[1] The cancer cells may metastasize (spread) from the prostate to other parts of the body, particularly the bones and lymph nodes. Prostate cancer may cause pain, difficulty in urinating, problems during sexual intercourse, or erectile dysfunction. Other symptoms can potentially develop during later stages of the disease.

Rates of detection of prostate cancers vary widely across the world, with South and East Asia detecting less frequently than in Europe, and especially the United States.[2] Prostate cancer tends to develop in men over the age of fifty and although it is one of the most prevalent types of cancer in men, many never have symptoms, undergo no therapy, and eventually die of other causes. This is because cancer of the prostate is, in most cases, slow-growing, symptom-free, and since men with the condition are older they often die of causes unrelated to the prostate cancer, such as heart/circulatory disease, pneumonia, other unconnected cancers, or old age. About two-thirds of cases are slow growing, the other third more aggressive and fast developing.[3]

Many factors, including genetics and diet, have been implicated in the development of prostate cancer. The presence of prostate cancer may be indicated by symptoms, physical examination, prostate-specific antigen (PSA), or biopsy. The PSA test increases cancer detection but does not decrease mortality.[4] Moreover, prostate test screening is controversial at the moment and may lead to unnecessary, even harmful, consequences in some patients.[5] Nonetheless, suspected prostate cancer is typically confirmed by taking a biopsy of the prostate and examining it under a microscope. Further tests, such as CT scans and bone scans, may be performed to determine whether prostate cancer has spread.

Treatment options for prostate cancer with intent to cure are primarily surgery, radiation therapy, stereotactic radiosurgery, and proton therapy. Other treatments, such as hormonal therapy, chemotherapy, cryosurgery, and high intensity focused ultrasound (HIFU) also exist, although not FDA approved, depending on the clinical scenario and desired outcome.

The age and underlying health of the man, the extent of metastasis, appearance under the microscope, and response of the cancer to initial treatment are important in determining the outcome of the disease. The decision whether or not to treat localized prostate cancer (a tumor that is contained within the prostate) with curative intent is a patient trade-off between the expected beneficial and harmful effects in terms of patient survival and quality of life.

[edit] Overview

See also: Prostate

The prostate is a part of the male reproductive system that helps make and store seminal fluid. In adult men, a typical prostate is about three centimeters long and weighs about twenty grams.[6] It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation.[7] Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about twenty percent of the fluid constituting semen.[8] In prostate cancer, the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, which is converted from testosterone within the prostate itself. Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.


An important part of evaluating prostate cancer is determining the stage, or how far the cancer has spread. Knowing the stage helps define prognosis and is useful when selecting therapies. The most common system is the four-stage TNM system (abbreviated from Tumor/Nodes/Metastases). Its components include the size of the tumor, the number of involved lymph nodes, and the presence of any other metastases.[9]

The most important distinction made by any staging system is whether or not the cancer is still confined to the prostate. In the TNM system, clinical T1 and T2 cancers are found only in the prostate, while T3 and T4 cancers have spread elsewhere. Several tests can be used to look for evidence of spread. These include computed tomography to evaluate spread within the pelvis, bone scans to look for spread to the bones, and endorectal coil magnetic resonance imaging to closely evaluate the prostatic capsule and the seminal vesicles. Bone scans should reveal osteoblastic appearance due to increased bone density in the areas of bone metastasis—opposite to what is found in many other cancers that metastasize.

After a prostate biopsy, a pathologist looks at the samples under a microscope. If cancer is present, the pathologist reports the grade of the tumor. The grade tells how much the tumor tissue differs from normal prostate tissue and suggests how fast the tumor is likely to grow. The Gleason system is used to grade prostate tumors from 2 to 10, where a Gleason score of 10 indicates the most abnormalities. The pathologist assigns a number from 1 to 5 for the most common pattern observed under the microscope, then does the same for the second-most-common pattern. The sum of these two numbers is the Gleason score. The Whitmore-Jewett stage is another method sometimes used.

 Signs and symptoms

Early prostate cancer usually causes no symptoms. Often it is diagnosed during the workup for an elevated PSA noticed during a routine checkup.

Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria (painful urination).

Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the vas deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function and performance, such as difficulty achieving erection or painful ejaculation.[10]

Advanced prostate cancer can spread to other parts of the body, possibly causing additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis, or ribs. Spread of cancer into other bones such as the femur is usually to the proximal part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and urinary and fecal incontinence.[11]

[edit] Causes

The specific causes of prostate cancer remain unknown.[12] The primary risk factors are age and family history. Prostate cancer is very uncommon in men younger than 45, but becomes more common with advancing age. The average age at the time of diagnosis is 70.[13] However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have found prostate cancer in thirty percent of men in their 50s, and in eighty percent of men in their 70s.[14] Men who have first-degree family members with prostate cancer appear to have double the risk of getting the disease compared to men without prostate cancer in the family.[15] This risk appears to be greater for men with an affected brother than for men with an affected father. In the United States in 2005, there were an estimated 230,000 new cases of prostate cancer and 30,000 deaths due to prostate cancer.[16] Men with high blood pressure are more likely to develop prostate cancer.[17] A 2010 study found that prostate basal cells were the most common site of origin for prostate cancers.[18]


Genetic background may contribute to prostate cancer risk, as suggested by associations with race, family, and specific gene variants. Men who have a first-degree relative (father or brother) with prostate cancer have twice the risk of developing prostate cancer, and those with two first-degree relatives affected have a fivefold greater risk compared with men with no family history.[19] In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men.[20] [21] In contrast, the incidence and mortality rates for Hispanic men are one third lower than for non-Hispanic whites. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors.[22]

No single gene is responsible for prostate cancer; many different genes have been implicated. Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer.[23] Other linked genes include the Hereditary Prostate cancer gene 1 (HPC1), the androgen receptor, and the vitamin D receptor.[20] TMPRSS2-ETS gene family fusion, specifically TMPRSS2-ERG or TMPRSS2-ETV1/4 promotes cancer cell growth.[24]

Loss of cancer suppressor genes, early in the prostatic carcinogenesis, have been localized to chromosomes 8p, 10q, 13q,and 16q. P53 mutations in the primary prostate cancer are relatively low and are more frequently seen in metastatic settings, hence, p53 mutations are late event in pathology of prostate cancer. Other tumor suppressor genes that are thought to play a role in prostate cancer include PTEN (gene) and KAI1. “Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis”[25] Relative frequency of loss of E-cadherin and CD44 has also been observed.


While a number of dietary factors have been linked to prostate cancer the evidence is still tentative.[26] Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence.[27] Red meat and processed meat also appear to have little effect.[28] Lower blood levels of vitamin D may increase the risk of developing prostate cancer.[29] This may be linked to lower exposure to ultraviolet (UV) light, since UV light exposure can increase vitamin D in the body.[30]

Green tea may be protective (due to its catechins content),[31] although the most comprehensive clinical study indicates that it has no protective effect.[32] Other holistic methods are also studied.[33]

Taking multivitamins more than seven times a week may increase the risks of contracting the disease.[34][35] This research was unable to highlight the exact vitamins responsible for this increase (almost double), although they suggest that vitamin A, vitamin E and beta-carotene may lie at its heart. It is advised that those taking multivitamins never exceed the stated daily dose on the label.

Folic acid supplements have recently been linked to an increase in risk of developing prostate cancer.[36] A ten-year research study led by University of Southern California researchers showed that men who took daily folic acid supplements of 1 mg were three times more likely to be diagnosed with prostate cancer than men who took a placebo.[36]

High alcohol intake may increase the risk of prostate cancer and interfere with folate metabolism.[37] Low folate intake and high alcohol intake may increase the risk of prostate cancer to a greater extent than the sole effect of either one by itself.[37] A case control study consisting of 137 veterans addressed this hypothesis and the results were that high folate intake was related to a 79% lower risk of developing prostate cancer and there was no association between alcohol consumption by itself and prostate cancer risk.[37] Folate’s effect however was only significant when coupled with low alcohol intake.[37] There is a significant decrease in risk of prostate cancer with increasing dietary folate intake but this association only remains in individuals with low levels of alcohol consumption.[37] There was no association found in this study between folic acid supplements and risk of prostate cancer.[37]

 Medication exposure

There are also some links between prostate cancer and medications, medical procedures, and medical conditions.[38] Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.[39]

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood to the area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk.[40] Finally, obesity[41] and elevated blood levels of testosterone[42] may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer however more research is needed to determine if this is a causative relationship.[43]

Research released in May 2007, found that US war veterans who had been exposed to Agent Orange had a 48% increased risk of prostate cancer recurrence following surgery.[44]


In 2006, researchers associated a previously unknown retrovirus, Xenotropic MuLV-related virus or XMRV, with human prostate tumors.[45] Subsequent reports on the virus have been contradictory. A group of US researchers found XMRV protein expression in human prostate tumors,[46] while German scientists failed to find XMRV-specific antibodies or XMRV-specific nucleic acid sequences in prostate cancer samples.[47]


When normal cells are damaged beyond repair, they are eliminated by apoptosis. Cancer cells avoid apoptosis and continue to multiply in an unregulated manner.

Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time, these cancer cells begin to multiply and spread to the surrounding prostate tissue (the stroma) forming a tumor. Eventually, the tumor may grow large enough to invade nearby organs such as the seminal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells that can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, and may invade rectum, bladder and lower ureters after local progression. The route of metastasis to bone is thought to be venous as the prostatic venous plexus draining the prostate connects with the vertebral veins.[48]

The prostate is a zinc accumulating, citrate producing organ. The protein ZIP1 is responsible for the active transport of zinc into prostate cells. One of zinc’s important roles is to change the metabolism of the cell in order to produce citrate, an important component of semen. The process of zinc accumulation, alteration of metabolism, and citrate production is energy inefficient, and prostate cells sacrifice enormous amounts of energy (ATP) in order to accomplish this task. Prostate cancer cells are generally devoid of zinc. This allows prostate cancer cells to save energy not making citrate, and utilize the new abundance of energy to grow and spread. The absence of zinc is thought to occur via a silencing of the gene that produces the transporter protein ZIP1. ZIP1 is now called a tumor suppressor gene product for the gene SLC39A1. The cause of the epigenetic silencing is unknown. Strategies which transport zinc into transformed prostate cells effectively eliminate these cells in animals. Zinc inhibits NF-κB pathways, is anti-proliferative, and induces apoptosis in abnormal cells. Unfortunately, oral ingestion of zinc is ineffective since high concentrations of zinc into prostate cells is not possible without the active transporter, ZIP1.[49]

RUNX2 is a transcription factor that prevents cancer cells from undergoing apoptosis thereby contributing to the development of prostate cancer.[50]

The PI3k/Akt signaling cascade works with the transforming growth factor beta/SMAD signaling cascade to ensure prostate cancer cell survival and protection against apoptosis.[51] X-linked inhibitor of apoptosis (XIAP) is hypothesized to promote prostate cancer cell survival and growth and is a target of research because if this inhibitor can be shut down then the apoptosis cascade can carry on its function in preventing cancer cell proliferation.[52] Macrophage inhibitory cytokine-1 (MIC-1) stimulates the focal adhesion kinase (FAK) signaling pathway which leads to prostate cancer cell growth and survival.[53]

The androgen receptor helps prostate cancer cells to survive and is a target for many anti cancer research studies; so far, inhibiting the androgen receptor has only proven to be effective in mouse studies.[54] Prostate specific membrane antigen (PSMA) stimulates the development of prostate cancer by increasing folate levels for the cancer cells to use to survive and grow; PSMA increases available folates for use by hydrolyzing glutamated folates.[55]

 Early Detection and Diagnosis

The American Cancer Society’s position regarding early detection is “Research has not yet proven that the potential benefits of testing outweigh the harms of testing and treatment. The American Cancer Society believes that men should not be tested without learning about what we know and don’t know about the risks and possible benefits of testing and treatment. Starting at age 50, (45 if African American or brother or father suffered from condition before age 65) talk to your doctor about the pros and cons of testing so you can decide if testing is the right choice for you.”[56]

The only test that can fully confirm the diagnosis of prostate cancer is a biopsy, the removal of small pieces of the prostate for microscopic examination. However, prior to a biopsy, less invasive testing can be conducted.

According to Professor Hardev Pandha, The Prostate Project Chair of Urological Oncology at the University of Surrey’s Postgraduate Medical School, a non-invasive test looking for the presence of the protein Engrailed-2 (EN2) in the urine to be more reliable and accurate than existing tests.

“In this study, we showed that the new test was twice as good at finding prostate cancer as the standard PSA test. Only rarely did we find EN2 in the urine of men who were cancer free, so if we find EN2 we can be reasonably sure that a man has prostate cancer. EN2 was not detected in men with non-cancer disorders of the prostate such as prostatitis or benign enlargement. These conditions often cause a high PSA result, causing considerable stress for the patient and sometimes also unnecessary further tests such as prostate biopsies.” [57]

There are also several other tests that can be used to gather more information about the prostate and the urinary tract. Digital rectal examination (DRE) may allow a doctor to detect prostate abnormalities. Cystoscopy shows the urinary tract from inside the bladder, using a thin, flexible camera tube inserted down the urethra. Transrectal ultrasonography creates a picture of the prostate using sound waves from a probe in the rectum.

Prostate Imaging

Ultrasound (US) and Magnetic Resonance Imaging (MRI)are the two main imaging methods used for prostate cancer detection. Urologists use transrectal ultrasound during prostate biopsy and can sometimes see a hypoechoic area. But US has poor tissue resolution and thus, is generally not clinically used. In contrast, prostate MRI has superior soft tissue resolution. MRI is a type of imaging that uses magnetic fields to locate and characterize prostate cancer. Multi-parametric prostate MRI consists of four types of MRI sequences called T2 weighted imaging, T1 weighted imaging, Diffusion Weighted Imaging, MR Spectrocopic Imaging and Dynamic-Contrast Enhanced Imaging.[58] Genitourinary radiologists use multi-parametric MRI to locate and identify prostate cancer. Currently, MRI is used to identify targets for prostate biopsy using fusion MRI with ultrasound (US) or MRI-guidance alone. In men who are candidates for active surveillance, fusion MR/US guided prostate biopsy detected 33% of cancers compared to 7% with standard ultrasound guided biopsy. [59] Prostate MRI is also used for surgical planning for men undergoing robotic prostatectomy. It has also shown to help surgeons decide whether to resect or spare the neurovascular bundle, determine return to urinary continence and help assess surgical difficulty. [60]. Some prostate advocacy groups believe prostate MRI should be used to screen for prostate cancer–”manogram”– like mammogram is for breast cancer. [61]


Main article: Prostate biopsy

Micrograph showing a prostate cancer (conventional adenocarcinoma) with perineural invasion. H&E stain.

If cancer is suspected, a biopsy is offered expediently. During a biopsy a urologist or radiologist obtains tissue samples from the prostate via the rectum. A biopsy gun inserts and removes special hollow-core needles (usually three to six on each side of the prostate) in less than a second. Prostate biopsies are routinely done on an outpatient basis and rarely require hospitalization. Fifty-five percent of men report discomfort during prostate biopsy.[62]

Gleason score

Main article: Gleason score

The tissue samples are then examined under a microscope to determine whether cancer cells are present, and to evaluate the microscopic features (or Gleason score) of any cancer found. Prostate specific membrane antigen is a transmembrane carboxypeptidase and exhibits folate hydrolase activity.[36] This protein is overexpressed in prostate cancer tissues and is associated with a higher Gleason score.[36]

Tumor markers

Tissue samples can be stained for the presence of PSA and other tumor markers in order to determine the origin of malignant cells that have metastasized.[63]

Small cell carcinoma is a very rare (1%[64]) type of prostate cancer that cannot be diagnosed using the PSA.[64][65] As of 2009[update] researchers are trying to determine the best way to screen for this type of prostate cancer because it is a relatively unknown and rare type of prostate cancer but very serious and quick to spread to other parts of the body.[65] Possible methods include chromatographic separation methods by mass spectrometry, or protein capturing by immunoassays or immunized antibodies. The test method will involve quantifying the amount of the biomarker PCI, with reference to the Gleason Score. Not only is this test quick, it is also sensitive. It can detect patients in the diagnostic grey zone, particularly those with a serum free to total Prostate Specific Antigen ratio of 10-20%.[66]

The oncoprotein BCL-2, has been associated with the development of androgen-independent prostate cancer due to its high levels of expression in androgen-independent tumours in advanced stages of the pathology. The upregulation of BCL-2 after androgen ablation in prostate carcinoma cell lines and in a castrated-male rat model further established a connection between BCL-2 expression and prostate cancer progression.[67]

The expression of Ki-67 by immunohistochemistry may be a significant predictor of patient outcome for men with prostate cancer.[68]

ERK5 is a protein that may be used as a marker. ERK5 is present in abnormally high levels of prostate cancer, including invasive cancer which has spread to other parts of the body. It is also present in relapsed cancer following previous hormone therapy. Research shows that reducing the amount of ERK5 found in cancerous cells reduces their invasiveness.[69]


Prostate cancer screening is an attempt to find unsuspected cancers, and may lead to more specific follow-up tests such as a biopsy, with cell samples taken for closer study. Options include the digital rectal exam (DRE) and the prostate-specific antigen (PSA) blood test. Such screening is controversial and, in some patients, may lead to unnecessary, even harmful, consequences.[5] A 2010 analysis concluded that routine screening with either a DRE or PSA is not supported by the evidence as there is no mortality benefit from screening.[4] More recently, the United States Preventive Services Task Force (USPSTF) recommended against the PSA test for prostate cancer screening in healthy men.[70] This USPSTF recommendation, released in October 2011, is based on “review of evidence” studies concluding that “Prostate-specific antigen–based screening results in small or no reduction in prostate cancer–specific mortality and is associated with harms related to subsequent evaluation and treatments, some of which may be unnecessary.”[71]

Modern screening tests have found cancers that might never have developed into serious disease, and that “the slight reduction of risk by surgically removing the prostate or treating it with radiation may not outweigh the substantial side effects of these treatments,” an opinion also shared by the CDC.[72][73]


There is a significant relation between lifestyle (including food consumption) and cancer prevention.[74] Exercise and diet may help prevent prostate cancer to the same extent as may medications such as alpha-blockers and 5-alpha-reductase inhibitors.


Two medications which block the conversion of testosterone to dihydrotestosterone, finasteride[75] and dutasteride,[76] have also shown some promise. The use of these medications for primary prevention is still in the testing phase, and they are not widely used for this purpose. A 2008 study found that finasteride reduces the incidence of prostate cancer by 30%, without any increase in the risk of High-Grade prostate cancer.[77] In the original study it turns out that the smaller prostate caused by finasteride means that a doctor is more likely to hit upon cancer nests and more likely to find aggressive-looking cells.[77]

Compared to placebo treatment, taking 5-alpha-reductase inhibitors (5-ARIs) can reduce a man’s risk of being diagnosed with prostate cancer from around 5–9% to around 4-6% during up to 7 years of treatment, according to a Cochrane Review of studies.[78]

 Ejaculation frequency

More frequent ejaculation also may decrease a man’s risk of prostate cancer. One study showed that men who ejaculated 3-5 times a week at the age of 15-19 had a decreased rate of prostate cancer when they are old, though other studies have shown no benefit.[79][80] The results contradict those of previous studies, that suggested that having many sexual partners, or a high frequency of sexual activity, increases the risk of prostate cancer by up to 40 percent. A key difference may be that these earlier studies defined sexual activity as sexual intercourse, whereas this study focused on the number of ejaculations, whether or not intercourse was involved.[81] Another study completed in 2004 reported that “Most categories of ejaculation frequency were unrelated to risk of prostate cancer. However, high ejaculation frequency was related to decreased risk of total prostate cancer.” The report abstract concluded, “Our results suggest that ejaculation frequency is not related to increased risk of prostate cancer.”[82]


Consuming fish appears to lower prostate cancer deaths but not the occurrence of prostate cancer.[83] Omega-3 fatty acids are unlikely to prevent prostate cancer.[84] There is no evidence that vitamin supplements affect risk.[85] Trans fats may be associated with an increased risk of cancer but the evidence is still limited.[86] The American Dietetic Association and Dieticians of Canada report a decreased incidence of prostate cancer for those following a vegetarian diet.[87]


Treatment for prostate cancer may involve active surveillance (monitoring for tumor progress or symptoms), surgery (i.e. radical prostatectomy), radiation therapy including brachytherapy (prostate brachytherapy) and external beam radiation therapy, High-intensity focused ultrasound (HIFU), chemotherapy, oral chemotherapeutic drugs (Temozolomide/TMZ), cryosurgery, hormonal therapy, or some combination.[88][89][90] William J. Catalona, MD: regarding Active Surveillance, “Watchful Waiting or for some patients, Wishful Waiting: Can delay prompt treatment of life-threatening tumors, it would require repeated biopsies that often make subsequent nerve-sparing surgery more difficult and it causes many patients anxiety about living with untreated cancer, thus diminishing their quality of life.” These men may have already been chemically castrated and impotent.

Which option is best depends on the stage of the disease, the Gleason score, and the PSA level. Other important factors are age, general health, and patient views about potential treatments and their possible side-effects. Because all treatments can have significant side-effects, such as erectile dysfunction and urinary incontinence, treatment discussions often focus on balancing the goals of therapy with the risks of lifestyle alterations. Prostate cancer patients are strongly recommended to work closely with their physicians and use a combination of the treatment options when managing their prostate cancer.[91][92][93]

Because of PSA screening, almost 90% of patients are diagnosed when the cancer is localized to the prostate gland and its removal by surgery or radiotherapy will in most cases lead to a cure. Because of this almost 94% of U.S. patients choose treatment. However, in 50% to 75% of these patients the cancer would not have affected their survival even without treatment, and by accepting treatment they have a high chance of sexual, urinary, and bowel side effects. For instance, two-thirds of treated patients cannot get sufficient erections for intercourse, and almost a third have urinary leakage. However, some cancers will grow faster and prostate cancer is the second most common reason of cancer death in U.S. men, after lung cancer. Even the most intelligent and educated patient faces this uncertainty, and 1 in 6 men will be diagnosed with prostate cancer in their life time. The National Comprehensive Cancer Network (NCCN) offers annually updated and the most evidence-based guidelines for prostate cancer, as for all cancers, that can help newly-diagnosed and established patients to choose the best option for their specific clinical situation. For prostate cancer the NCCN guideline has been rated the most highly. However, all guidelines including the NCCN guideline need a good estimation of the patient’s long-term health-adjusted life expectancy, because this factor is the most important determinant of survival in newly diagnosed patients. Primary care physicians and urologists find it hard to make this estimate – which might be the reason why guidelines are not used even though the treatment choice is so complex. An easy and evidence-based approach ([94] to decision-making has been published in the August 15, 2011 issue of the American Family Physician, the most commonly read journal in primary care. The authors have shown how to estimate health-adjusted life expectancy and have simplified NCCN guidelines so that patients can have a roadmap to reach the decision recommended for their clinical situation from where they can use personal preferences based on side-effect profiles of different treatment options. Patients can use a newly-developed 18-item questionnaire to find if they have good knowledge and understanding about treatment options before they choose an option; over half of 184 surveyed patients who had been newly-diagnosed and had already met with their urologist after the diagnosis and had chosen a treatment option could not correctly answer over half of questions even though 90% patients had good health literacy and over 60% were college-educated. The authors have also provided a one-page patient information handout.

Although the widespread use of prostate specific antigen (PSA) screening in the USA has resulted in diagnosis at earlier age and cancer stage, the vast majority of cases are still diagnosed in men older than 65 years, and approximately 25% of cases are diagnosed in men older than 75 years.[95] Though US National Comprehensive Cancer Network guidelines[96] recommend using life expectancy greater than or less than 10 years to help make treatment decisions, in practice, many elderly patients are not offered curative treatment options such as radical prostatectomy (RP) or radiation therapy and are instead treated with hormonal therapy or watchful waiting. This pattern can be attributed to factors such as medical co-morbidity and patient preferences is regard to quality of life in addition to prostate cancer specific risk factors such as pretreatment PSA, Gleason score and clinical stage. As the average life expectancy increases due to advances in treatment of cardiovascular, pulmonary and other chronic disease, it is likely that more elderly patients will be living long enough to suffer the consequences of their prostate cancer. Therefore, there is currently much interest in the role of aggressive prostate cancer treatment modalities such as with surgery or radiation in the elderly population who have localized disease. The results of one randomized controlled trial published by the Scandinavian Prostate Cancer Group 4 [97] evaluated cancer-specific mortality in patients treated with RP compared with watchful waiting. The patients receiving radical prostatectomy had a relative risk reduction of 30.7% [95% confidence interval 2.5%-50.7%], but an absolute risk reduction of 6% [95% confidence interval 0.5%-11.5%]. The number needed to treat was calculated to be 16. This means that, over the median follow up period of approximately 10 years, 16 patients with localized prostate cancer would need to receive radical prostatectomy rather than watchful waiting in order to prevent one death due to prostate cancer. Further subset analysis revealed that this benefit did not apply to all ages equally. In men younger than 65 years, patients randomized to receive radical prostatectomy actually had a 10-18% absolute risk reduction in cancer-specific mortality compared to those randomized to watchful waiting. However, in men older than 65, there was no statistically significant risk reduction even when adjusted for PSA level, Gleason score and tumor stage. Randomized, controlled trials comparing radical prostatectomy, radiation therapy, hormonal therapy and watchful waiting would provide the best evidence for how to best treat elderly patients. Such trials are urgently needed, as the elderly population is rapidly growing and is expected to continue to do so. Study results in 2011 suggest active surveillance is the best choice for older ‘low-risk’ patients.[98]

The selection of treatment options may be a complex decision involving many factors. For example, radical prostatectomy after primary radiation failure is a very technically challenging surgery and may not be an option, while salvage radiation therapy after surgical failure may have many complications.[99] This may enter into the treatment decision.

If the cancer has spread beyond the prostate, treatment options significantly change, so most doctors that treat prostate cancer use a variety of nomograms to predict the probability of spread. Treatment by watchful waiting/active surveillance, external beam radiation therapy, brachytherapy, cryosurgery, HIFU, and surgery are, in general, offered to men whose cancer remains within the prostate. Hormonal therapy and chemotherapy are often reserved for disease that has spread beyond the prostate. However, there are exceptions: radiation therapy may be used for some advanced tumors, and hormonal therapy is used for some early stage tumors. Cryotherapy (the process of freezing the tumor), hormonal therapy, and chemotherapy may also be offered if initial treatment fails and the cancer progresses.[100]

Castration-resistant prostate cancer

Most hormone dependent cancers become refractory after one to three years and resume growth despite hormone therapy. Previously considered “hormone-refractory prostate cancer” or “androgen-independent prostate cancer”, the term castration-resistant has replaced “hormone refractory” because while they are no longer responsive to castration treatment (reduction of available androgen/testosterone/DHT by chemical or surgical means), these cancers still show reliance upon hormones for androgen receptor activation.[101] Before 2004, all treatments for castration-resistant prostate cancer (CRPC) were considered[who?] palliative and not shown to prolong survival.[citation needed] However, there are now several treatments available to treat CRPC that improve survival.

The cancer chemotherapic docetaxel has been used as treatment for (CRPC) with a median survival benefit of 2 to 3 months.[102][103] Docetaxel’s FDA approval in 2004 was significant as it was the first treatment proven to prolong survival in CRPC. In 2010, the FDA approved a second-line chemotherapy treatment known as cabazitaxel.[104]

Off-label use of the oral drug ketoconazole is sometimes used as a way to further manipulate hormones with a therapeutic effect in CRPC. However, many side effects are possible with this drug and abiraterone is likely to supplant usage since it has a similar mechanism of action with less toxic side effects.

A combination of bevacizumab (Avastin), docetaxel, thalidomide and prednisone appears effective in the treatment of CRPC.[105]

The immunotherapy treatment with sipuleucel-T is also effective in the treatment of CRPC with a median survival benefit of 4.1 months.[106]

The second line hormonal therapy abiraterone (Zytiga) completed a phase 3 trial for CRPC patients who have failed chemotherapy in 2010. Results were positive with overall survival increased by 4.6 months when compared to placebo. On April 28, 2011, the U.S. Food and Drug Administration approved abiraterone acetate in combination with prednisone to treat patients with late-stage (metastatic) castration-resistant prostate cancer who have received prior docetaxel (chemotherapy).[107]

Alpharadin completed a phase 3 trial for CRPC patients with bone metastasis. A pre-planned interim analysis showed improved survival and quality of life. The study was stopped for ethical reasons to give the placebo group the same treatment. Apharadin uses bone targeted Radium-223 isotopes to kill cancer cells by alpha radiation. Alpharadin is an investigational agent and is not approved for marketing by the European Medicines Agency (EMA), the U.S. Food and Drug Administration (FDA), or any other health authorities.[108]

There are also several treatments currently in clinical trials to treat CRPC. These include the 2nd generation hormonal therapies MDV3100 and orteronel (TAK-700), the immunotherapy PROSTVAC, and the bone metastasis-targeting cabozantinib (XL-184).


Prostate cancer rates are higher and prognosis poorer in developed countries than the rest of the world. Many of the risk factors for prostate cancer are more prevalent in the developed world, including longer life expectancy and diets high in red meat. (People who consume larger amounts of meat and dairy also tend to consume fewer portions of fruits and vegetables. It is not currently clear whether both of these factors, or just one of them, contribute to the occurrence of prostate cancer.[109]) Also, where there is more access to screening programs, there is a higher detection rate. Prostate cancer is the ninth-most-common cancer in the world, but is the number-one non-skin cancer in men from the United States. Prostate cancer affected eighteen percent of American men and caused death in three percent in 2005.[110] In Japan, death from prostate cancer was one-fifth to one-half the rates in the United States and Europe in the 1990s.[111] In India in the 1990s, half of the people with prostate cancer confined to the prostate died within ten years.[112] African-American men have 50–60 times more prostate cancer and prostate cancer deaths than men in Shanghai, China.[113] In Nigeria, two percent of men develop prostate cancer, and 64% of them are dead after two years.[114]

In patients who undergo treatment, the most important clinical prognostic indicators of disease outcome are stage, pre-therapy PSA level, and Gleason score. In general, the higher the grade and the stage, the poorer the prognosis. Nomograms can be used to calculate the estimated risk of the individual patient. The predictions are based on the experience of large groups of patients suffering from cancers at various stages.[115]

In 1941, Charles Huggins reported that androgen ablation therapy causes regression of primary and metastatic androgen-dependent prostate cancer.[116] He was awarded the 1966 Nobel Prize for Physiology or Medicine for this discovery. Androgen ablation therapy causes remission in 80-90% of patients undergoing therapy, resulting in a median progression-free survival of 12 to 33 months. After remission, an androgen-independent phenotype typically emerges, wherein the median overall survival is 23–37 months from the time of initiation of androgen ablation therapy.[117] The actual mechanism contributes to the progression of prostate cancer is not clear and may vary between individual patient. A few possible mechanisms have been proposed.[118]

Classification systems

Many prostate cancers are not destined to be lethal, and most men will ultimately die from causes other than of the disease. Decisions about treatment type and timing may, therefore, be informed by an estimation of the risk that the tumor will ultimately recur after treatment and/or progress to metastases and mortality. Several tools are available to help predict outcomes, such as pathologic stage and recurrence after surgery or radiation therapy. Most combine stage, grade, and PSA level, and some also add the number or percent of biopsy cores positive, age, and/or other information.

  • The D’Amico classification stratifies men by low, intermediate, or high risk based on stage, grade, and PSA. It is used widely in clinical practice and research settings. The major downside to the 3-level system is that it does not account for multiple adverse parameters (e.g., high Gleason score and high PSA) in stratifying patients.
  • The Partin tables predict pathologic outcomes (margin status, extraprostatic extension, and seminal vesicle invasion) based on the same three variables and are published as lookup tables.
  • The Kattan nomograms predict recurrence after surgery and/or radiation therapy, based on data available either at time of diagnosis or after surgery. The nomograms can be calculated using paper graphs or software available on a website or for handheld computers. The Kattan score represents the likelihood of remaining free of disease at a given time interval following treatment.
  • The UCSF Cancer of the Prostate Risk Assessment (CAPRA) score predicts both pathologic status and recurrence after surgery. It offers comparable accuracy as the Kattan preoperative nomogram, and can be calculated without paper tables or a calculator. Points are assigned based on PSA, Grade, stage, age, and percent of cores positive; the sum yields a 0–10 score, with every 2 points representing roughly a doubling of risk of recurrence. The CAPRA score was derived from community-based data in the CaPSURE database. It has been validated among over 10,000 prostatectomy patients, including patients from CaPSURE;[119] the SEARCH registry, representing data from several Veterans Administration and active military medical centers;[120] a multi-institutional cohort in Germany;[121] and the prostatectomy cohort at Johns Hopkins University.[122] More recently, it has been shown to predict metastasis and mortality following prostatectomy, radiation therapy, watchful waiting, or androgen deprivation therapy.[123]


Age-standardized death from prostate cancer per 100,000 inhabitants in 2004.[124]

  no data
  less than 4
  more than 44

Rates of prostate cancer vary widely across the world. Although the rates vary widely between countries, it is least common in South and East Asia, more common in Europe, and most common in the United States.[2] According to the American Cancer Society, prostate cancer is least common among Asian men and most common among black men, with figures for white men in between.[125][126] The average annual incidence rate of prostate cancer between 1988 and 1992 among Chinese men in the United States was 15 times higher than that of their counterparts living in Shanghai and Tianjin.[125][126][127] However, these high rates may be affected by increasing rates of detection.[128] Many suggest that prostate cancer may be under reported, yet BPH incidence in China and Japan is similar to rates in Western countries.,[129][130]

Prostate cancer develops primarily in men over fifty. It is the most common type of cancer in men in the United States, with 186,000 new cases in 2008 and 28,600 deaths.[131] It is the second leading cause of cancer death in U.S. men after lung cancer. In the United Kingdom it is also the second most common cause of cancer death after lung cancer, where around 35,000 cases are diagnosed every year and of which around 10,000 die of it. Many factors, including genetics and diet, have been implicated in the development of prostate cancer. The Prostate Cancer Prevention Trial found that finasteride reduces the incidence of prostate cancer by 30%. There had been a controversy about this also increasing the risk of more aggressive cancers, but more recent research showed this may not be the case.[77][132]

More than 80% of men will develop prostate cancer by the age of 80.[133] However, in the majority of cases, it will be slow-growing and harmless. In such men, diagnosing prostate cancer is overdiagnosis—the needless identification of a technically aberrant condition that will never harm the patient—and treatment in such men exposes them to all of the adverse effects, with no possibility of extending their lives.[134]


Although the prostate was first described by Venetian anatomist Niccolò Massa in 1536, and illustrated by Flemish anatomist Andreas Vesalius in 1538, prostate cancer was not identified until 1853.[135] Prostate cancer was initially considered a rare disease, probably because of shorter life expectancies and poorer detection methods in the 19th century. The first treatments of prostate cancer were surgeries to relieve urinary obstruction.[136] Removal of the entire gland (radical perineal prostatectomy) was first performed in 1904 by Hugh H. Young at Johns Hopkins Hospital.[137] Surgical removal of the testes (orchiectomy) to treat prostate cancer was first performed in the 1890s, but with limited success. Transurethral resection of the prostate (TURP) replaced radical prostatectomy for symptomatic relief of obstruction in the middle of the 20th century because it could better preserve penile erectile function. Radical retropubic prostatectomy was developed in 1983 by Patrick Walsh.[138] This surgical approach allowed for removal of the prostate and lymph nodes with maintenance of penile function.

In 1941, Charles B. Huggins published studies in which he used estrogen to oppose testosterone production in men with metastatic prostate cancer. This discovery of “chemical castration” won Huggins the 1966 Nobel Prize in Physiology or Medicine.[139] The role of the hormone GnRH in reproduction was determined by Andrzej W. Schally and Roger Guillemin, who both won the 1977 Nobel Prize in Physiology or Medicine for this work.

Receptor agonists, such as leuprolide and goserelin, were subsequently developed and used to treat prostate cancer.[140][141]

Radiation therapy for prostate cancer was first developed in the early 20th century and initially consisted of intraprostatic radium implants. External beam radiation became more popular as stronger radiation sources became available in the middle of the 20th century. Brachytherapy with implanted seeds was first described in 1983.[142]

Systemic chemotherapy for prostate cancer was first studied in the 1970s. The initial regimen of cyclophosphamide and 5-fluorouracil was quickly joined by multiple regimens using a host of other systemic chemotherapy drugs.[143]

On 30 July 2010 Owen Witte M.D. et al. of UCLA published a series of studies in Science during which they had introduced viruses known to cause cancerous mutation in prostate cells: AKT, ERG, and AR into isolated samples of basal and luminal cells and grafted the treated tissue into mice. After 16 weeks, none of the luminal samples had undergone malignant mutation, while the basal samples had mutated into prostate-like tubules which had then developed malignancy and formed cancerous tumors, which appeared identical to human samples under magnification. This led to the conclusion that the prostate basal cell may be the most likely “site of origin” of prostate cancer.[144]

Society and culture


People with prostate cancer generally encounter significant disparities in awareness, funding, media coverage, and research—and therefore, inferior treatment and poorer outcomes—compared to other cancers of equal prevalence.[145] In 2001 The Guardian noted that Britain had 3,000 nurses specializing in breast cancer, compared to only one for prostate cancer. It also discovered that the waiting time between referral and diagnosis was two weeks for breast cancer but three months for prostate cancer.[146] A 2007 report by The National Prostate Cancer Coalition stated that for every prostate cancer drug on the market, there were seven used to treat breast cancer. The Times also noted an “anti-male bias in cancer funding” with a four to one discrepancy in the United Kingdom by both the government and by cancer charities such as Cancer Research UK.[145][147] Equality campaigners such as author Warren Farrell cite such stark spending inequalities as a clear example of governments unfairly favouring women’s health over men’s health.[148]

Disparities also extend into areas such as detection, with governments failing to fund or mandate prostate cancer screening while fully supporting breast cancer programs. For example, a 2007 report found 49 U.S. states mandate insurance coverage for routine breast cancer screening, compared to 28 for prostate cancer.[145][149] Prostate cancer also experiences significantly less media coverage than other, equally prevalent cancers, with a study by Prostate Coalition showing 2.6 breast cancer stories for each one covering cancer of the prostate.[145]

Prostate cancer awareness month

Prostate cancer awareness month takes place in September in a number of countries. A blue ribbon is used to promote the cause.[150][151]


Androgen at a concentration of 10-fold higher than the physiological concentration has also been shown to cause growth suppression and reversion of androgen-independent prostate cancer xenografts or androgen-independent prostate tumors derived in vivo model to an androgen-stimulated phenotype in athymic mice.[152][153] These observation suggest the possibility to use androgen to treat the development of relapsed androgen-independent prostate tumors in patients.

Oral infusion of green tea catechins, a potential alternative therapy for prostate cancer by natural compounds, has been shown to inhibit the development, progression, and metastasis as well in autochthonous transgenic adenocarcinoma of the mouse prostate (TRAMP) model, which spontaneously develops prostate cancer.[154]

The insulin-like growth factor signaling axis is thought to play a key role in the progression of prostate carcinoma. It consists of two ligands (IGF-1 and IGF-2), two receptors (IGF-IR and IGF-IIR) and six related high-affinity IGF-binding proteins (IGFBP 1-6).[155] Altered expression of IGF axis members has been implicated in the development of many different types of cancers, including prostate.[156][157]

A genistein derivative KBU2046 is under investigation for prostate cancer.[158] MDV3100 is in phase III trials for HRPC (chemo-naive and post-chemo patient populations).[159]

 Prostate cancer models

Scientists have established a few prostate cancer cell lines to investigate the mechanism involved in the progression of prostate cancer. LNCaP, PC-3 (PC3), and DU-145 (DU145) are commonly used prostate cancer cell lines. The LNCaP cancer cell line was established from a human lymph node metastatic lesion of prostatic adenocarcinoma. PC-3 and DU-145 cells were established from human prostatic adenocarcinoma metastatic to bone and to brain, respectively. LNCaP cells express androgen receptor (AR); however, PC-3 and DU-145 cells express very little or no AR. AR, an androgen-activated transcription factor, belongs to the steroid nuclear receptor family. Development of the prostate is dependent on androgen signaling mediated through AR, and AR is also important during the development of prostate cancer. The proliferation of LNCaP cells is androgen-dependent but the proliferation of PC-3 and DU-145 cells is androgen-insensitive. Elevation of AR expression is often observed in advanced prostate tumors in patients.[160][161] Some androgen-independent LNCaP sublines have been developed from the ATCC androgen-dependent LNCaP cells after androgen deprivation for study of prostate cancer progression. These androgen-independent LNCaP cells have elevated AR expression and express prostate specific antigen upon androgen treatment. The paradox is that androgens inhibit the proliferation of these androgen-independent prostate cancer cells.[162][163][164]


At present, an active area of research and non-clinically applied investigations involve non-invasive methods of prostate tumor detection. Adenoviruses modified to transfect tumor cells with harmless yet distinct genes (such as luciferase) have proven capable of early detection. So far, however, this area of research has been tested only in animal and LNCaP cell models.[165]


Presence of the EN2 (gene) in urine has been correlated to a high probability of prostate cancer.[166] Co-researchers Hardev Pandha, and Richard Morgan published their findings in the 1 March 2011 issue of the journal Clinical Cancer Research.[167] A laboratory test currently identifies EN2 in urine, and a home test kit is envisioned similar to a home pregnancy test strip. According to Morgan, “We are preparing several large studies in the UK and in the US and although the EN2 test is not yet available, several companies have expressed interest in taking it forward.” [168]


Another potential non-invasive method of early prostate tumor detection is through a molecular test that detects the presence of cell-associated PCA3 mRNA in fluid massaged from the prostate by the doctor and first-void urinated out within a limited amount of urine into the specimen container. PCA3 mRNA is expressed almost exclusively by prostate cells and has been shown to be highly over-expressed in prostate cancer cells. The test result is currently reported as a specimen ratio of PCA3 mRNA to PSA mRNA. Although not a replacement for serum PSA level, the PCA3 test is an additional tool to help decide whether, in men suspected of having prostate cancer (especially if an initial biopsy fails to explain the elevated serum PSA), a biopsy/rebiopsy is really needed. The higher the expression of PCA3 in the sample, the greater the likelihood of a positive biopsy; i.e., the presence of cancer cells in the prostate.

Early prostate cancer antigen-2

It was reported in April 2007 that research is being conducted on a new blood test for early prostate cancer antigen-2 (EPCA-2) that may alert men if they have prostate cancer and how aggressive it will be.[169][170]

Thrombophlebitis is associated with an increased risk of prostate cancer and may be a good way for physicians to remind themselves to screen patients with thrombophlebitis for prostate cancer as well since these two are closely linked.[171]


Epithelial cells of the prostate secrete prostasomes as well as PSA. Prostasomes are membrane–surrounded, prostate-derived organelles that appear extracellularly, and one of their physiological functions is to protect the sperm from attacks by the female immune system. Cancerous prostate cells continue to synthesize and secrete prostasomes, and may be shielded against immunological attacks by these prostasomes. Research of several aspects of prostasomal involvement in prostate cancer has been performed

Indonesia version

Kanker Prostat
Klasifikasi dan sumber daya eksternal

Mikrograf adenokarsinoma prostat, asinar jenis, jenis yang paling umum dari kanker prostat. Gleason pola 4. Biopsi jarum. H & E noda.
ICD-10 C61
ICD-9 185
OMIM 176807
DiseasesDB 10780
MedlinePlus 000380
eMedicine radio/574
MESH D011471

Kanker prostat adalah bentuk kanker yang berkembang di prostat, sebuah kelenjar dalam sistem reproduksi laki-laki. Kanker prostat paling lambat tumbuh, namun, ada kasus-kasus kanker prostat agresif [1] Sel-sel kanker dapat bermetastasis (menyebar) dari prostat ke bagian lain dari tubuh, khususnya tulang dan kelenjar getah bening.. Kanker prostat dapat menyebabkan rasa sakit, kesulitan dalam buang air kecil, masalah selama hubungan seksual, atau disfungsi ereksi. Gejala lain yang berpotensi dapat mengembangkan selama tahap-tahap akhir dari penyakit.

Tingkat deteksi kanker prostat sangat bervariasi di seluruh dunia, dengan Asia Selatan dan Timur mendeteksi lebih jarang daripada di Eropa, dan terutama Amerika Serikat [2] Kanker prostat cenderung untuk mengembangkan pada pria di atas usia lima puluh dan meskipun. Ini adalah salah satu jenis yang paling umum dari kanker pada pria, banyak yang tidak pernah memiliki gejala, menjalani terapi tidak ada, dan akhirnya meninggal karena penyebab lain. Hal ini karena kanker prostat adalah, dalam banyak kasus, lambat tumbuh, gejala-bebas, dan karena laki-laki dengan kondisi lebih tua mereka sering meninggal karena penyebab yang tidak terkait dengan kanker prostat, seperti jantung / penyakit peredaran darah, radang paru-paru, lainnya tidak berhubungan kanker, atau usia tua. Sekitar dua-pertiga kasus lambat tumbuh, ketiga lainnya lebih agresif dan cepat berkembang [3].

Banyak faktor, termasuk genetika dan diet, telah terlibat dalam perkembangan kanker prostat. Kehadiran kanker prostat dapat diindikasikan dengan gejala-gejala, pemeriksaan fisik, antigen spesifik prostat-(PSA), atau biopsi. Tes PSA meningkatkan deteksi kanker tetapi tidak menurunkan angka kematian [4]. Selain itu, tes skrining prostat adalah kontroversial saat ini dan dapat menyebabkan tidak perlu, bahkan berbahaya, konsekuensi pada beberapa pasien. [5] Meskipun demikian, diduga kanker prostat biasanya dikonfirmasi dengan mengambil biopsi prostat dan memeriksanya di bawah mikroskop. Tes lebih lanjut, seperti CT scan dan scan tulang, dapat dilakukan untuk menentukan apakah kanker prostat telah menyebar.

Pilihan pengobatan untuk kanker prostat dengan maksud untuk menyembuhkan terutama pembedahan, terapi radiasi, radiosurgery stereotactic, dan terapi proton. Pengobatan lain, seperti terapi hormonal, kemoterapi, cryosurgery, dan intensitas tinggi terfokus USG (HIFU) juga ada, meskipun tidak disetujui FDA, tergantung pada skenario klinis dan hasil yang diinginkan.

Usia dan kesehatan mendasar dari manusia, sejauh mana metastasis, penampilan di bawah mikroskop, dan respon kanker terhadap pengobatan awal adalah penting dalam menentukan hasil dari penyakit. Keputusan apakah atau tidak untuk mengobati kanker prostat lokal (suatu tumor yang terkandung dalam prostat) dengan maksud penyembuhan adalah trade off-pasien antara efek menguntungkan dan merugikan yang diharapkan dalam hal kelangsungan hidup pasien dan kualitas hidup.


Prostat adalah bagian dari sistem reproduksi laki-laki yang membantu membuat dan menyimpan cairan seminal. Pada pria dewasa, prostat tipikal adalah sekitar tiga sentimeter panjang dan berat sekitar dua puluh gram [6]. Hal ini terletak di panggul, di bawah kandung kemih dan di depan rektum. Prostat mengelilingi bagian dari urethra, tabung yang membawa urin dari kandung kemih saat buang air kecil dan air mani saat ejakulasi [7] Karena lokasinya, prostat sering mempengaruhi penyakit kencing, ejakulasi, dan jarang buang air besar.. Berisi kelenjar prostat kecil yang membuat sekitar dua puluh persen dari cairan mani yang merupakan [8] Pada kanker prostat, sel-sel kelenjar prostat ini bermutasi menjadi sel kanker.. Kelenjar prostat memerlukan hormon laki-laki, yang dikenal sebagai androgen, untuk bekerja dengan baik. Androgen termasuk testosteron, yang dibuat di testis, dehydroepiandrosterone, yang dibuat di kelenjar adrenal, dan dihidrotestosteron, yang dikonversi dari testosteron dalam prostat itu sendiri. Androgen juga bertanggung jawab untuk karakteristik seks sekunder seperti rambut wajah dan massa otot meningkat.

Artikel utama: Manajemen kanker prostat
Pengobatan untuk kanker prostat mungkin melibatkan surveilans aktif (pemantauan untuk kemajuan tumor atau gejala), operasi (yaitu prostatektomi radikal), terapi radiasi termasuk brachytherapy (brachytherapy prostat) dan terapi radiasi sinar eksternal, intensitas tinggi terfokus USG (HIFU), kemoterapi, lisan obat-obat kemoterapi (Temozolomide / TMZ), cryosurgery, terapi hormonal, atau beberapa kombinasi [88] [89] [90] William J. Catalona, ​​MD:. tentang Pengawasan aktif, “Menunggu Waspada atau untuk beberapa pasien, Menunggu Wishful: Dapatkah keterlambatan perawatan segera dari kehidupan-mengancam tumor, itu akan memerlukan biopsi berulang yang sering membuat selanjutnya saraf-sparing lebih sulit dan hal itu menyebabkan kecemasan banyak pasien tentang hidup dengan kanker tidak diobati, sehingga mengurangi kualitas hidup mereka. ” Orang-orang ini mungkin telah dikebiri dan tidak berdaya kimia.

Pilihan mana yang terbaik tergantung pada tahap penyakit, skor Gleason, dan tingkat PSA. Faktor penting lainnya adalah usia, kesehatan umum, dan pandangan pasien tentang perawatan potensial dan kemungkinan efek samping. Karena semua perawatan dapat memiliki efek samping yang signifikan, seperti disfungsi ereksi dan inkontinensia urin, diskusi pengobatan sering fokus pada menyeimbangkan tujuan terapi dengan risiko perubahan gaya hidup. Kanker prostat pasien sangat dianjurkan untuk bekerja sama dengan dokter mereka dan menggunakan kombinasi pilihan pengobatan kanker prostat ketika mengelola mereka [91] [92] [93].

Karena skrining PSA, hampir 90% dari pasien yang didiagnosis ketika kanker terlokalisasi kelenjar prostat dan penghapusan dengan pembedahan atau radioterapi di kebanyakan kasus akan mengarah untuk menyembuhkan. Karena ini hampir 94% dari pasien AS memilih pengobatan. Namun, dalam 50% sampai 75% dari pasien kanker tidak akan terpengaruh kelangsungan hidup mereka bahkan tanpa pengobatan, dan dengan menerima perlakuan mereka memiliki kesempatan tinggi seksual, urin, dan efek samping usus. Sebagai contoh, dua pertiga dari pasien yang diobati tidak bisa mendapatkan ereksi yang cukup untuk melakukan hubungan, dan hampir sepertiga memiliki kebocoran kemih. Namun, beberapa kanker akan tumbuh lebih cepat dan kanker prostat adalah alasan kedua yang paling umum kematian kanker pada pria AS, setelah kanker paru-paru. Bahkan pasien yang paling cerdas dan berpendidikan wajah ketidakpastian ini, dan 1 di 6 orang akan didiagnosis dengan kanker prostat dalam waktu kehidupan mereka. Jaringan Kanker Komprehensif Nasional (NCCN) menawarkan setiap tahun diperbaharui dan pedoman berbasis bukti paling untuk kanker prostat, seperti untuk semua kanker, yang dapat membantu yang baru didiagnosis dan mendirikan pasien untuk memilih pilihan terbaik untuk situasi yang spesifik klinis mereka. Untuk kanker prostat pedoman NCCN telah dinilai yang paling tinggi. Namun, semua pedoman termasuk pedoman NCCN membutuhkan estimasi yang baik jangka panjang kesehatan disesuaikan Harapan hidup pasien, karena faktor ini adalah determinan paling penting dari kelangsungan hidup pada pasien yang baru didiagnosis. Dokter perawatan primer dan urolog merasa sulit untuk membuat perkiraan ini – yang mungkin menjadi alasan mengapa pedoman tidak digunakan meskipun pilihan pengobatan sangat kompleks. Sebuah pendekatan yang mudah dan berbasis bukti ( [94] untuk pengambilan keputusan telah diterbitkan dalam edisi 15 Agustus 2011 dari Dokter Keluarga Amerika, paling sering membaca jurnal dalam perawatan primer. Para penulis telah menunjukkan bagaimana untuk memperkirakan kesehatan disesuaikan harapan hidup dan telah menyederhanakan NCCN pedoman sehingga pasien dapat memiliki peta jalan untuk mencapai keputusan yang direkomendasikan untuk situasi klinis mereka dari mana mereka dapat menggunakan preferensi pribadi berdasarkan profil efek samping pilihan pengobatan yang berbeda . Pasien dapat menggunakan baru dikembangkan 18-item kuesioner untuk menemukan jika mereka memiliki pengetahuan dan pemahaman yang baik tentang pilihan pengobatan sebelum mereka memilih pilihan; lebih dari setengah dari 184 pasien yang disurvei yang telah baru didiagnosis dan telah bertemu dengan urolog mereka setelah diagnosis dan memilih pilihan pengobatan tidak bisa menjawab secara benar lebih dari setengah pertanyaan meskipun 90% pasien memiliki melek kesehatan yang baik dan lebih dari 60% adalah berpendidikan tinggi. Para penulis juga memberikan selebaran satu halaman informasi pasien.

Meskipun meluasnya penggunaan skrining prostat spesifik (PSA) antigen di Amerika Serikat telah mengakibatkan diagnosis pada usia awal dan tahap kanker, sebagian besar kasus masih didiagnosis pada pria lebih tua dari 65 tahun, dan sekitar 25% dari kasus yang didiagnosis di pria yang lebih tua dari 75 tahun [95] Meskipun. US National Comprehensive Cancer pedoman Jaringan [96] pilihan pengobatan merekomendasikan menggunakan harapan hidup lebih besar dari atau kurang dari 10 tahun untuk membantu membuat keputusan pengobatan, dalam praktek, pasien usia lanjut banyak yang tidak ditawarkan kuratif seperti prostatektomi radikal (RP) atau terapi radiasi dan malah diobati dengan terapi hormon atau menunggu waspada. Pola ini dapat dikaitkan dengan faktor-faktor seperti medis co-morbiditas dan pasien preferensi yang berkaitan dengan kualitas hidup di samping faktor risiko kanker prostat tertentu seperti pretreatment PSA, skor Gleason dan stadium klinis. Sebagai harapan hidup rata-rata meningkat karena kemajuan dalam pengobatan kardiovaskular, penyakit kronis paru dan lainnya, kemungkinan bahwa lebih banyak pasien lansia akan tinggal cukup lama menderita akibat kanker prostat mereka. Oleh karena itu, saat ini ada minat banyak peran agresif modalitas pengobatan kanker prostat seperti dengan operasi atau radiasi pada populasi lanjut usia yang memiliki penyakit lokal. Hasil dari salah satu uji coba terkontrol secara acak yang diterbitkan oleh Kelompok Kanker Prostat Skandinavia 4 [97] dievaluasi spesifik kanker kematian pada pasien yang diobati dengan RP dibandingkan dengan menunggu waspada. Pasien yang menerima prostatektomi radikal mengalami penurunan risiko relatif dari 30,7% [95% confidence interval 2,5% -50,7%], tetapi pengurangan risiko absolut dari 6% [95% confidence interval 0,5% -11,5%]. Jumlah yang diperlukan untuk mengobati dihitung menjadi 16. Ini berarti bahwa, selama median masa tindak lanjut sekitar 10 tahun, 16 pasien dengan kanker prostat lokal akan perlu untuk menerima prostatektomi radikal daripada menunggu waspada untuk mencegah satu kematian akibat kanker prostat. Analisis subset lebih lanjut mengungkapkan bahwa manfaat ini tidak berlaku untuk semua usia sama. Pada pria yang lebih muda dari 65 tahun, pasien diacak untuk menerima prostatektomi radikal benar-benar memiliki 10-18% pengurangan risiko absolut kanker kematian spesifik dibandingkan dengan mereka secara acak menunggu waspada. Namun, pada pria lebih tua dari 65, tidak ada pengurangan risiko statistik signifikan bahkan ketika disesuaikan dengan PSA, skor Gleason dan stadium tumor. Acak, percobaan dikontrol membandingkan prostatektomi radikal, terapi radiasi, terapi hormonal dan menunggu waspada akan memberikan bukti terbaik untuk cara terbaik untuk mengobati pasien usia lanjut. Percobaan tersebut sangat dibutuhkan, karena populasi lansia berkembang pesat dan diperkirakan akan terus melakukannya. Hasil penelitian pada 2011 menunjukkan surveilans aktif adalah pilihan terbaik untuk ‘risiko rendah’ ​​tua pasien. [98]

Pemilihan pilihan pengobatan mungkin keputusan yang kompleks yang melibatkan banyak faktor. Sebagai contoh, prostatektomi radikal setelah kegagalan radiasi utama adalah operasi yang sangat teknis menantang dan tidak mungkin menjadi pilihan, sementara menyelamatkan terapi radiasi setelah kegagalan bedah mungkin memiliki banyak komplikasi [99]. Hal ini dapat masuk ke dalam keputusan pengobatan.

Jika kanker telah menyebar keluar prostat, pilihan pengobatan secara signifikan berubah, sehingga kebanyakan dokter yang mengobati kanker prostat menggunakan berbagai nomogram untuk memprediksi kemungkinan menyebar. Pengobatan dengan menunggu waspada / surveilans aktif, terapi sinar radiasi eksternal, brakiterapi, cryosurgery, HIFU, dan operasi, secara umum, ditawarkan kepada laki-laki yang kanker masih dalam prostat. Terapi hormonal dan kemoterapi yang sering disediakan untuk penyakit yang telah menyebar ke luar prostat. Namun, ada pengecualian: terapi radiasi dapat digunakan untuk beberapa tumor maju, dan terapi hormonal digunakan untuk beberapa tumor tahap awal. Cryotherapy (proses pembekuan tumor), terapi hormonal, dan kemoterapi juga dapat ditawarkan jika pengobatan awal gagal dan kanker berkembang. [100]

Pengebirian-tahan kanker prostat
Kebanyakan kanker tergantung hormon menjadi refrakter setelah satu sampai tiga tahun dan melanjutkan pertumbuhan meskipun terapi hormon. Sebelumnya dianggap “hormon-refraktori kanker prostat” atau “androgen-independen kanker prostat”, istilah pengebirian-tahan telah menggantikan “hormon refraktori” karena sementara mereka tidak lagi responsif terhadap pengobatan pengebirian (pengurangan androgen tersedia / testosteron / DHT oleh kimia atau cara bedah), kanker ini masih menunjukkan ketergantungan pada hormon untuk aktivasi reseptor androgen [101] Sebelum 2004, semua pengobatan untuk pengebirian-tahan kanker prostat (CRPC) dianggap. [siapa?] paliatif dan tidak ditampilkan untuk memperpanjang kelangsungan hidup. [kutipan diperlukan] Namun, sekarang ada beberapa perawatan yang tersedia untuk mengobati CRPC yang meningkatkan kelangsungan hidup.

Kanker chemotherapic docetaxel telah digunakan sebagai pengobatan untuk (CRPC) dengan manfaat kelangsungan hidup rata-rata 2 sampai 3 bulan [102]. [103] docetaxel yang disetujui FDA pada 2004 sangat signifikan itu adalah pengobatan pertama terbukti memperpanjang kelangsungan hidup di CRPC. Pada tahun 2010, FDA menyetujui pengobatan kemoterapi lini kedua dikenal sebagai cabazitaxel. [104]

Off-label penggunaan obat oral ketoconazole kadang-kadang digunakan sebagai cara untuk lebih memanipulasi hormon dengan efek terapeutik pada CRPC. Namun, banyak efek samping yang mungkin dengan obat ini dan abiraterone kemungkinan untuk menggantikan penggunaan karena memiliki mekanisme serupa tindakan dengan efek samping yang kurang beracun.

Sebuah kombinasi bevacizumab (Avastin), docetaxel, thalidomide dan prednison muncul efektif dalam pengobatan CRPC [105].

Perlakuan imunoterapi dengan sipuleucel-T juga efektif dalam pengobatan CRPC dengan manfaat kelangsungan hidup rata-rata 4,1 bulan. [106]

Baris kedua terapi hormon abiraterone (Zytiga) menyelesaikan fase 3 percobaan untuk pasien CRPC yang telah gagal kemoterapi pada 2010. Hasilnya positif dengan kelangsungan hidup secara keseluruhan meningkat sebesar 4,6 bulan bila dibandingkan dengan plasebo. Pada tanggal 28 April 2011, US Food and Drug Administration disetujui asetat abiraterone dalam kombinasi dengan prednisone untuk mengobati pasien dengan stadium akhir (metastasis) pengebirian-tahan kanker prostat yang telah menerima docetaxel sebelumnya (kemoterapi) [107].

Alpharadin menyelesaikan fase 3 percobaan untuk pasien dengan metastasis tulang CRPC. Sebuah analisis pra-direncanakan sementara menunjukkan peningkatan kelangsungan hidup dan kualitas hidup. Penelitian ini dihentikan karena alasan etis untuk memberikan kelompok plasebo perlakuan yang sama. Apharadin menggunakan tulang ditargetkan Radium-223 isotop untuk membunuh sel kanker dengan radiasi alpha. Alpharadin adalah agen diteliti dan tidak disetujui untuk pemasaran oleh European Medicines Agency (EMA), US Food and Drug Administration (FDA), atau otoritas kesehatan lainnya. [108]

Ada juga beberapa perawatan saat ini dalam uji klinis untuk mengobati CRPC. Ini termasuk generasi 2 hormon terapi MDV3100 dan orteronel (TAK-700), yang PROSTVAC imunoterapi, dan tulang metastasis-penargetan cabozantinib (XL-184).

Kanker prostat tingkat lebih tinggi dan prognosis yang lebih buruk di negara maju daripada seluruh dunia. Banyak faktor risiko untuk kanker prostat lebih umum di negara maju, termasuk harapan hidup lebih lama dan diet tinggi daging merah. (Orang yang mengkonsumsi sejumlah besar daging dan susu juga cenderung mengkonsumsi lebih sedikit porsi buah-buahan dan sayuran Hal ini tidak jelas apakah kedua faktor ini, atau hanya salah satu dari mereka, berkontribusi terhadap terjadinya kanker prostat.. [109]) Juga, di mana ada lebih banyak akses ke program skrining, ada tingkat deteksi lebih tinggi. Kanker prostat adalah kanker kesembilan yang paling umum di dunia, tetapi nomor-satu non-kanker kulit pada pria dari Amerika Serikat. Terkena kanker prostat delapan belas persen pria Amerika dan menyebabkan kematian dalam tiga persen pada tahun 2005 [110] Di Jepang, kematian akibat kanker prostat seperlima satu setengah tingkat di Amerika Serikat dan Eropa pada 1990-an. [111]. Di India pada 1990-an, setengah dari orang dengan kanker prostat terbatas pada prostat meninggal dalam sepuluh tahun [112] Afrika-Amerika laki-laki memiliki kanker prostat 50-60 kali lebih dan kematian akibat kanker prostat daripada laki-laki di Shanghai, Cina.. [113 ] Di Nigeria, dua persen pria menderita kanker prostat, dan 64% dari mereka yang tewas setelah dua tahun [114].

Pada pasien yang menjalani pengobatan, prognosis indikator paling penting dari hasil klinis penyakit tahap, pra-terapi tingkat PSA, dan skor Gleason. Secara umum, semakin tinggi kelas dan panggung, miskin prognosis. Nomogram dapat digunakan untuk menghitung risiko yang diperkirakan dari masing-masing pasien. Prediksi didasarkan pada pengalaman kelompok besar pasien yang menderita kanker pada berbagai tahap. [115]

Pada tahun 1941, Charles Huggins melaporkan bahwa terapi ablasi androgen menyebabkan regresi primer dan metastasis androgen tergantung kanker prostat [116]. Dia dianugerahi Hadiah Nobel 1966 untuk Fisiologi atau Kedokteran untuk penemuan ini. Terapi ablasi androgen menyebabkan remisi pada 80-90% dari pasien yang menjalani terapi, sehingga kelangsungan hidup bebas perkembangan penyakit rata-rata 12 sampai 33 bulan. Setelah remisi, fenotip androgen-independen biasanya muncul, dimana kelangsungan hidup secara keseluruhan median 23-37 bulan dari saat inisiasi terapi ablasi androgen [117]. Mekanisme yang sebenarnya memberikan kontribusi terhadap perkembangan kanker prostat tidak jelas dan dapat bervariasi antara pasien individu. Sebuah mekanisme beberapa kemungkinan telah diusulkan

Artikel utama: Prostat stadium kanker
Suatu bagian penting dari mengevaluasi kanker prostat adalah menentukan panggung, atau seberapa jauh kanker telah menyebar. Mengetahui panggung membantu menentukan prognosis dan berguna ketika memilih terapi. Sistem yang paling umum adalah empat tahap sistem TNM (disingkat dari Tumor / Nodes / Metastasis). Komponen-komponennya termasuk ukuran tumor, jumlah kelenjar getah bening yang terlibat, dan kehadiran dari setiap metastasis lainnya. [9]

Perbedaan yang paling penting yang dibuat oleh sistem staging adalah apakah atau tidak kanker masih terbatas pada prostat. Dalam sistem TNM, T1 T2 klinis dan kanker hanya ditemukan di prostat, sementara kanker T3 dan T4 telah menyebar di tempat lain. Beberapa tes dapat digunakan untuk mencari bukti penyebaran. Ini termasuk computed tomography untuk mengevaluasi menyebar di dalam panggul, tulang scan untuk mencari menyebar ke tulang, dan kumparan pencitraan resonansi magnetik untuk endorectal erat mengevaluasi kapsul prostat dan vesikula seminalis. Scan tulang harus mengungkapkan penampilan osteoblastik karena kepadatan tulang meningkat di daerah tulang metastasis-berlawanan dengan apa yang ditemukan pada kanker lain yang bermetastasis.

Setelah biopsi prostat, ahli patologi melihat sampel di bawah mikroskop. Jika kanker hadir, ahli patologi laporan grade dari tumor. Kelas memberitahu berapa banyak jaringan tumor berbeda dari jaringan prostat normal dan menunjukkan seberapa cepat tumor cenderung tumbuh. Sistem Gleason digunakan untuk tumor prostat kelas 2 sampai 10, di mana skor Gleason dari 10 menunjukkan kelainan yang paling. Ahli patologi memberikan nomor dari 1 sampai 5 untuk pola yang paling umum diamati di bawah mikroskop, kemudian melakukan hal yang sama untuk pola kedua-paling-umum. Jumlah dari kedua angka ini adalah skor Gleason. Tahap Whitmore-Jewett adalah metode lain kadang-kadang digunakan.

 Klasifikasi sistem
Kanker prostat Banyak yang tidak ditakdirkan untuk menjadi mematikan, dan kebanyakan pria pada akhirnya akan mati dari penyebab lain dari penyakit. Keputusan tentang jenis pengobatan dan waktu mungkin, karena itu, akan diinformasikan oleh perkiraan resiko bahwa tumor akhirnya akan kambuh setelah pengobatan dan / atau kemajuan untuk metastasis dan kematian. Beberapa alat yang tersedia untuk membantu memprediksi hasil, seperti tahap patologis dan kekambuhan setelah operasi atau terapi radiasi. Kebanyakan tahap menggabungkan, kelas, dan tingkat PSA, dan beberapa juga menambahkan jumlah atau persen dari core biopsi positif, usia, dan / atau informasi lainnya.D’Amico klasifikasi stratifies pria dengan risiko rendah, menengah, atau tinggi berdasarkan tahap, kelas, dan PSA. Hal ini digunakan secara luas dalam praktek klinis dan pengaturan penelitian. Kelemahan utama sistem 3-tingkat adalah bahwa hal itu tidak memperhitungkan parameter yang merugikan (misal, tinggi skor Gleason dan PSA tinggi) pada pasien stratifikasi.
Tabel Partin memprediksi hasil patologis (margin status, ekstensi extraprostatic, dan invasi vesikula seminalis) berdasarkan tiga variabel yang sama dan diterbitkan sebagai tabel lookup.
Para nomogram Kattan memprediksi kekambuhan setelah operasi dan / atau terapi radiasi, berdasarkan data yang tersedia baik pada saat diagnosis atau setelah operasi. Para nomogram dapat dihitung menggunakan grafik kertas atau perangkat lunak yang tersedia di situs Web atau untuk komputer genggam. Skor Kattan mewakili kemungkinan tetap bebas dari penyakit pada interval waktu tertentu setelah pengobatan.
Kanker UCSF skor Penilaian Risiko Prostat (Capra) memprediksi baik status yang patologis dan kekambuhan setelah operasi. Ia menawarkan akurasi yang sebanding sebagai nomogram Kattan praoperasi, dan dapat dihitung tanpa tabel kertas atau kalkulator. Poin ditetapkan berdasarkan PSA, Kelas, panggung, usia, dan persen dari core positif; jumlah tersebut menghasilkan nilai 0-10, dengan setiap 2 poin mewakili sekitar dua kali lipat risiko kekambuhan. Capra skor berasal dari data berbasis masyarakat dalam database CaPSURE. Ini telah divalidasi di antara lebih dari 10.000 pasien prostatektomi, termasuk pasien dari CaPSURE; [119] registri SEARCH, yang mewakili data dari Administrasi Veteran dan aktif beberapa pusat medis militer; [120] kohort multi-institusi di Jerman; [121] dan prostatektomi kohort di Johns Hopkins University [122]. Baru-baru ini, telah ditunjukkan untuk memprediksi metastasis dan kematian setelah prostatektomi, terapi radiasi, menunggu waspada, atau terapi androgen kekurangan. [123]

Umur-standar kematian dari kanker prostat per 100.000 penduduk pada tahun 2004 [124].

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Tingkat kanker prostat sangat bervariasi di seluruh dunia. Meskipun tarif sangat bervariasi antar negara, itu paling umum di Asia Selatan dan Timur, lebih umum di Eropa, dan yang paling umum di Amerika Serikat. [2] Menurut American Cancer Society, kanker prostat paling umum di antara pria Asia dan paling umum di kalangan laki-laki hitam, dengan angka untuk orang kulit putih di antara [125] [126]. Tingkat kejadian tahunan rata-rata kanker prostat antara 1988 dan 1992 di kalangan pria Cina di Amerika Serikat adalah 15 kali lebih tinggi daripada rekan-rekan mereka yang tinggal di Shanghai dan Tianjin [125]. [126] [127] Namun, harga ini tinggi mungkin dipengaruhi oleh tingkat peningkatan deteksi. [128] Banyak menunjukkan bahwa kanker prostat mungkin kurang dilaporkan, namun kejadian BPH di Cina dan Jepang mirip dengan tarif di negara-negara Barat., [129] [130]

Kanker prostat berkembang terutama pada pria di atas lima puluh. Ini adalah jenis yang paling umum dari kanker pada pria di Amerika Serikat, dengan 186.000 kasus baru pada 2008 dan 28.600 kematian [131]. Ini adalah penyebab kedua kematian kanker pada pria Amerika Serikat setelah kanker paru-paru. Di Inggris juga merupakan penyebab paling umum kedua kematian kanker setelah kanker paru-paru, di mana sekitar 35.000 kasus didiagnosis setiap tahun dan yang sekitar 10.000 mati itu. Banyak faktor, termasuk genetika dan diet, telah terlibat dalam perkembangan kanker prostat. Kanker Prostat Pencegahan Trial menemukan bahwa finasterida mengurangi insiden kanker prostat sebesar 30%. Ada telah menjadi kontroversi tentang ini juga meningkatkan risiko kanker yang lebih agresif, tetapi penelitian yang lebih baru menunjukkan bahwa hal ini tidak mungkin terjadi. [77] [132]

Lebih dari 80% pria akan mengembangkan kanker prostat pada usia 80 [133] Namun, pada kebanyakan kasus, akan tumbuh lambat dan tidak berbahaya.. Pada pria tersebut, mendiagnosis kanker prostat adalah overdiagnosis-identifikasi perlu dari suatu kondisi teknis menyimpang yang tidak akan pernah merugikan pasien dan pengobatan pada pria tersebut menghadapkan mereka ke semua efek samping, tanpa kemungkinan memperpanjang hidup mereka. [134]

Meskipun prostat pertama kali dijelaskan oleh ahli anatomi Venesia NiccoMassa di 1536, dan diilustrasikan oleh Flemish anatomi Andreas Vesalius pada tahun 1538, kanker prostat tidak teridentifikasi sampai 1853. [135] Kanker prostat awalnya dianggap sebagai penyakit langka, mungkin karena harapan hidup lebih pendek dan metode deteksi miskin di abad ke-19. Perlakuan pertama kanker prostat operasi untuk menghilangkan obstruksi kemih. [136] Penghapusan dari seluruh kelenjar (prostatektomi radikal perineum) pertama kali dilakukan pada tahun 1904 oleh Hugh H. Young di Johns Hopkins Hospital. [137] Operasi pengangkatan testis ( orchiectomy) untuk mengobati kanker prostat pertama kali dilakukan di tahun 1890, tetapi dengan keberhasilan yang terbatas. Reseksi transurethral dari prostat (TURP) diganti prostatektomi radikal untuk mengurangi gejala-gejala obstruksi pada pertengahan abad ke-20 karena lebih bisa memelihara fungsi ereksi penis. Prostatektomi radikal retropubik dikembangkan pada tahun 1983 oleh Patrick Walsh. [138] Hal ini memungkinkan untuk pendekatan bedah pengangkatan prostat dan kelenjar getah bening dengan pemeliharaan fungsi penis.

Pada tahun 1941, Charles B. Huggins menerbitkan studi di mana ia digunakan estrogen untuk menentang produksi testosteron pada pria dengan kanker prostat metastasis. Ini penemuan “pengebirian kimiawi” memenangkan Huggins tahun 1966 Penghargaan Nobel dalam Fisiologi atau Kedokteran. [139] Peran GnRH hormon dalam reproduksi ditentukan oleh Andrzej W. Schally dan Roger Guillemin, yang keduanya memenangkan Hadiah Nobel 1977 dalam Fisiologi atau Kedokteran untuk pekerjaan ini.

Reseptor agonis, seperti leuprolid dan goserelin, yang kemudian dikembangkan dan digunakan untuk mengobati kanker prostat [140]. [141]

Terapi radiasi untuk kanker prostat pertama kali dikembangkan pada awal abad 20 dan pada awalnya terdiri dari implan intraprostatic radium. Radiasi sinar eksternal menjadi lebih populer sebagai sumber radiasi kuat menjadi tersedia pada pertengahan abad ke-20. Brachytherapy dengan biji ditanamkan pertama kali dijelaskan pada tahun 1983. [142]

Kemoterapi sistemik untuk kanker prostat pertama kali dipelajari tahun 1970-an. Regimen awal siklofosfamid dan 5-fluorouracil segera bergabung dengan beberapa rejimen menggunakan sejumlah obat kemoterapi sistemik lainnya. [143]

Pada 30 Juli 2010 Owen Witte M.D. et al. dari UCLA menerbitkan serangkaian studi di Science di mana mereka telah memperkenalkan virus diketahui menyebabkan kanker mutasi dalam sel prostat: Akt, ERG, dan AR ke dalam sampel diisolasi dari sel-sel basal dan luminal dan dicangkokkan jaringan diperlakukan ke tikus. Setelah 16 minggu, tidak ada sampel telah mengalami mutasi luminal ganas, sementara sampel basal telah bermutasi menjadi prostat seperti tubulus yang kemudian berkembang dan membentuk tumor keganasan kanker, yang tampaknya identik dengan sampel manusia di bawah pembesaran. Hal ini membawa pada kesimpulan bahwa sel prostat basal mungkin “tempat asal” yang paling mungkin dari kanker prostat [144].

Masyarakat dan budaya
Orang dengan kanker prostat umumnya menemukan perbedaan yang signifikan dalam kesadaran, dana, liputan media, dan penelitian-dan karena itu, pengobatan lebih rendah dan lebih miskin dibandingkan dengan hasil-kanker lain dari prevalensi yang sama [145] Pada tahun 2001. The Guardian mencatat bahwa Inggris memiliki 3.000 perawat yang mengkhususkan diri pada kanker payudara, dibandingkan dengan hanya satu untuk kanker prostat. Hal ini juga menemukan bahwa waktu tunggu antara rujukan dan diagnosis adalah dua minggu untuk kanker payudara namun tiga bulan untuk kanker prostat. [146] Sebuah laporan tahun 2007 oleh Koalisi Kanker Prostat Nasional menyatakan bahwa untuk setiap obat kanker prostat di pasar, ada tujuh digunakan untuk mengobati kanker payudara. Times juga mencatat sebuah “anti-laki-laki bias dalam pendanaan kanker” dengan perbedaan 4-1 di Inggris oleh pemerintah maupun oleh badan amal kanker seperti Cancer Research Inggris [145]. [147] Kesetaraan juru kampanye seperti penulis Warren Farrell mengutip kesenjangan pengeluaran tersebut sebenarnya sebagai contoh yang jelas dari pemerintah tidak adil mendukung kesehatan perempuan atas kesehatan pria [148].

Disparitas juga memperluas ke daerah-daerah seperti deteksi, dengan pemerintah gagal untuk mendanai atau mandat skrining kanker prostat sementara sepenuhnya mendukung program kanker payudara. Misalnya, laporan tahun 2007 menemukan 49 negara bagian AS mandat cakupan asuransi untuk skrining kanker payudara rutin, dibandingkan dengan 28 untuk kanker prostat [145]. [149] Kanker prostat juga mengalami liputan media yang secara signifikan lebih sedikit daripada yang lain, kanker juga lazim, dengan studi oleh Koalisi Prostat menampilkan cerita payudara kanker 2,6 untuk setiap satu meliputi kanker prostat. [145]

Kanker prostat kesadaran bulan
Kanker prostat bulan kesadaran berlangsung pada bulan September di sejumlah negara. Sebuah pita biru digunakan untuk mempromosikan menyebabkan [150]. [151]

Androgen pada konsentrasi 10-kali lipat lebih tinggi daripada konsentrasi fisiologis juga telah terbukti menyebabkan penekanan pertumbuhan dan pengembalian androgen-independen kanker prostat atau androgen xenografts-independen tumor prostat diturunkan dalam model vivo untuk fenotip androgen pada tikus athymic dirangsang. [152] [153] Observasi ini menunjukkan kemungkinan untuk menggunakan androgen untuk mengobati pengembangan kambuh androgen-independen tumor prostat pada pasien.

Infus oral katekin teh hijau, terapi alternatif yang potensial untuk kanker prostat oleh senyawa-senyawa alami, telah terbukti dapat menghambat pembangunan, kemajuan, dan metastasis juga dalam adenocarcinoma transgenik asli dari prostat mouse (gelandangan) model, yang secara spontan mengembangkan kanker prostat [154].

Insulin-seperti faktor pertumbuhan signaling sumbu berpikir untuk memainkan peran kunci dalam perkembangan kanker prostat. Ini terdiri dari dua ligan (IGF-1 dan IGF-2), dua reseptor (IGF-IR dan IGF-IIR) dan enam protein tinggi afinitas pengikatan IGF-terkait (IGFBP 1-6) [155] ekspresi. Perubahan IGF sumbu anggota telah terlibat dalam pengembangan berbagai jenis kanker, termasuk prostat [156]. [157]

Sebuah turunan genistein KBU2046 sedang diselidiki untuk kanker prostat. [158] MDV3100 dalam uji fase III untuk HRPC (kemo-naif dan pasca-populasi pasien kemo). [159]

 Kanker prostat model
Para ilmuwan telah membentuk garis sel kanker prostat beberapa untuk menyelidiki mekanisme yang terlibat dalam perkembangan kanker prostat. LNCaP, PC-3 (PC3), dan DU-145 (DU145) yang umumnya digunakan garis sel kanker prostat. Kanker LNCaP garis sel didirikan dari lesi metastasis kelenjar getah bening manusia adenokarsinoma prostat. PC-3 dan DU-145 sel didirikan dari adenokarsinoma prostat manusia metastasis ke tulang dan ke otak, masing-masing. LNCaP sel mengekspresikan reseptor androgen (AR), namun, PC-3 dan DU-145 sel mengekspresikan AR sangat sedikit atau tidak ada. AR, faktor transkripsi androgen diaktifkan, milik keluarga reseptor steroid nuklir. Pengembangan prostat tergantung pada sinyal androgen dimediasi melalui AR, dan AR juga penting selama perkembangan kanker prostat. Proliferasi sel LNCaP adalah androgen tergantung tetapi proliferasi PC-3 dan DU-145 sel adalah androgen sensitif. Ketinggian ekspresi AR sering diamati pada tumor prostat pada pasien [160]. [161] Beberapa androgen-independen sublines LNCaP telah dikembangkan dari sel tergantung androgen ATCC LNCaP setelah kekurangan androgen untuk studi perkembangan kanker prostat. Ini androgen-independen sel LNCaP telah mengangkat AR ekspresi dan mengekspresikan antigen spesifik prostat pada pengobatan androgen. Paradoksnya adalah bahwa androgen menghambat proliferasi dari androgen-independen sel kanker prostat. [162] [163] [164]

Saat ini, area aktif penelitian dan investigasi non-klinis diterapkan melibatkan non-invasif metode deteksi tumor prostat. Adenovirus dimodifikasi untuk transfect sel tumor dengan gen tidak berbahaya namun berbeda (seperti luciferase) telah terbukti mampu deteksi dini. Sejauh ini, bagaimanapun, ini daerah penelitian telah diuji hanya pada model sel hewan dan LNCaP. [165]

Kehadiran EN2 (gen) dalam urin telah berkorelasi dengan probabilitas tinggi kanker prostat [166]. Co-peneliti Hardev Pandha, dan Richard Morgan menerbitkan temuan mereka pada edisi 1 2011 Maret jurnal Clinical Cancer Research. [167 ] Sebuah tes laboratorium saat ini mengidentifikasi EN2 dalam urin, dan test kit rumah dibayangkan mirip dengan strip tes kehamilan di rumah. Menurut Morgan, “Kami sedang mempersiapkan beberapa penelitian besar di Inggris dan di Amerika Serikat dan meskipun tes EN2 belum tersedia, beberapa perusahaan telah menyatakan minatnya dalam mengambil ke depan.” [168]

Metode lain non-invasif potensi deteksi tumor prostat dini adalah melalui tes molekuler yang mendeteksi adanya sel-terkait PCA3 mRNA dalam cairan memijat dari prostat oleh dokter dan pertama-kekosongan kencing keluar dalam jumlah terbatas ke dalam spesimen urin kontainer. PCA3 mRNA dinyatakan hampir secara eksklusif oleh sel prostat dan telah terbukti sangat lebih-disajikan dalam sel-sel kanker prostat. Hasil tes saat ini dilaporkan sebagai rasio spesimen PCA3 mRNA untuk mRNA PSA. Meskipun tidak pengganti untuk tingkat serum PSA, tes PCA3 adalah alat tambahan untuk membantu memutuskan apakah, pada pria diduga menderita kanker prostat (terutama jika biopsi awal gagal untuk menjelaskan serum PSA tinggi), sebuah rebiopsy biopsi / adalah benar-benar dibutuhkan . Semakin tinggi ekspresi PCA3 dalam sampel, semakin besar kemungkinan biopsi yang positif, yaitu, adanya sel-sel kanker dalam prostat.

Awal kanker prostat antigen-2
Hal itu dilaporkan pada April 2007 bahwa penelitian sedang dilakukan pada tes darah baru untuk kanker prostat dini antigen-2 (EPCA-2) yang dapat mengingatkan pria jika mereka memiliki kanker prostat dan seberapa agresif itu akan [169] [170].

Tromboflebitis dikaitkan dengan peningkatan risiko kanker prostat dan mungkin cara yang baik bagi dokter untuk mengingatkan diri untuk pasien layar dengan tromboflebitis untuk kanker prostat juga karena kedua terkait erat [171].

Sel epitel dari prostat mensekresi prostasomes serta PSA. Prostasomes yang dikelilingi membran-, prostat yang diturunkan dari organel yang muncul ekstrasel, dan salah satu fungsi fisiologis mereka adalah untuk melindungi sperma dari serangan oleh sistem kekebalan tubuh wanita. Sel-sel kanker prostat terus mensintesis dan mensekresi prostasomes, dan mungkin dilindungi terhadap serangan imunologi oleh prostasomes. Penelitian beberapa aspek keterlibatan prostasomal pada kanker prostat telah dilakukan






the end @ copyright dr iwan suwandy 2011

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