What is pathophysiology of Prostate cancer?

['Harim dispela pes']

Wanem samting i mekim na man i kisim sik kensa bilong prostet?

Ol i tok, dispela i mekim na ol man i no inap kisim ol marasin bilong daunim sik bilong prostet.

Dispela sik i save kamap long ol sel bilong prostate glan, em wanpela liklik hap bilong bodi i luk olsem hani, na i stap aninit long skin bilong man.

Prostate gland i save kamapim wara bilong sem, em i save givim kaikai long ol pikinini bilong sem na karim ol i go long narapela hap.

Ol i no save gut long as tru bilong sik kensa bilong prostet, tasol i gat sampela samting i save mekim na man inap kisim dispela sik.

Ol dispela samting i olsem: krismas, famili, skin, na sampela senis i kamap long jin.

Planti man i gat sik kensa bilong prostet, ol i gat 65 krismas samting.

Na tu, ol man i gat famili i gat sik kensa bilong prostet, ol inap kisim dispela sik, na ol man Afrika Amerika na ol man bilong Karibian tu.

Ol i tok, dispela sik i save kamap taim ol sel bilong prostet i no wok long kamap planti na i wok long bruk bruk.

Dispela inap kamap long rot bilong sampela senis i kamap long jin bilong ol man na dispela i mekim na sampela jin bilong kamap bikpela i wok strong tumas o ol jin bilong daunim ol buk i no wok.

Ol dispela senis inap mekim na ol sel i no gro gut, na dispela i mekim na ol buk i kamap.

Taim buk i go bikpela, em inap go insait long ol hap bilong bodi i stap klostu, olsem waitlewa, pekpek, na ol liklik rop bilong waitlewa.

Sampela taim ol sel bilong kensa inap lusim namba wan buk na i go long ol narapela hap bilong bodi long rot bilong blut o ol rop bilong blut.

Taim sik kensa i go bikpela, i hatwok moa long oraitim.

Ol homon i save mekim sampela samting long skin bilong man, olsem homon androgen, em testosterone.

Testosteron inap kirapim ol sel bilong sik kensa long kamap planti, na planti marasin bilong daunim dispela sik i bilong daunim mak bilong dispela homon o pasim wok bilong en.

Olsem na ol i tok, sik bilong kensa bilong prostet i save kamap taim ol sel i no wok long kamap planti na brukim ol yet.

Bilong kisim save long ol samting i mekim na man i kisim sik kensa bilong prostet, em i bikpela samting long kisim ol gutpela marasin bilong helpim dispela sik.

['Ol Tok Bilong Bipo']

PubMed/Medline https://www.nlm.nih.gov/databases/download/pubmed_medline.html

RefinedWeb https://arxiv.org/abs/2306.01116

Zobniw CM, Causebrook A, Fong MK: Clinical use of abiraterone in the treatment of metastatic castration-resistant prostate cancer. Res Rep Urol. 2014, 6 (): 97-105.

Lim HY, Agarwal AM, Agarwal N, Ward JH: Recurrent epistaxis as a presenting sign of androgen-sensitive metastatic prostate cancer. Singapore Med J. 2009, 50 (5): e178-80.

Kohli M, Qin R, Jimenez R, Dehm SM: Biomarker-based targeting of the androgen-androgen receptor axis in advanced prostate cancer. Adv Urol. 2012, 2012 (): 781459.

Nelson JB, Hedican SP, George DJ, Reddi AH, Piantadosi S, Eisenberger MA, Simons JW: Identification of endothelin-1 in the pathophysiology of metastatic adenocarcinoma of the prostate. Nat Med. 1995, 1 (9): 944-9.

Msaouel P, Nandikolla G, Pneumaticos SG, Koutsilieris M: Bone microenvironment-targeted manipulations for the treatment of osteoblastic metastasis in castration-resistant prostate cancer. Expert Opin Investig Drugs. 2013, 22 (11): 1385-400.

Kotani K, Sekine Y, Ishikawa S, Ikpot IZ, Suzuki K, Remaley AT: High-density lipoprotein and prostate cancer: an overview. J Epidemiol. 2013, 23 (5): 313-9.

Jadvar H: Molecular imaging of prostate cancer: a concise synopsis. Mol Imaging. , 8 (2): 56-64.

['Toksave: sik']

['Dispela Web-sait i bilong skulim na givim save tasol long ol man, na i no bilong givim tok bilong helpim ol sikman o helpim ol narapela long sait bilong helt.']

['Ol i no ken yusim ol dispela tok bilong helpim ol long save long sik bilong ol, na ol man i laik kisim helpim long ol samting bilong helt, ol i mas toktok wantaim wanpela dokta.']

['Tingim, ol kompiuta i save yusim ol kompiuta long kamapim ol bekim bilong ol askim, tasol ol i no save kolim stret ol namba, olsem namba bilong ol man i gat wanpela sik.']

['Oltaim yu mas kisim tingting bilong dokta o narapela lain i gat save long helpim yu long sait bilong helt sapos yu gat sik. No ken sakim tok bilong dokta o wet long kisim tingting bilong dokta, long wanem, yu ritim sampela tok long dispela Web-sait. Sapos yu ting yu gat sik, ringim 911 o go long haus sik i stap klostu.']

['Toksave: raits bilong man i bosim']

['Digital Millennium Copyright Act bilong 1998, 17 U.S.C. § 512 (the DMCA) i tok ol papa bilong ol samting i gat rait long wokim ol samting, sapos ol i ting ol samting i stap long Intenet i brukim ol lo bilong ol long Amerika.']

['Sapos yu bilip olsem sampela samting i stap long dispela Web-sait o ol sevis bilong mipela i brukim lo bilong kopirait bilong yu, yu (o agent bilong yu) inap salim toksave long mipela na askim mipela long rausim o pasim rot bilong yu long kisim dispela samting.']

['Ol i mas salim ol toksave long rot bilong e-mail (lukim hap "Kontek" bilong lukim e-mail atres). ']

['Lo bilong DMCA i tok olsem toksave bilong yu long ol man i bin brukim lo bilong kopirait i mas i gat ol dispela tok: (1) stori long ol samting i gat kopirait long en, em ol man i tok ol i bin brukim; (2) stori long ol samting i gat kopirait na ol tok bilong helpim mipela long painim ol dispela samting; (3) ol tok bilong yu bilong salim pas long mipela, olsem atres, telefon namba, na e-meil atres; (4) tok yu bin mekim olsem yu bilip tru olsem man i gat kopirait o agent bilong em i no orait long ol samting i stap long dispela websait.']

['(5) Yu mas raitim wanpela pepa na putim han bilong yu bilong tokaut olsem ol tok bilong dispela pepa i stret na yu gat namba long mekim ol samting bilong lukautim ol rait bilong man i bin wokim ol samting.']

['Na (6) wanpela sain o sain bilong man i gat rait long wokim dispela samting o bilong wanpela man i gat namba long mekim wok bilong dispela man.']

['Sapos yu no raitim olgeta dispela tok, dispela inap mekim na ol i no stretim kwik komplen bilong yu.']

['Kontektim']

['Plis salim e-mail long mipela sapos yu gat sampela askim o tingting.']

What is pathophysiology of prostate cancer?

The pathophysiology of prostate cancer refers to the underlying mechanisms and processes that lead to the development and progression of the disease.

Prostate cancer is a malignant tumor that arises from the cells of the prostate gland, which is a small, walnut-shaped organ located below the bladder in men.

The prostate gland produces seminal fluid, which nourishes and transports sperm.

The exact cause of prostate cancer is not fully understood, but several factors are known to increase the risk of developing the disease.

These include age, family history, race, and certain genetic mutations.

Prostate cancer is more common in older men, with the majority of cases occurring in men over the age of 65.

Additionally, men with a family history of prostate cancer are at an increased risk, as are African American men and men of Caribbean descent.

The pathophysiology of prostate cancer involves the uncontrolled growth and division of cells within the prostate gland.

This can occur due to genetic mutations that lead to the overexpression of certain growth factors or the inactivation of tumor suppressor genes.

These mutations can result in the unregulated growth of cells, leading to the formation of a tumor.

As the tumor grows, it can invade nearby tissues and organs, such as the bladder, rectum, and nearby lymph nodes.

In some cases, cancer cells can break away from the primary tumor and spread to other parts of the body through the bloodstream or lymphatic system, a process known as metastasis.

Once the cancer has spread, it can be more difficult to treat.

Prostate cancer can also be influenced by hormonal factors, particularly the androgen hormone testosterone.

Testosterone can stimulate the growth of prostate cancer cells, and many treatments for prostate cancer aim to reduce the levels of this hormone or block its effects.

In summary, the pathophysiology of prostate cancer involves the uncontrolled growth and division of cells within the prostate gland, which can be influenced by genetic, hormonal, and environmental factors.

Understanding the underlying mechanisms of the disease is crucial for developing effective treatments and improving outcomes for patients with prostate cancer.

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