Pathophysiology kanker prostat e ro mattuujui lao mekanisme nenniya proses dasar e iya nassabari allebbangenna nenniya allebbangenna lasa e.
Kanker prostat iyanaritu tumor ganas iya mompo pole sel kelenjar prostat, iyanaritu organ mabeccu, mabbentu' kenari iya engkae ri yawa kandung kemih ri urane.
Iyyae muttama umuru, sejarah kaluwarga, ras, nenniya mutasi genetik mattentu.
Kanker prostat lebbi macahoro ri urane iya lebbi macowa, sibawa macahoro kasus kajajiang ri urane iya lebbi macowa pole 65 taung.
Rilainnaero, urane sibawa sejarah kaluwarga kanker prostat engka ri resiko lebbi maraja, pappada urane Afrika Amerika nenniya urane pole Karibia.
Pathophysiology kanker prostat nauttamaki allebbangenna nenniya abbagengeng sel iya de na riatoro rilaleng kelenjar prostat.
Iyya wedding kajajiang nasaba mutasi genetik iya nassabari'e ekspresi lebbi pole faktor pertumbuhan tertentu iyarega de'na aktif gen penekan tumor.
Iyae mutasi e wedding nassabari allebangeng sel iya de'e naatur, nassabari bentu' tumor.
Ri wettu tumor e mallebbang, ullei na'invasi jaringan nenniya organ macawe', pappada kandung kemih, rektum, nenniya kelenjar getah bening macawe.
Rilaleng siare kasus, sel kanker nulle leppe pole tumor primer nenniya mallebbang lao ri bageang laingna watakkalena laloi aliran dara iyarega sistem limfatik, seddi proses iya risseng e riyaseng metastasis.
Narekko kanker e mallebbang, nulle lebbi masussa ripajjappa.
Kanker prostat wedding toi ripigau pole faktor hormonal, utamana hormon androgen testosteron.
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.
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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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