La fisiopatologia del cancer de prostata la se riferiss ai mecanism e ai process che g'hann per fondament el svilup e la progression de la malatia.
El cancher de prostata l"è un tumur malign che el nass de le cellule de la prostata, qe l"è un organ piscinin a forma de noce qe 'l se troeuva sota la vescica ind i om.
La prostata la prodüss el fluid seminal, che nutriss e trasporta el sperma.
La causa precisa del cancer de prostata l"è minga capida del tut, ma se sa che divèrsi fattur aumenten el ris'c de sviluppà la malattia.
Chesti i cumprenden l'età, la storia familiara, la razza e certi mutaziun genetich.
El cancher de prostata l"è püsee comun in di òmen püssee vecc, cun la magiur part di cas che succeden in di òmen püssee vecc de 65 agn.
Inoltra, i omm cun una storia familiara de cancher de prostata g'han un ris'c püsee grand, cuma i omm afro-american e i omm de discendenza caraibica.
La fisiopatologia del cancer de prostata la coinvolge la cressita e la divisiun incontrolada di cellule ind la ghiandola prostatica.
Chesto el pœl suceder per via de mutazion genetich qe i pœl portar a la sovraespression de cert fator de cress o a l'inactivasion de geni suppressor de tumor.
Cheste mutazion pœden portà a una cressida minga regulada de cellule, qe la porta a la formazion de un tumor.
Intant che el tumur el cress, el pœl invader i tessud e i orghen vesin, comè la vescica, el retto e i linfonod vesin.
In certi cas, i cellule cancerose pœden separass del tumor primari e spantegar-s in olter part del corp travers el flus sanguigno o el sistema linfatich, un process cognossud comè metastasi.
Una volta che el cancher l"è spantegaa, el pœu vesser püssee dificil de curar.
El cancher de prostata pœl vesser influenzad anca de fatur urmonal, in particolar de l'ormon androgen testosterone.
El testosterone el pœl stimolà la cressida de cellule del cancher de prostata, e tanti tratament per el cancher de prostata g'han per obietiv de redur i livèll de'st'ormon o blocar i sò efètt.
In sintesi, la fisiopatologia del cancher de prostata la coinvolge la cressita e la divisiun incontrolada di celul ind la prostata, che pœden vesser influenzade de fatur genetich, urmonal e ambient.
Capir i mecanism che g'han de la malattia l"è crucial per sviluppà di tratament eficaz e migliorar i resultad per i pazient cun el cancer de prostata.
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.
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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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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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