Il- patofiżjoloġija tal- kanċer tal- prostata tirreferi għall- mekkaniżmi u l- proċessi sottostanti li jwasslu għall- żvilupp u l- progressjoni tal- marda.
Il- kanċer tal- prostata huwa tumur malinn li jirriżulta miċ- ċelloli tal- glandola tal- prostata, li hija organu żgħir f' forma ta ' walnut li jinsab taħt il- bużżieqa fl- irġiel.
Il- glandola tal- prostata tipproduċi likwidu seminali, li jnutri u jġorr is- spermatozoi.
Il- kawża eżatta tal- kanċer tal- prostata mhix mifhuma bis- sħiħ, imma diversi fatturi huma magħrufa li jżidu r- riskju li tiżviluppa l- marda.
Dawn jinkludu l- età, l- istorja tal- familja, ir- razza, u ċerti mutazzjonijiet ġenetiċi.
Il- kanċer tal- prostata huwa aktar komuni fl- irġiel anzjani, u l- biċċa l- kbira tal- każijiet iseħħu fl- irġiel li għandhom aktar minn 65 sena.
Barra minn hekk, l- irġiel b'istorja tal- familja taʼ kanċer tal- prostata huma f'riskju akbar, kif ukoll l- irġiel Afro-Amerikani u l- irġiel taʼ dixxendenza tal- Karibew.
Il- patofiżjoloġija tal- kanċer tal- prostata tinvolvi t- tkabbir u d- diviżjoni mhux ikkontrollati taċ- ċelloli fi ħdan il- glandola tal- prostata.
Dan jista ' jseħħ minħabba mutazzjonijiet ġenetiċi li jwasslu għall- espressjoni eċċessiva ta ' ċerti fatturi tat- tkabbir jew l- inattivazzjoni ta ' ġeni soppressuri tat- tumur.
Dawn il- mutazzjonijiet jistgħu jirriżultaw fit- tkabbir mhux regolat taċ- ċelloli, li jwassal għall- formazzjoni ta ' tumur.
Hekk kif it- tumur jikber, jistaʼ jinvadi t- tessuti u l- organi fil- viċin, bħall- bużżieqa, ir- rektum, u n- noduli limfatiċi fil- viċin.
F' xi każijiet, iċ- ċelloli tal- kanċer jistgħu jinfirdu mit- tumur primarju u jinfirxu lejn partijiet oħra tal- ġisem permezz tas- sistema tad- demm jew tal- limfa, proċess magħruf bħala metastażi.
Ladarba l- kanċer jinfirex, jista ' jkun iktar diffiċli li jiġi kkurat.
Il- kanċer tal- prostata jista ' jkun influwenzat ukoll minn fatturi ormonali, b' mod partikolari l- ormon androgen testosterone.
It- testosterone jista ' jistimula t- tkabbir taċ- ċelloli tal- kanċer tal- prostata, u ħafna trattamenti għall- kanċer tal- prostata jimmiraw biex inaqqsu l- livelli ta ' dan l- ormon jew jimblukkaw l- effetti tiegħu.
Fil- qosor, il- patofiżjoloġija tal- kanċer tal- prostata tinvolvi t- tkabbir u d- diviżjoni mhux ikkontrollati taċ- ċelloli fi ħdan il- glandola tal- prostata, li jistgħu jiġu influwenzati minn fatturi ġenetiċi, ormonali, u ambjentali.
Il-fehim tal-mekkaniżmi sottostanti tal-marda huwa kruċjali għall-iżvilupp ta' trattamenti effettivi u t-titjib tar-riżultati għall-pazjenti b'kanċer tal-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.
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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Jekk jogħġbok ibgħatilna email b'kull mistoqsija / suġġeriment.
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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