What is pathophysiology of Prostate cancer?

['Sel i usebter-agi']

D acu-tt tfizitulujit n waṭṭan n kuruna n tdawsa?

Tasnudert n tdawsa n tdawsa n tdawsa d tamsalt n tnefsit d tdamsa i d-yettawin ɣer usnerni d usnerni n waṭṭan.

Aṭṭan n tgezzayt d afurk amezzangu i d-yettlalen seg izerfan n tgezzayt n uwgelhen, d agman amecṭuḥ, yettcabin ɣer uḥeccad, yezga-d ddaw n tgerjumt deg yirgazen.

Taɣezzfant n uwgelhen tessufuɣ-d aman n tadist, i yettṛebbin yerna yettḥewwiṣen irden.

Ssebba n swaswa n ukansir n tdawsa ur tettwafham ara akken ilaq, maca llan aṭas n yimgan yettwassnen i yesnernayen amihi n usnulfu n waṭṭan.

Gar-asen leɛmer, amezruy n twacult, tawsit, d kra n yimuttiyen ijinitikanen.

Aṭṭan n tgezzayt n uwday d win yettmagaren ugar deg yirgazen meqqren deg leɛmer, s tuget n liḥalat i d-iḍerrun deg yirgazen yesɛan ugar n 65 n yiseggasen.

Rnu ɣer waya, irgazen yesεan amezruy n twacult n ukansir n tbiṭar i yellan deg umihi meqqren, am yergazen n Marikan n Tefriqt akk d yergazen n tegzirt n Karibik.

Tasnudert n tdawsa n tdawsa n uwgelhen tettawi-d ɣef unefli ur nettwaḥkem akked beṭṭu n izerfan deg tdawsa n uwgelhen.

Aya yezmer ad d-yeḍru ɣef lǧal n ubeddel n ujinit yettawin ɣer usemɣer n kra n yimgan n unefli neɣ asedrem n yijiniten imḥettmen n ugama.

Imuttiyen-a zemren ad d-awin ɣer unefli ur nettwassen ara n tsilunin, yettawin ɣer usnulfu n tumert.

Akken ara timɣur tgeṭṭumt, tezmer ad tekcem deg yiẓeḍwan d izerfan iqerben ɣur-s, am tεebbuḍt, tadist, d yiẓeḍwan imsellumen iqerben ɣur-s.

Deg kra n tegnatin, izirigen n ukunsir zemren ad d-ffɣen seg weglim amezwaru u ad ttwazerɛen ɣer tamiwin nniḍen n tfekka s ubrid n yidammen neɣ n unagraw anmazray, d talilt yettwasnen s yisem n metastase.

Ma ifat yenṭeḍ kanser, yezmer ad yuεer ad t-yeḥlu yiwen.

Aṭṭan n tgezzayt yezmer daɣen ad yettwaḥaz s yimgan ihurmunen, ladɣa ahurmun n androgen testosterone.

Testosterone yezmer ad yessebɣes anerni n tewsitin n ukunsir n tdawsa, dɣa aṭas n yisufar n ukunsir n tdawsa ttnadin ad ssneqsen idisan n urmud-a neɣ ad ḥebsen igmaḍ-is.

S umata, tafizikt n waṭṭan n kuruna n tdawsa tettawi-d ɣef unefli ur nettwaḥkem d beṭṭu n izerfan yellan deg tdawsa, izemren ad ilin ssebba n kra n yimgan amujini, ahurmun d wid n twennaḍt.

Asefhem n yimikanen yellan ddaw n waṭṭan-a d ayen yesɛan azal meqqren i usnerni n yisufar imellḥen d usnerni n yigmaḍ i yimuḍinen yesεan akunsir n tdawsa.

['Tiɣbula']

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.

['Anfafad: amejjay']

['Asmel-a web yettunefk-d kan i yiswiyen n uselmed d usissen, ur d-yettak ara iwellihen imejjayen neɣ isefka udmawanen.']

['Isallen i d-yettunefken ur ilaq ara ad ttwasqedcen i usebded neɣ i usemḥi n kra n wugur n tezmert neɣ aṭṭan, yerna wid yettnadin ɣef yiwellihen imsujjiyen udmawanen yessefk ad ẓren amejjay yesɛan turagt.']

['Ttxil-k ẓer belli azeṭṭa amseddayan i d-yettaken tiririyin i tuttriwin, ur iṣeḥḥa ara mliḥ ma yella d ayen yerzan uḍḍun. D amedya, amḍan n yimdanen yettwaḍḍfen s kra n waṭṭan.']

['Ssutur dima ṛṛay n ṭṭbib-ik neɣ n kra n umejjay-nniḍen ara iwalmen ɣef waṭṭan-ik. Ɣur-k ad tḥeqreḍ ṛṛay n ṭṭbib amsadur neɣ ad tεeṭṭleḍ deg usuter-is ɣef lǧal n kra i teɣriḍ deg usmel-a. Ma tɣileḍ ahat tesεiḍ liḥala n tεeǧlanit deg tezmert, siwel 911 neɣ ṛuḥ ɣer texxamt n tεeǧlanit i d-iqerben. Ulac assaɣ gar ṭṭbib d umuḍin i d-yettnulfun s usmel-a neɣ aseqdec-is. BioMedLib neɣ ixeddamen-is, neɣ kra n win yettekkiyen deg usmel-a, ur d-ttaken ara yakk kra n yisumren, s wawal neɣ s usemres, ɣef ayen yerzan isallen i d-yettunefken dagi neɣ aseqdec-is.']

['Anekcum: azref n uḍfar']

['Asaḍuf n umeskar n yizerfan n wemdan n alfin (Digital Millennium Copyright Act) n 1998, 17 U.S.C. § 512 (DMCA) yettak-d ttawil i yimeskaren n yizerfan n wemdan i yumnen belli ayen i d-yettbanen deg Internet yettḍurru izerfan-nsen ddaw usaḍuf n umeskar n yizerfan n wemdan n Marikan. ']

['Ma tumneḍ s wul yelhan belli kra n taɣult neɣ taɣawsa yettwafken deg unermes-nneɣ neɣ deg yiqeddacen-nneɣ tegzem azref-ik n uḥraz, tzemreḍ (neɣ amsedday-ik) ad aɣ-d-tazneḍ izen akken ad nessuter asuffeɣ n taɣult neɣ n taɣawsa-nni, neɣ ad nessader tuqqna ɣer-s. ']

['Isental yessefk ad ttwazen s tira s yimayl (ẓer asebter "Contact" i tansa n yimayl).']

['DMCA teḥwaǧ isalli-inek n tukksa n yizerfan yettwanekṛen ad d-yeglu s yisallen-a: (1) asegzi n umahil yettwaḥerzen s yizerfan yettwanekṛen i d-yettwanekren; (2) asegzi n uḍris yettwanekren d yisallen ara aɣ-yeǧǧen ad d-naf uḍris-nni; (3) isallen n usiwel inek, ladɣa tansa-inek, uṭṭun n tilifun d tansa imayl; (4) awal sɣur-k d akken tumneḍ s wayen yelhan belli aḍris-nni s wamek i d-tettcetkiḍ ur yettwasemres ara sɣur bab n yizerfan, neɣ amesten-is, neɣ s useqdec n kra n usaḍuf; ']

['(5) yiwet n tseddi sɣur-k, yettwatten s uḥasef n lekdeb, d akken isallen yellan deg uzenzi d iṣeḥḥan u tesεiḍ azref ad tesseḍruḍ izerfan umeskar i d-yeqqaren ttwarẓen; ']

['akked (6) azmul n tfekka neɣ n tuqqna tagensit n bab n yizerfan neɣ n umdan yettwafernen ad yexdem s yisem n bab n yizerfan. ']

['Ma ur d-terriḍ ara isallen-agi akk, yezmer ad d-yeglu s uεeṭṭel deg usefrek n ucetki-inek.']

['Assaɣ']

['Ttxil-k azen-aɣ-d imayl ma tesεiḍ asteqsi / asumer.']

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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