Journals / Mustafa Kemal Üniversitesi Tıp Dergisi / 2020 / Cilt: 11 - Sayı: 41

Molecular Pathways of Prostate Carcinoma

Prostat Karsinomunun Moleküler Yolakları

Pages
118–123
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Therefore, we talked about the major genetic and epigenetic changes involved in prostate carcinoma.

📌 3 Key Takeaways

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Objective & Hypothesis:Prostate cancer is one of the most common types of cancer with rapidly growing incidence rates in the world.
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Key Findings & Data:The incidence and mortality rates of prostate cancer are widely variable in different populations.
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Conclusion & Impact:Therefore, we talked about the major genetic and epigenetic changes involved in prostate carcinoma.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:prostat karsinomu · moleküler yolaklar · tedavi

Abstract

Prostate cancer is one of the most common types of cancer with rapidly growing incidence rates in the world. The incidence and mortality rates of prostate cancer are widely variable in different populations. The prostate cancer includes multiple genetic modifications such as deletion in specific genome sequences of tumor-suppressor genes and alterations in specific chromosomal sites associated with oncogene activation. It is difficult to determine whether the hereditary changes leading to prostate cancer are associated with one or more specific genetic features. Prostate carcinogenesis is complex and has not been fully explained. If we can better understand prostate carcinogenesis, we can also find targeted therapy. Therefore, we talked about the major genetic and epigenetic changes involved in prostate carcinoma.

Özet

Prostat kanseri, dünyada hızla artan insidans oranlarına sahip en yaygın kanser türlerinden biridir. Prostat kanseri insidansı ve mortalite oranları farklı popülasyonlarda büyük ölçüde değişkendir. Prostat kanseri, tümör baskılayıcı genlerin spesifik genom sekanslarında delesyon ve onkogen aktivasyonu ile ilişkili spesifik kromozomal bölgelerdeki değişiklikler gibi çoklu genetik modifikasyonları içerir. Prostat kanseri yol açan kalıtsal değişikliklerin bir veya daha fazla spesifik genetik özellik ile ilişkili olup olmadığını belirlemek zordur. Prostat karsinogenezi çok karmaşık olup hala mekanizmaları olarak açıklanmamıştır. Eğer prostat karsinogenezini daha iyi anlayabilirsek bu hastalar için hedefe yönelik tedavi de bulabiliriz. Bu nedenle biz burada prostat karsinomunda yer alan büyük genetik ve epigenetik değişikliklerden bahsetmek istedik.

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Cite This Article

BAYRAMOĞLU, Z., ÜNAL, B. (2020). Molecular Pathways of Prostate Carcinoma. Mustafa Kemal Üniversitesi Tıp Dergisi, Cilt: 11 - Sayı: 41, 118–123. https://ajindex.com/articles/288545

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References (14)

  1. Ferlay J, Colombet M, Soerjomataram I, Mathers C, Parkin DM, Piñeros M, et al. GLOBACAN 2018 Cancer incidence and mortality data: sources and methods by country, GLOBOCAN2018, Available from: http://gco.iarc.fr. Accessed 10 November 2019. https://doi.org/10.1002/ijc.31937
  2. Getaneh AM, Heijnsdijk E, de Koning H. The role of modelling in the policy decision making process for cancer screening: example of prostate specific antigen screening. Public health research & practice. 2019; 29(2). https://doi.org/10.17061/phrp2921912
  3. Cooperberg MR, Carroll PR, Klotz L. Active surveillance for prostate cancer: progress and promise. J Clin Oncol. 2011; 29 (27): 3669-76. https://doi.org/10.1200/JCO.2011.34.9738
  4. Jeldres C, Suardi N, Walz J, Hutterer GC, Ahyai S, Lattouf JB, et al. Validation of the contemporary epstein criteria for insignificant prostate cancer in European men. European urology 2008;54(6), 1306-1313. https://doi.org/10.1016/j.eururo.2007.11.057
  5. Lu-Yao GL, Albertsen PC, Moore DF, Lin Y, DiPaola RS, Yao SL. Fifteen-year outcomes following conservative management among men aged 65 years or older with localized prostate cancer. European urology, 2015;68(5), 805-811. https://doi.org/10.1016/j.eururo.2015.03.021
  6. Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran pathologic basis of disease, professional edition e-book. Elsevier health sciences; 2014.p.266-80.
  7. Dutt S, Gao AC. The molecular basis of prostate carcinogenesis. In The Molecular Basis of Human Cancer 2017;pp. 423-445.
  8. Humana Press,
  9. New York, NY. https://doi.org/10.1007/978-1-59745-458-2_27
  10. Rodrigues DN, Butler LM, Estelles DL, De Bono JS. Molecular pathology and prostate cancer therapeutics: from biology to bedside. The Journal of pathology, 2014;232(2), 178-184. https://doi.org/10.1002/path.4272
  11. Falzarano SM, Zhou M, Carver P, Tsuzuki T, Simmerman K, He H, et al. ERG gene rearrangement status in prostate cancer detected by immunohistochemistry. Virchows Archiv, 2011;459(4), 441. https://doi.org/10.1007/s00428-011-1128-4
  12. King JC, Xu J, Wongvipat J, Hieronymus H, Carver BS, Leung DH, et al. Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis. Nature genetics, 2009;41(5), 524. https://doi.org/10.1038/ng.371
  13. Tomlins SA, Day JR, Lonigro RJ, Hovelson DH, Siddiqui J, Kunju LP, et al. Urine TMPRSS2: ERG plus PCA3 for individualized prostate cancer risk assessment. European urology, 2016;70(1), 45-53. https://doi.org/10.1016/j.eururo.2015.04.039
  14. Korkolopoulou P, Levid