Genetics of Prostate Carcinoma

Authors

  • Božo Krušlin Ljudevit Jurak Department of Pathology and Cytology, Sestre Milosrdnice University Hospital Centre, Zagreb ; Department of Pathology, School of Medicine, University of Zagreb, Zagreb
  • Lucija Škara University of Zagreb, School of Medicine, Scientific Group for Research on Epigenetic Biomarkers, Zagreb
  • Tonći Vodopić Department of Pathology, Cytology and Forensic Medicine, Varaždin General Hospital, Varaždin
  • Borna Vrhovec Department of Urology, Sestre Milosrdnice University Hospital Centre, Zagreb
  • Jure Murgić Department of Oncology, Sestre Milosrdnice University Hospital Centre, Zagreb
  • Goran Štimac Department of Urology, Sestre Milosrdnice University Hospital Centre, Zagreb
  • Ana Fröbe Department of Pathology, School of Medicine, University of Zagreb, Zagreb ; Department of Oncology, Sestre Milosrdnice University Hospital Centre, Zagreb
  • Cvjetko Lež Department of Pathology and Cytology, Zabok General Hospital, Bračak and Josip Juraj Strossmayer University of Osijek, Faculty of Dental Medicine and Health Osijek
  • Monika Ulamec Ljudevit Jurak Department of Pathology and Cytology, Sestre Milosrdnice University Hospital Centre, Zagreb ; Department of Pathology, School of Medicine, University of Zagreb, Zagreb
  • Koraljka Gall-Trošelj Laboratory for Epigenomics, Division of Molecular Medicine, Ruđer Bošković Institute, Zagreb

DOI:

https://doi.org/10.5644/ama2006-124.327

Keywords:

Prostate Cancer, Genetic Changes, Molecular Subtypes, Treatment

Abstract

The aim of this review is to provide a brief overview of some current approaches regarding diagnostics, pathologic features, treatment, and genetics of prostate carcinoma (PCa). Prostate carcinoma is the most common visceral tumor and the second most common cancer-related cause of death in males. Clinical outcomes for patients with localized prostate cancer are excellent, but despite advances in prostate cancer treatments, castrate-resistant prostate cancer and metastatic prostate cancer patients have a poor prognosis. Advanced large-scale genomic studies revealed a large number of genetic alterations in prostate cancer. The meaning of these alterations needs to be validated in the specific prostate cancer molecular subtype context. Along these lines, there is a critical need for establishing genetically engineered mouse models, which would include speckle type BTB/POZ protein and isocitrate Dehydrogenase (NADP (+)) 1 mutant, as well as androgen receptor neuroendocrine subtypes of prostate cancer. Another urgent need is developing highly metastatic prostate cancer models, as only up to 17% of available models dis- play bone metastases and exhibit a less typical neuroendocrine prostate cancer or sarcomatoid carcinoma. Moreover, androgen deprivation and relapse should be mimicked in the genetically engineered mouse models, as androgen independence may yield a better model for metastatic castrate-resistant prostate cancer. The development of such refined animal models should be guid- ed by comparative genomics of primary versus corresponding metastatic tumors. Such an approach will have the potential to illuminate the key genetic events associated with specific molecular prostate cancer subsets and indicate directions for effective therapy.

Conclusion. Despite excellent results in the treatment of localized prostatic carcinoma, castrate-resistant prostate can- cer and metastatic prostate cancer have a poor prognosis. Advanced large-scale genomic studies revealed a large number of ge- netic alterations in PCa. Experimental models of prostate carcinoma in genetically modified mice could provide new data about the genetic changes in such cancers and help in developing better animal models for treatment resistant prostate carcinomas.

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Published

2021-05-26

How to Cite

Krušlin, B., Škara, L., Vodopić, T., Vrhovec, B., Murgić, J., Štimac, G., Fröbe, A., Lež, C., Ulamec, M., & Gall-Trošelj, K. (2021). Genetics of Prostate Carcinoma. Acta Medica Academica, 50(1), 71–87. https://doi.org/10.5644/ama2006-124.327

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