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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration
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Germline pathogenic variants in prostate cancer.

Yousif M Shakroo1, Charles A Seabury1, Kenneth A Iczkowski2

  • 1Virginia Urology, Richmond, VA 23235, United States.

Pathology, Research and Practice
|November 14, 2024
PubMed
Summary

A study found that 12% of prostate cancer patients meeting genetic testing guidelines had pathogenic germline variants. Family history significantly increased the likelihood of carrying these variants, highlighting the role of hereditary factors in prostate cancer.

Keywords:
BRCA2Genetic testingGermline mutationHOXB13MUTYHProstate cancer

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Area of Science:

  • Oncology
  • Human Genetics
  • Cancer Genomics

Background:

  • Prostate cancer (PC) is often sporadic, but a hereditary component is recognized.
  • Germline genetic variants are implicated in PC heritability.
  • Identifying these variants is crucial for understanding PC risk and treatment.

Purpose of the Study:

  • To investigate the prevalence of germline pathogenic variants in prostate cancer patients.
  • To correlate genetic findings with clinicopathologic and demographic data.
  • To assess the impact of family history on the presence of germline variants.

Main Methods:

  • Retrospective chart review and analysis of germline genetic testing results.
  • Classification of genetic variants using ACMG/AMP 2015 guidelines.
  • Data collection included clinicopathologic, demographic, and genetic information from 160 PC patients meeting NCCN guidelines.

Main Results:

  • 12% (19/160) of patients harbored pathogenic or likely pathogenic germline variants.
  • Variants were identified in genes including MUTYH, ATM, BRCA2, CHEK2, PALB2, and HOXB13.
  • No significant differences in clinicopathologic data or variants of uncertain significance were observed between racial/ethnic groups.
  • A family history of cancer was significantly associated with carrying pathogenic/likely pathogenic variants (p=0.002).

Conclusions:

  • Germline pathogenic variants are present in a notable proportion of prostate cancer patients.
  • Family history is a key indicator for hereditary risk in prostate cancer.
  • Larger studies are needed to elucidate the relationship between clinicopathologic features and germline variants in prostate cancer.