HOXB13 and other high penetrant genes for prostate cancer.

Document Type

Article

Publication Date

7-2016

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This article has been peer reviewed. It is the author’s final published version in Asian Journal of Andrology

Volume 18, Issue 4, July 2016, Pages 530-532.

The published version is available at DOI: 10.4103/1008-682X.175785. Copyright © AJA, SIMM & SJTU

Abstract

Cancer initiation and progression is the result of an accumulation of mutations in key tumor suppressor genes, mismatch repair genes, or oncogenes, which impact cancer cell growth, death, and differentiation. Mutations occurring in cancer tissue are termed somatic; whereas, heritable mutations that may be passed onto subsequent generations occur in germline DNA. It is these germline mutations that can lead to cancer family syndromes whereby family members carrying a deleterious germline mutation have an increased susceptibility to certain cancer phenotypes. Common features of hereditary cancer syndromes include early age-of-onset, multiple affected generations, rare tumor types, and/or multiple primary malignancies. Approximately, 5%-10% of all common cancers, including prostate cancer, have a hereditary component and are attributable to highly penetrant germline mutations.1 Across all cancer types, known cancer susceptibility syndromes number >100; however, it is important to note that mutations in high-penetrance genes explain only a fraction of heritable cancers.2 Well-known examples of hereditary cancer syndromes include Lynch (HNPCC), Cowden (PHTS), Li-Fraumeni, and Hereditary Breast and Ovarian Cancer (HBOC) syndromes, which are attributable to mutations in mismatch repair genes, PTEN, p53, and BRCA1/2, respectively.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License.

PubMed ID

27034017

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