GENETIC PROSTATE CANCER
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DNA Repair & Cancer Predisposition Genes
ATM (Ataxia-Telangiectasia Mutated) – Involved in DNA damage repair; mutations increase the risk of breast, pancreatic, and prostate cancer, as well as ataxia-telangiectasia, a neurodegenerative disorder.
BRCA1 (Breast Cancer 1) – A tumour suppressor gene crucial for DNA repair; mutations significantly increase the risk of breast, ovarian, prostate, and pancreatic cancer.
BRCA2 (Breast Cancer 2) – Works similarly to BRCA1 in DNA repair; mutations raise the risk of breast, ovarian, prostate, and pancreatic cancer, as well as male breast cancer.
CHEK2 (Checkpoint Kinase 2) – Regulates the DNA damage response; mutations increase the risk of breast, prostate, and colorectal cancer.
EPCAM (Epithelial Cell Adhesion Molecule) – Affects cell adhesion and indirectly silences MSH2, leading to Lynch syndrome, which increases colorectal, endometrial, and other cancer risks.
Mismatch Repair & Prostate Cancer Genes
HOXB13* (Homeobox B13) – Regulates prostate development; mutations are associated with hereditary prostate cancer.
MLH1 (MutL Homolog 1) – A key DNA mismatch repair (MMR) gene; mutations cause Lynch syndrome, leading to increased risk of colorectal, endometrial, and other cancers.
MSH2 (MutS Homolog 2) – Works with MLH1 in mismatch repair; mutations lead to Lynch syndrome, predisposing individuals to colorectal and endometrial cancer.
MSH6 (MutS Homolog 6) – Works with MSH2 in mismatch repair; mutations cause Lynch syndrome, with a higher risk of endometrial and colorectal cancer.
NBN (Nibrin, also known as NBS1) – Part of the DNA damage repair complex; mutations increase the risk of breast, prostate, and other cancers, and can cause Nijmegen breakage syndrome.
Other Cancer-Related Genes
PALB2 (Partner and Localizer of BRCA2) – Works with BRCA2 in DNA repair; mutations significantly increase the risk of breast, ovarian, and pancreatic cancer.
PMS2 (PMS1 Homolog 2, Mismatch Repair System Component) – Another MMR gene; mutations contribute to Lynch syndrome, though with a slightly lower cancer risk than MLH1 or MSH2 mutations.
RAD51D (RAD51 Homolog D) – Involved in homologous recombination repair; mutations increase the risk of ovarian and breast cancer.
TP53 (Tumour Protein p53) – Known as the "guardian of the genome", this tumour suppressor regulates cell growth and apoptosis; mutations cause Li-Fraumeni syndrome, leading to a very high risk of multiple early-onset cancers, including breast, brain, sarcomas, and leukaemias.
*The HOXB13 gene encodes a transcription factor involved in prostate gland development and cell differentiation.
HOXB13 G84E Variant (rs138213197)
This specific missense mutation (G84E) results in an amino acid change from glycine (G) to glutamic acid (E).
Clinical significance:
This variant is strongly associated with an increased risk of hereditary prostate cancer, particularly in Northern European populations.
Carriers of this mutation have a 2- to 5-fold increased risk of developing early-onset and familial prostate cancer.
It is not linked to aggressive prostate cancer, but rather to an increased lifetime risk of developing the disease.
Other Considerations
Testing for HOXB13 G84E is generally recommended for individuals with a strong family history of prostate cancer.
Unlike BRCA1/BRCA2 mutations, the impact on other cancers is limited, though some studies suggest a possible minor increase in breast cancer risk.