VUS: BP1 (Strong) is supported by residue 2233 being outside BRCA2 critical domains and SpliceAI maximum delta 0.014 indicating no predicted splicing impact.
BRCA2 encodes a DNA repair protein that maintains genome stability by repairing double-strand breaks through homologous recombination and by protecting DNA replication forks. It acts as a tumor suppressor, and inherited loss-of-function changes cause hereditary breast and ovarian cancer syndrome, with elevated lifetime risks of breast, ovarian, prostate, and pancreatic cancers; biallelic changes cause Fanconi anemia complementation group D1. Reduced or altered BRCA2 activity is implicated in multiple tumor types, and PARP inhibitors are an approved treatment for BRCA2-associated ovarian and breast cancers.
This missense change affects BRCA2, a tumor-suppressor gene whose DNA double-strand-break repair function supports genome stability and whose inherited loss of function causes hereditary breast and ovarian cancer syndrome.
VUS: BP1 (Strong) is supported by residue 2233 being outside BRCA2 critical domains and SpliceAI maximum delta 0.014 indicating no predicted splicing impact.