PARP Inhibitor Biomarkers: Understanding the
Role of BRCA Mutations and Other Predictors of Response

Poly
(ADP-ribose) polymerases or PARP inhibitors are a class of targeted cancer
drugs that have shown promising results in the treatment of certain cancers.
PARP inhibitors work by blocking an enzyme called poly (ADP-ribose) polymerase
(PARP) that plays a key role in DNA repair. By blocking PARP, these drugs
prevent cancer cells from repairing damage to their DNA caused by chemotherapy,
radiation therapy or other cancer treatments. This leads to cancer cell death.



Initial clinical trials showed PARP
Inhibitor Biomarkers to be most beneficial for patients with tumors
having defects in the homologous recombination repair (HRR) pathway, the main
pathway cells use for repairing double-stranded DNA breaks. The most common HRR
pathway defects are germline (inherited) mutations in the BRCA1 and BRCA2
genes. Women who inherit mutations in these genes have greatly increased
lifetime risks of developing breast and ovarian cancers. Tumors with BRCA
mutations have proven highly responsive to PARP inhibitor treatment.



BRCA Mutations as Predictors of Response



BRCA1 and BRCA2 gene mutations account for the majority of cancers associated
with defective HRR. Clinical trials have demonstrated remarkable responses to
PARP inhibitors in patients with BRCA-mutated breast, ovarian and prostate
cancers. PARP inhibitors have shown objective response rates of around 60% in
platinum-resistant or platinum-refractory high-grade serous ovarian cancer
patients with known BRCA mutations.

Get More
Insights On, PARP
Inhibitor Biomarkers