Research detection kit Lucksen®

for BRAF mutationsleadfor TP53 gene

Homologous Recombination Deficiency (HRD) typically refers to a cellular-level impairment in homologous recombination repair (HRR) functionality. This condition can result from various factors, including germline mutations in HRR-related genes, somatic mutations, and epigenetic inactivation [1]. TCGA studies suggest that approximately half of high-grade serous ovarian cancer (HGSOC) may exhibit HRD, but only about 20% of patients carry pathogenic BRCA1/2 mutations. HRD can also result from other factors such as BRCA1 methylation and mutations in other HRR genes [2]. HRD can lead to specific, quantifiable, and stable genomic alterations. Loss of Heterogeneity (LOH), Telomeric Allelic Imbalance (TAI), and Large-scale State Transitions (LST), are used as indicators of Genomic Scar. The unweighted sum of these markers is used as an HRD score [3]. Combining pathogenic mutations in BRCA1/2 with the HRD score can nearly double the population benefiting from testing compared to testing for BRCA1/2 gene mutations alone. HRD STATUS INDICATES EFFICACY OF PARP INHIBITORS Clinical testing for HRD has significant application value in predicting the efficacy of PARP inhibitors in the treatment of advanced ovarian cancer. It can stratify ovarian cancer patients, optimize treatment decisions, and maximize the clinical benefit of PARP inhibitors. Furthermore, in breast cancer, pancreatic cancer, and prostate cancer, HRD testing may also have potential guidance value for the clinical use of PARP inhibitors or platinum compounds [1].