ABSTRACT
Colorectal cancer is one of the most common malignant tumors, and its morbidity and mortality increase year by year. In recent years, some patients with colorectal cancer have benefited from precision targeted therapies, but the overall prognosis is still unsatisfactory. Treatment of homologous recombination deficiency represented by BRCA1/2 has become a hot research direction at present. With the wide application and exact curative effect of poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors in ovarian cancer, breast cancer, pancreatic cancer and other malignant tumors, PARP inhibitors are also gradually being used in colorectal cancer. This review summarizes the current research progress of PARP inhibitors in treatment of colorectal cancer.
ABSTRACT
Although adding platinum to taxane- and anthracycline-based neoadjuvant chemotherapy regimens for triple-negative breast cancer (TNBC) patients can significantly improve the pathological complete response (pCR) rate and long-term survival, it is associated with higher treatment-related adverse events (AEs) . Current researches focus on the response predictors to select patients who may benefit from platinum-based chemotherapy. Homologous recombination deficiency (HRD) can identify patients who truly need platinum drugs, that is, those with BRCA wild-type but HRD tumors. Results suggest that anthracycline-based chemotherapy is sufficient for BRCA mutation carriers and that non-HRD carriers will not benefit from the added carboplatin.
ABSTRACT
Subject(s)
Humans , Arm , Asian People , Bias , Carboplatin , Disease-Free Survival , Doxorubicin , Drug Therapy , Follow-Up Studies , Maintenance Chemotherapy , Ovarian Neoplasms , Prognosis , Quality of Life , Recombination, Genetic , Sample SizeABSTRACT
Ovarian cancer patients with homologous recombination deficiencies exhibit specific clinical behaviors, and improved responses to treatments, such as platinum-based chemotherapy and poly (ADP-ribose) polymerase (PARP) inhibitors, have been observed. Germline mutations in the BRCA 1/2 genes are the most well-known mechanisms of homologous recombination deficiency. However, other mechanisms, such as germline and somatic mutations in other homologous recombination genes and epigenetic modifications, have also been implicated in homologous recombination deficiency. The epidemiology and implications of these other mechanisms need to be better understood to improve the treatment strategies for these patients. Furthermore, an evaluation of various diagnostic tests to investigate homologous recombination deficiency is essential. Comprehension of the role of homologous recombination deficiency in ovarian cancer also allows the development of therapeutic combinations that can improve the efficacy of treatment. In this review, we discuss the epidemiology and management of homologous recombination deficiency in ovarian cancer patients.