Targeting P53 Gene in Breast Cancer

Abstract

Infectious diseases and breast cancer rely heavily on p53, a tumor suppressor that protects genetic integrity. It is present on chromosome 17p13 and controls angiogenesis, programmed cell death, and cell proliferation. The expression of p53 and its isoforms is more predictive of treatment outcomes and responses to chemotherapy for breast cancer patients than the presence or absence of TP53 mutations. Subtype-dependent mutations of p53's negative regulator MDM2 can both be signs of p53 deactivation in breast cancer. Targeting both wild-type and p53 mutant across various subtypes of breast cancer is one possible treatment strategy. Notably, through paracrine signaling, mutant p53 in stromal fibroblasts speeds up the formation of breast tumors. In the progression and trajectory of breast cancer, the pivotal involvement of the p53 gene, alongside the bcl-2 proto-oncogene, is noteworthy. Addressing the role of p53 is crucial in the context of breast cancer development and its course.