在全球范围内，在众多癌症亚型中，乳腺癌 (BC) 是影响女性人群最常见的癌症形式之一。女性的家族史显着增加了患乳腺癌的风险。乳腺癌是由异常乳腺细胞增殖并发展成肿瘤引起的。据估计，5-10% 的乳腺癌是遗传性的，并涉及确保乳腺癌细胞存活和预后的基因突变。最常见的遗传变异导致遗传性乳腺癌，但不限于 p53、BRCA1 和 BRCA2。 BRCA1 和 BRCA2 参与基因组重组、细胞周期监测、程序性细胞死亡和转录调控。当乳腺癌中存在 BRCA1 和 2 遗传变异时，p53 不规则性变得更加普遍。 BRCA1/2 和 p53 基因都参与细胞周期监测。本文讨论了乳腺癌研究的现状，重点关注抑癌基因（BRCA1/2 和 p53）以及结构活性关系研究、FDA 批准的药物以及治疗 BC 的几种治疗方式。目前市场上销售的乳腺癌药物具有不同的副作用，包括贫血、肺炎、恶心、嗜睡和呕吐。因此，开发副作用最小的新型 p53 和 BRCA1/2 抑制剂至关重要。我们在本概述中涵盖了随后（2020 年起）检查的化合物，这些化合物可用作先导化合物。此外，我们还介绍了机械途径，以展示关键的药物靶点以及针对这些靶点的临床和临床后药物在 BC 中的实用性。© 2024。作者获得 Springer Nature Switzerland AG 的独家许可。

Globally, among numerous cancer subtypes, breast cancer (BC) is one of the most prevalent forms of cancer affecting the female population. A female's family history significantly increases her risk of developing breast cancer. BC is caused by aberrant breast cells that proliferate and develop into tumors. It is estimated that 5-10% of breast carcinomas are inherited and involve genetic mutations that ensure the survival and prognosis of breast cancer cells. The most common genetic variations are responsible for hereditary breast cancer but are not limited to p53, BRCA1, and BRCA2. BRCA1 and BRCA2 are involved in genomic recombination, cell cycle monitoring, programmed cell death, and transcriptional regulation. When BRCA1 and 2 genetic variations are present in breast carcinoma, p53 irregularities become more prevalent. Both BRCA1/2 and p53 genes are involved in cell cycle monitoring. The present article discusses the current status of breast cancer research, spotlighting the tumor suppressor genes (BRCA1/2 and p53) along with structural activity relationship studies, FDA-approved drugs, and several therapy modalities for treating BC. Breast cancer drugs, accessible today in the market, have different side effects including anemia, pneumonitis, nausea, lethargy, and vomiting. Thus, the development of novel p53 and BRCA1/2 inhibitors with minimal possible side effects is crucial. We have covered compounds that have been examined subsequently (2020 onwards) in this overview which may be utilized as lead compounds. Further, we have covered mechanistic pathways to showcase the critical druggable targets and clinical and post-clinical drugs targeting them for their utility in BC.© 2024. The Author(s), under exclusive licence to Springer Nature Switzerland AG.