Manisha Gupta, Umesh Kumar, Shoorvir Singh
Breast cancer is a very diverse illness that is caused by a complex interaction of environmental, molecular, and hereditary variables. Notch signaling, the PI3K/AKT/mTOR pathway, the MAPK/ERK pathway, and the NF-κB pathway are important participants in the development, progression, and metastasis of breast cancer. These pathways control vital biological functions including metastasis, apoptosis, cell survival, and proliferation. Furthermore, mutations in the BRCA1/BRCA2-mediated DNA damage repair pathways are closely linked to hereditary breast malignancies and are essential for preserving genomic integrity. Many breast cancer subtypes are characterised by disruptions in the hormonal signaling pathways, namely HER2 receptor signaling, and Estrogen Receptor (ER) signaling, which inform treatment approaches. Additionally, breast cancer frequently exhibits dysregulation of apoptotic pathways, encompassing both intrinsic and extrinsic mechanisms, which contributes to resistance to treatment. Comprehending the complex network of these pathways not only aids in clarifying the biology of breast cancer but also creates new opportunities for targeted treatments, including kinase inhibitors for PI3K/AKT-driven subtypes and PARP inhibitors for tumors with BRCA mutations. Precision treatment and better patient outcomes are made possible by this thorough understanding of the molecular processes underlying breast cancer.