Molecular heterogeneity and MYC dysregulation in triple-negative breast cancer: genomic advances and therapeutic implications.

Triple-negative breast cancer (TNBC) is characterized by a diverse range of molecular features that have been extensively studied. MYC plays a critical role in regulating metabolism, differentiation, proliferation, cell growth, and apoptosis. Dysregulation of MYC is associated with poor prognosis and contributes to the development and progression of breast cancer. A particularly intriguing aspect of TNBC is its association with tumors in BRCA1 mutation carriers, especially in younger women. MYC may also contribute to resistance to adjuvant treatments. For TNBC, targeting MYC-regulated pathways in combination with inhibitors of other carcinogenic pathways offers a promising therapeutic approach. Several signaling pathways regulate TNBC, and targeting these pathways could lead to effective therapeutic strategies for breast cancer. Advances in genomic tools, such as CRISPR-Cas9, next-generation sequencing, and whole-exome sequencing, are revolutionizing breast cancer diagnoses. These technologies have significantly enhanced our understanding of MYC oncogenesis, particularly through CRISPR-Cas9 and NGS. Targeting MYC and its partner MAX could provide valuable insights into TNBC. Moreover, the therapeutic potential of targeting MYC-driven signaling mechanisms and their interactions with other oncogenic pathways, including PI3K/AKT/mTOR and Wnt/β-catenin, is increasingly recognized. Next-generation sequencing and CRISPR-Cas9 represent significant breakthroughs in genomic tools that open new opportunities to explore MYC's role in TNBC and facilitate the development of personalized treatment plans. This review discusses the future clinical applications of personalized treatment strategies for patients with TNBC.