Triple-negative breast cancer is characterized by distinct molecular profiles,
unique metastatic patterns, aggressive behavior, lacks the targeted therapeutic
approach, and caused significant mortality worldwide. The molecular complexity of
angiogenesis, autophagy, apoptosis, and metastasis process in TNBC has fostered
research efforts to unleash the molecular, pathological, and genetic drivers of their
lethal cascade. This complex disease entity involves PI3k/Akt/mTOR, NF-kB, ERRs,
and miRNA trafficking which has further worsened the clinical outcome. Due to their
heterogeneous nature, none of the drugs were able to completely target the TNBC
tumor spectrum. This chapter highlights the classification of TNBC on the basis of
aberrated copy number, histology, proteomic, and mutational profiles to understand the
aetiology of the disease. The identification of therapeutic vulnerabilities was also
carried out by gaining insights into the above-mentioned signalling pathways and their
role in further complicating the disease.
Keywords: Androgen receptors, Angiogenesis, Apoptosis, Autophagy, Copier overdrive, Invasion, Lymphoplasmacytic infiltration, Metastasis, MiRNAs, Monoclonal antibodies, MTOR, Mutational analysis, Oncogenes, PI3k/Akt, Proproliferative, Pro-survival, Tumor suppressor.
