Molecular sub-typing and exploration of key signalling pathways involved in complicating the disease

Nikhil Ponnoor Anto, Amitha Muraleedharan, Rashmi Mittal

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations

Abstract

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.

Original languageEnglish
Title of host publicationTherapeutic Drug Targets and Phytomedicine For Triple Negative Breast Cancer
PublisherBentham Science Publishers
Pages47-72
Number of pages26
ISBN (Electronic)9789815079784
ISBN (Print)9789815079791
DOIs
StatePublished - 13 Jan 2023

Keywords

  • Androgen receptors
  • Angiogenesis
  • Apoptosis
  • Autophagy
  • Copier overdrive
  • Invasion
  • Lymphoplasmacytic infiltration
  • MTOR
  • Metastasis
  • MiRNAs
  • Monoclonal antibodies
  • Mutational analysis
  • Oncogenes
  • PI3k/Akt
  • Pro-survival
  • Proproliferative
  • Tumor suppressor

ASJC Scopus subject areas

  • General Medicine

Fingerprint

Dive into the research topics of 'Molecular sub-typing and exploration of key signalling pathways involved in complicating the disease'. Together they form a unique fingerprint.

Cite this