Molecular oncology of breast cancer

Himanshu Joshi, Michael F. Press

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

16 Scopus citations


Breast cancer, like other cancers, is a genetic disease. The disease is caused by acquired molecular alterations during the lifetime of an individual and by inherited mutant genes. Risk for breast cancer development is also impacted by hormonal factors through control of breast proliferative activity. Although most DNA sequence alterations have no carcinogenic potential, functional changes in critical regulatory genes have the potential to affect important pathways that provide growth advantages for the cells having these alterations. While a wide range of alterations are known, expression array analyses have permitted identification of intrinsic breast cancer subtypes (luminal A, luminal B, HER2-enriched, basal-like), which are associated with differences in patient outcomes as well as responsiveness to therapies. Currently, only a limited number of molecular alterations (expression levels of estrogen receptor-alpha, progesterone receptor, and HER2) are established as critically important for breast cancer patient treatment decisions. These predictive markers permit selection of patients for antihormone, anti-HER2, and CDK4/6 inhibitor therapies. Nevertheless, it is anticipated that better understanding of genome-wide alterations provided by recent genomic, transcriptomic, and epigenomic studies will not only lead to a better understanding of the biological pathways that transform normal cells to malignant growth but will also identify critical alterations that may be susceptible to development of new targeted therapies.

Original languageEnglish
Title of host publicationThe Breast
Subtitle of host publicationComprehensive Management of Benign and Malignant Diseases
PublisherElsevier Inc.
ISBN (Print)9780323359559
StatePublished - 2018
Externally publishedYes


  • Acquired alterations
  • Cancer stem cells
  • Familial breast cancer
  • Gene amplification
  • Genomics
  • Intrinsic subtypes
  • Mutations
  • Predictive markers


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