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Molecular aspects of breast cancer resistance to drugs (Review)

Gloria M Calaf1, Andrea B Zepeda2, Rodrigo L Castillo3

  • 1Instituto de Alta Investigación, Universidad de Tarapacá, Arica 1001236, Chile.

International Journal of Oncology
|June 23, 2015
PubMed

Insights

Breast cancer remains a major global health threat. Understanding its causes, including genetic mutations like BRCA1/BRCA2 and HER-2/neu overexpression, is key to improving patient outcomes and developing targeted therapies.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Breast cancer is a leading cause of death in women globally, despite ongoing research.
  • Carcinogenesis involves a complex progression from genetic mutations to metastasis.
  • Hereditary factors account for only 8% of breast cancers, primarily linked to BRCA1/BRCA2 mutations.

Purpose of the Study:

  • To review the pathophysiology of breast cancer.
  • To highlight the role of genetic mutations and specific biomarkers in breast cancer development and treatment.
  • To underscore the significance of understanding breast cancer etiology for improved patient management.

Main Methods:

  • Literature review of breast cancer pathophysiology.
  • Analysis of genetic factors (BRCA1/BRCA2) and their associated risks.
  • Examination of the role of HER-2/neu overexpression in treatment response.

Main Results:

  • Somatic mutations, DNA repair alterations, and growth suppressor inhibition drive carcinogenesis.
  • BRCA1/BRCA2 mutations increase the risk of second primary breast and ovarian cancers.
  • HER-2/neu overexpression (~30% of tumors) predicts response to chemotherapy and endocrine therapy.

Conclusions:

  • Understanding the multifactorial etiology of breast cancer, including genetic predispositions and molecular markers, is crucial.
  • Targeted therapies based on genetic profiles and biomarkers like HER-2/neu can improve treatment efficacy.
  • Further research into unknown etiologies is necessary to reduce breast cancer mortality.

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