Non-steroidal anti-inflammatory drugs (NSAIDs) and breast cancer risk: differences by molecular subtype

Theodore M Brasky1, Matthew R Bonner, Kirsten B Moysich

  • 1Department of Social and Preventive Medicine, School of Public Health and Health Professions, University at Buffalo, Buffalo, NY, USA. tbrasky@fhcrc.org

Insights

Aspirin use may lower breast cancer risk, but ibuprofen use appears to increase risk for certain subtypes. This highlights how different non-steroidal anti-inflammatory drugs (NSAIDs) affect breast cancer risk differently.

Area of Science:

  • Oncology
  • Epidemiology
  • Pharmacology

Background:

  • Non-steroidal anti-inflammatory drug (NSAID) use has shown inconsistent associations with breast cancer risk.
  • Breast cancer heterogeneity, defined by molecular subtypes, may explain these inconsistencies.
  • Understanding NSAID effects across different breast cancer subtypes is crucial for risk assessment.

Purpose of the Study:

  • To investigate the association between aspirin and ibuprofen use and breast cancer risk across molecular subtypes.
  • To explore whether NSAID effects on breast cancer risk differ by tumor characteristics.
  • To provide insights into the heterogeneous etiologies of breast cancer.

Main Methods:

  • Population-based case-control study in Western New York.
  • Inclusion of 1,170 primary breast cancer cases and 2,115 controls.
  • Logistic regression analysis of recent and lifetime NSAID use (aspirin, ibuprofen).

Main Results:

  • Recent and lifetime aspirin use was associated with reduced breast cancer risk, irrespective of subtype.
  • Recent ibuprofen use was linked to an increased risk of estrogen receptor-positive/progesterone receptor-positive (ER+/PR+), HER2-negative (HER2-), and p53-positive breast cancers.
  • Ibuprofen use was also associated with increased risk for Luminal A and B breast cancer subtypes.

Conclusions:

  • Findings support the hypothesis that breast cancer subtypes have distinct etiologies.
  • Aspirin and ibuprofen demonstrate differential effects on breast cancer risk.
  • Further research is warranted to elucidate the mechanisms behind these varied NSAID effects.