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[Cyclooxygenase 2 and breast cancer. From biological concepts to therapeutic trials]

Jean-Paul Guastalla1, Thomas Bachelot, Isabelle Ray-Coquard

  • 1Centre Léon-Bérard, 28, rue Laennec, 69008 Lyon. guastall@lyon.fnclcc.fr

Bulletin Du Cancer
|July 9, 2004
PubMed

Insights

Cyclooxygenases (Cox) are key enzymes in breast cancer development. Research suggests non-steroidal anti-inflammatory drugs (NSAIDs) may reduce breast cancer risk, with ongoing trials exploring Cox inhibitors for prevention and treatment.

Area of Science:

  • Biochemistry
  • Oncology
  • Molecular Biology

Context:

  • Cyclooxygenases (Cox) are prostaglandin synthetase enzymes implicated in mammary carcinogenesis.
  • Existing research links Cox enzymes to various oncogenes, dietary factors, transcription factors, apoptosis regulators, and angiogenesis pathways.
  • No correlation has been found between Cox2 expression and hormonal receptors in breast cancer.

Purpose:

  • To explore the multifaceted role of cyclooxygenases (Cox) in mammary carcinogenesis.
  • To review the associations between Cox enzymes and oncogenes, dietary components, and molecular pathways relevant to breast cancer.
  • To examine the potential of Cox inhibitors in breast cancer prevention and therapy.

Summary:

  • Cox enzymes are central to breast cancer development, interacting with numerous molecular and cellular pathways.
  • Epidemiological data suggest long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) may lower breast cancer risk.
  • Dietary factors like resveratrol and unsaturated fatty acids show potential in reducing Cox2 expression, warranting further human studies.

Impact:

  • Findings highlight Cox enzymes as potential therapeutic targets for breast cancer prevention and treatment.
  • Clinical trials are investigating the anti-Cox2 drug celecoxib for various breast cancer settings, including prevention, adjuvant therapy, and metastatic disease.
  • This research could lead to novel strategies for managing and preventing breast cancer by targeting the Cox pathway.

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