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Coxibs: pharmacology, toxicity and efficacy in cancer clinical trials

Luis A Garcia Rodriguez1, Lucia Cea-Soriano, Stefania Tacconelli

  • 1Centro Español de Investigacion Farmacoepidemiologica, Madrid, Spain. lagarcia@ceife.es

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer
|August 16, 2012
PubMed

Insights

Nonsteroidal anti-inflammatory drugs (NSAIDs), particularly coxibs, show promise in reducing colorectal cancer (CRC) risk but pose cardiovascular risks. Low-dose aspirin may offer a safer chemoprevention strategy for CRC.

Area of Science:

  • Oncology
  • Pharmacology
  • Cardiovascular Medicine

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs), especially cyclooxygenase (COX)-2 selective inhibitors (coxibs), have demonstrated a reduced risk of colorectal cancer (CRC) onset and progression in epidemiological and experimental studies.
  • The clinical application of coxibs for cancer chemoprevention was curtailed due to identified cardiovascular (CV) risks.
  • Understanding the mechanisms behind NSAID-associated CV toxicity is crucial for evaluating their therapeutic potential.

Purpose of the Study:

  • To summarize current knowledge on the role of NSAIDs, particularly coxibs, in colorectal cancer.
  • To discuss the clinical data and plausible mechanisms of cardiovascular hazards associated with NSAIDs and coxibs.
  • To explore the potential for chemoprevention of CRC using NSAIDs, considering both benefits and risks.

Main Methods:

  • Review of epidemiological and experimental studies on NSAIDs, coxibs, and colorectal cancer.
  • Analysis of clinical data regarding cardiovascular risks associated with NSAIDs and coxibs.
  • Discussion of proposed mechanisms for NSAID- and coxib-induced cardiovascular toxicity.

Main Results:

  • NSAIDs and coxibs have been reported to reduce the risk of developing colonic tumors.
  • Cardiovascular risks associated with NSAIDs and coxibs have led to the halting of their use in chemoprevention.
  • Potential mechanisms for CV toxicity involve the differential inhibition of COX-1 and COX-2 pathways, affecting prostacyclin and thromboxane A(2) (TXA(2)) biosynthesis.

Conclusions:

  • Coxibs may be considered for specific patient groups, such as younger individuals with familial adenomatous polyposis (FAP), but CV risk remains a concern.
  • Recent findings indicate enhanced thromboxane A(2) biosynthesis in colon tumorigenesis, suggesting a role for COX-1 inhibition.
  • Low-dose aspirin, primarily inhibiting platelet COX-1, may represent a viable option for CRC chemoprevention, while the use of coxibs depends on identifying patients susceptible to thrombotic events through COX-2 inhibition biomarkers.

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