Does the lipid-lowering peroxisome proliferator-activated receptors ligand bezafibrate prevent colon cancer in patients with coronary artery disease?

doi:10.1186/1475-2840-7-18

Cardiovascular Diabetology

Volume 7

Viewing options:

Abstract
Full text
PDF (353KB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Tenenbaum A
Boyko V
Fisman EZ
Goldenberg I
Adler Y
Feinberg MS
Motro M
Tanne D
Shemesh J
Schwammenthal E
Behar S

on PubMed

Tenenbaum A
Boyko V
Fisman EZ
Goldenberg I
Adler Y
Feinberg MS
Motro M
Tanne D
Shemesh J
Schwammenthal E
Behar S
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Original investigation

Does the lipid-lowering peroxisome proliferator-activated receptors ligand bezafibrate prevent colon cancer in patients with coronary artery disease?

Alexander Tenenbaum¹ , Valentina Boyko² , Enrique Z Fisman¹ , Ilan Goldenberg² , Yehuda Adler¹ , Micha S Feinberg¹ , Michael Motro¹ , David Tanne² , Joseph Shemesh¹ , Ehud Schwammenthal¹ and Solomon Behar²

¹Cardiac Rehabilitation Institute, the Chaim Sheba Medical Center, Tel-Hashomer, affiliated with the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

²Bezafibrate Infarction Prevention Study Coordinating Center, Neufeld Cardiac Research Institute, the Chaim Sheba Medical Center, Tel-Hashomer, affiliated with the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

author email corresponding author email

Cardiovascular Diabetology 2008, 7:18doi:10.1186/1475-2840-7-18


Published:	19 June 2008

Abstract

Background

Epidemiologic studies have suggested that hypertriglyceridemia and insulin resistance are related to the development of colon cancer. Nuclear peroxisome proliferator-activated receptors (PPAR), which play a central role in lipid and glucose metabolism, had been hypothesized as being involved in colon cancerogenesis. In animal studies the lipid-lowering PPAR ligand bezafibrate suppressed colonic tumors. However, the effect of bezafibrate on colon cancer development in humans is unknown. Therefore, we proposed to investigate a possible preventive effect of bezafibrate on the development of colon cancer in patients with coronary artery disease during a 6-year follow-up.

Methods

Our population included 3011 patients without any cancer diagnosis who were enrolled in the randomized, double blind Bezafibrate Infarction Prevention (BIP) Study. The patients received either 400 mg of bezafibrate retard (1506 patients) or placebo (1505 patients) once a day. Cancer incidence data were obtained by matching a subject's identification numbers with the National Cancer Registry. Each matched record was checked for correct identification.

Results

Development of new cancer (all types) was recorded in 177 patients: in 79 (5.25%) patients from the bezafibrate group vs. 98 (6.51%) from the placebo group. Development of colon cancer was recorded in 25 patients: in 8 (0.53%) patients from the bezafibrate group vs. 17 (1.13%) from the placebo group, (Fisher's exact test: one side p = 0.05; two side p = 0.07).

A difference in the incidence of cancer was only detectable after a 4 year lag and progressively increased with continued follow-up. On multivariable analysis the colon cancer risk in patients who received bezafibrate tended to be lower with a hazard ratio of 0.47 and 95% confidence interval 0.2–1.1.

Conclusion

Our data, derived from patients with coronary artery disease, support the hypothesis regarding a possible preventive effect of bezafibrate on the development of colon cancer.