ArticleCancer research2009
Inhibition of azoxymethane-induced colorectal cancer by CP-31398, a TP53 modulator, alone or in combination with low doses of celecoxib in male F344 rats.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Resveratrol and p53: How are they involved in CRC plasticity and apoptosis?Journal of advanced research · 2024Review
- Animal Models of Colorectal Cancer: From Spontaneous to Genetically Engineered Models and Their Applications.Veterinary sciences · 2021Review
- Targeting cancer stem cells with p53 modulators.Oncotarget · 2016Article
- Targeting mTOR and p53 Signaling Inhibits Muscle Invasive Bladder Cancer In Vivo.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Anti-LeY antibody enhances therapeutic efficacy of celecoxib against gastric cancer by downregulation of MAPKs/COX-2 signaling pathway: correlation with clinical study.Journal of cancer research and clinical oncology · 2015Article
- Effects of metformin, buformin, and phenformin on the post-initiation stage of chemically induced mammary carcinogenesis in the rat.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- CP-31398 prevents the growth of p53-mutated colorectal cancer cells in vitro and in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- TP53 modulating agent, CP-31398 enhances antitumor effects of ODC inhibitor in mouse model of urinary bladder transitional cell carcinoma.American journal of cancer research · 2015Article
- Targeting the p53 pathway.Surgical oncology clinics of North America · 2013Review
- Chemopreventive effects of the p53-modulating agents CP-31398 and Prima-1 in tobacco carcinogen-induced lung tumorigenesis in A/J mice.Neoplasia (New York, N.Y.) · 2013Article
- Heritable one-hit events defining cancer prevention?Cell cycle (Georgetown, Tex.) · 2013Article
- p53-stabilizing agent CP-31398 prevents growth and invasion of urothelial cancer of the bladder in transgenic UPII-SV40T mice.Neoplasia (New York, N.Y.) · 2013Article
- Article
- Towards an understanding of the role of p53 in adrenocortical carcinogenesis.Molecular and cellular endocrinology · 2012Review
- Translational approaches targeting the p53 pathway for anti-cancer therapy.British journal of pharmacology · 2012Review
- Determination and stability of CP-31398 in plasma from experimental animals by LC-MS/MS.Journal of pharmaceutical and biomedical analysis · 2011Article
- Subchronic oral toxicity and metabolite profiling of the p53 stabilizing agent, CP-31398, in rats and dogs.Toxicology · 2011Article
- Pharmacological activation of p53 in cancer cells.Current pharmaceutical design · 2011Review
- A molecular signature of normal breast epithelial and stromal cells from Li-Fraumeni syndrome mutation carriers.Oncotarget · 2010Article
- NSAIDs and Cell Proliferation in Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2010Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor suppressor p53 plays a major role in colorectal cancer development. The present study explores the effects of p53-modulating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F344 rats. Maximum tolerated doses were 400 and 3,000 ppm for CP-31398 and celecoxib, respectively. ACF and tumor efficacy endpoints were carried out on azoxymethane-treated 7-week-old rats (48 per group) fed the control AIN-76A diet. Two weeks after carcinogen treatment, rats were fed the diets containing 0, 150, or 300 ppm CP-31398, 300 ppm celecoxib, or 150 ppm CP-31398 plus 300 ppm celecoxib. ACF and colon adenocarcinomas were determined at 8 and 48 weeks after azoxymethane treatment, respectively. Dietary CP-31398 was shown to suppress mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 at 150 and 300 ppm suppressed adenocarcinoma incidence by 30.4% (P < 0.02) and 44% (P < 0.005), respectively, and adenocarcinoma multiplicity by 51% (P < 0.005) and 65% (P < 0.0001), respectively. Dietary celecoxib suppressed colon adenocarcinoma incidence (60%; P < 0.0003) and multiplicity (70%; P < 0.0001). Importantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 78% and multiplicity by 90%. Rats that were fed the high-dose CP-31398 or a combination of low-dose CP-31398 and celecoxib showed considerable enhancement of p53 and p21(WAF1/CIP) expression, apoptosis, and reduced tumor cell proliferation in colonic tumors. These observations show, for the first time, that CP-31398 possesses significant dose-dependent chemopreventive activity in a well-established colon cancer model and that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreventive efficacy.
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