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Trial of Eflornithine Plus Sulindac in Patients With Familial Adenomatous Polyposis (FAP)

ABSTRACT: The purpose of this randomized, double-blind, Phase III trial is to determine if the combination of eflornithine plus sulindac is superior to sulindac or eflornithine as single agents in delaying time to the first occurrence of any FAP-related event. This includes: 1) FAP related disease progression indicating the need for excisional intervention involving the colon, rectum, pouch, duodenum and/or 2) clinically important events which includes progression to more advanced duodenal polyposis, cancer or death.

DISEASE(S): Familial Adenomatous Polyposis (fap),Adenomatous Polyposis Coli,Colorectal Neoplasms,Familial Adenomatous Polyposis,Nasopharyngeal Neoplasms

PROVIDER: 2116545 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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A Trial of Low Dose Sulindac Combined With Eflornithine in Patients With Familial Adenomatous Polyposis (FAP)

Project description:The purpose of this phase III study is to evaluate the safety and efficacy of the combination of eflornithine and sulindac compared to single agent sulindac or eflornithine in reducing the number of polyps in patients with familial adenomatous polyposis (FAP).

| 2098444 | ecrin-mdr-crc

Eflornithine and Sulindac in Preventing Colorectal Cancer in Patients With Colon Polyps

Project description:This randomized phase III trial is studying eflornithine and sulindac to see how well they work compared to a placebo in preventing colorectal cancer in patients with colon polyps. Chemoprevention is the use of certain drugs to keep cancer from forming, growing, or coming back. The use of eflornithine and sulindac may prevent colorectal cancer. It is not yet known whether eflornithine and sulindac are more effective than a placebo in preventing colorectal cancer

| 2013368 | ecrin-mdr-crc

Effect of NO-sulindac treatment on hypoxic prostate cancer cells

Project description:The hypoxia response contributes to radio and chemo-resistance in cancer cells. Our previous work has shown that the nitric oxide donating non-steroidal anti-inflammatory drug (NO-NSAID) NO-sulindac is a potent inhibitor of the hypoxia response in prostate cancer cells and leads to increased susceptibilty to radiation. In this study we used microarrays to investigated the global impact of NO-sulindac on the hypoxia response in prostate cancer cells with a view to determining the mechanism of action. PC3 hormone-insensitive prostate cancer cells were grown under normoxic or hypoxic conditions and treated with NO-sulindac, unnitrated sulindac or vehicle control. Global gene expression in response to treatment was examined using microarrays and the bioconductor software suite. Gene set enrichment analysis (GSEA), Gene ontology (GO) analysis and pathway analysis were used to examine the biological impact of treatments.

2012-12-01 | E-GEOD-34112 | biostudies-arrayexpress

Chemoprevention with COX2 and EGFR inhibition in FAP patients: mRNA signatures of duodenal neoplasia

Project description:RNA sequencing of duodenal polyps in FAP patients treated with plabebo or the drug combination, erlotinib + sulindac

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Effect of NO-sulindac treatment on hypoxic prostate cancer cells

2012-12-01 | GSE34112 | GEO

Expression data from murine colon tumors induced by azoxymethane. Tumors from control, obese, formerly obese, or sulindac-treated mice.

Project description:Obesity is associated with an increased risk of colon cancer. Our current study examines whether weight loss and/or treatment with the non-steroidal anti-inflammatory drug (NSAID) sulindac suppresses the protumor effects of obesity in a mouse model of colon cancer. Azoxymethane-treated male FVB/N mice were fed a low-fat diet (LFD) or high-fat diet (HFD) for 15 weeks, then HFD mice were randomized to remain on HFD (obese) or switch to LFD (formerly obese (FOb-LFD)). Within the control (LFD), obese, and FOb-LFD groups, half the mice were also randomized to start sulindac treatment (140 ppm in the diet). All mice were euthanized seven weeks later. FOb-LFD mice had intermediate levels of body weight, lower than obese but higher than control mice (P<0.05). Sulindac did not affect body weight. Obese mice had greater tumor multiplicity and burden than all other groups (P<0.05). Transcriptomic profiling indicated that both weight loss and sulindac modulate the expression of tumor genes related to invasion and may promote a more anti-tumor immune landscape. Furthermore, the fecal microbes Prevotella and Akkermansia muciniphila, both known to be elevated in colorectal cancer patients, were positively correlated with tumor multiplicity and reduced by sulindac in obese mice. In sum, either moderate weight loss or sulindac treatment completely reversed the effects of chronic obesity on colon tumorigenesis. Our findings suggest that an investigation regarding the effects of NSAID treatment on colon cancer risk and/or progression in obese individuals is warranted, particularly for those unable to achieve moderate weight loss.

2022-08-10 | GSE197846 | GEO

Transcription profiling by array of intestinal adenomas from Apc -/+ mice after sulindac treament

Project description:Transcriptional profile of tumors of ApcMin/+ mice after sulindac treatment

2008-06-03 | E-MEXP-1401 | biostudies-arrayexpress

Transcriptional profiling of mouse intestinal tissue, with or without antibiotic or sulindac treatment

Project description:Loss of APC or activation of Braf V600E mutation in combination with Alk5 loss in the intestinal epithelium under the control of VilCreER, with or without antibiotic/sulindac treatment

2021-04-01 | GSE168478 | GEO

Ornithine decarboxylase-1 polymorphism, chemoprevention with eflornithine and sulindac, and outcomes among colorectal adenoma patients.

Project description:The ornithine decarboxylase-1 (ODC1) polymorphism at position +316 affects binding by transcriptional activators and repressors and modulates the risk of metachronous colorectal adenomas, particularly in association with aspirin use. We investigated the effects of ODC1 after treatment with difluoromethylornithine (eflornithine)/sulindac or placebo. Two hundred twenty-eight colorectal adenoma patients in a randomized phase III trial were genotyped for ODC1. We used Wilcoxon rank sums tests on non-normally distributed continuous variables across two genotype groups, χ(2) or Fisher exact test to assess the association between baseline categorical variables and genotype group, and log binomial regression for the primary (adenoma recurrence) and secondary outcomes (tissue polyamine response, cardiovascular toxicity, gastrointestinal toxicity, and ototoxicity). All statistical tests were two-sided. In binomial regression models with variables age, sex, race, aspirin use, treatment, and ODC1 genotype, treatment was the only statistically significant factor associated with differences in adenoma recurrence or tissue polyamine response. A statistically significant interaction was detected between ODC1 genotype and treatment with respect to adenoma recurrence (placebo group: GG, 50%, AA/GA: 34%; treatment group: GG, 11%, AA/GA, 21%; P(interaction) = .038). Excess ototoxicity was observed among ODC1 AA patients receiving treatment, but the interaction of genotype and treatment on ototoxicity was not statistically significant (P = .45).

| S-EPMC2950167 | biostudies-literature

Differential Chemopreventive Activity of Sulindac and/or Atorvastatin in Apc+/Min-FCCC Mice With or Without Colorectal Adenomas

Project description:Emerging data suggest that some high-risk subjects benefit more than others from preventive intervention. The goal of this study was to determine the efficacy of sulindac (Sul) and/or atorvastatin (Atorva) against spontaneous colorectal adenomas in Apc+/Min-FCCC mice in which the tumor-bearing status was known at the time of treatment initiation. Administration of Sul/Atorva to tumor-bearing mice led to a 43% reduction in the multiplicity of colorectal adenomas as compared to that of untreated tumor-bearing mice. Atorvastatin completely inhibited the formation of microadenomas in mice that were tumor-free at baseline, with associated decreases in the expression of inflammatory mediators observed. Expression of Hoxb13 and Rprm was enhanced significantly following Sul/Atorva treatment, suggesting the importance of cell cycle regulation in colon tumor inhibition. The tumor status of animals at treatment initiation dictates response to atorvastatin, sulindac and Sul/Atorva. The tumor inhibition observed with Sul/Atorva in tumor-bearing mice was greater than that achieved with either agent alone.

2018-08-31 | GSE81375 | GEO

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