We are analyzing https://link.springer.com/article/10.1007/s10552-005-0411-6.

Title:
PPARγ and Colon and Rectal Cancer: Associations with Specific Tumor Mutations, Aspirin, Ibuprofen and Insulin-Related Genes (United States) | Cancer Causes & Control
Description:
We hypothesize that the peroxisome proliferator-activated receptor-γ (PPARγ) is associated with colorectal cancer given its association with insulin, diabetes, obesity, and inflammation. In this study, we evaluated the association between colorectal cancer and specific tumor mutations and the Pro12Ala (P12A) PPARγ polymorphism. We also evaluated interactions between the PPARγ gene and other insulin-related genes and use of aspirin and non-steroidal anti-inflammatory drug use. Data were available from 1,577 cases of colon cancer that were matched to 1,971 population-based controls and 794 cases of rectal cancer that were matched to 1,001 population-based controls. Colon tumors from the case subjects were evaluated for p53 and Ki-ras mutations and microsatellite instability (MSI). Insulin-related genes evaluated were the Bsm1, polyA, and Fok1 polymorphisms of the VDR gene; the G972R IRS1 polymorphism; the G1057D IRS2 polymorphism; the 19CA repeat polymorphism of the IGF1 gene; and the –200A>C IGFBP3 polymorphism. The odds ratio (OR) between the PA/AA genotypes and proximal tumors was 0.83 (95% CI: 0.69–1.01); for distal tumors was 1.00 (95% CI: 0.83–1.21); and for rectal tumors was 1.04 (95% CI: 0.86–1.25). Evaluation of specific types of tumor mutations showed that colon cancer cases with the PA or AA genotypes were less likely to have p53 tumor mutations (OR 0.78; 95% CI: 0.62–0.99), specifically transition mutations (OR 0.74; 95% CI: 0.56–0.97). Colon cancer cases also were less likely to have a tumor with MSI if they had the PA or AA PPARγ genotype (OR 0.68; 95% CI: 0.47–0.98); differences in Ki-ras mutations were not seen in colon tumors by PPARγ genotype. Those who did not take ibuprofen-type drugs and had the PA or AA genotypes were at a significantly greater risk of rectal cancer (OR 2.11; 95% CI: 1.52–2.92; p interaction 0.03) than people with the PP genotype regardless of ibuprofen-type drug use. There was a significant interaction between the −200A>C IGFBP3 polymorphism and the Pro12Ala PPARγ polymorphism and risk of colon cancer (p for interaction = 0.02) with individuals being at significantly lower risk if they had both the CC IGFBP3 genotype and the PA/AA PPARγ genotype. For rectal cancer there was a significant interaction between the Bsm1/polyA polymorphisms (p = 0.001) of the VDR gene and the PA/AA Pro12Ala PPARγ polymorphism with the highest risk group being those with both the PA/AA Pro12Ala PPARγ and the BB/SS VDR genotypes. These data suggest that PPARγ may be associated with many aspects of colorectal cancer including insulin- and inflammation-related mechanisms.
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Keywords {🔍}

cancer, google, scholar, cas, pubmed, article, colon, receptor, slattery, colorectal, insulin, pparγ, polymorphism, gene, risk, ppargamma, mutations, tumors, vitamin, peroxisome, proliferatoractivated, curtin, study, interaction, med, growth, research, tumor, diabetes, proala, gamma, endocrinol, control, rectal, association, vdr, role, res, data, associations, aspirin, genes, polymorphisms, irs, genotype, access, human, metab, clin, factor,

Topics {✒️}

peroxisome proliferator-activated receptor-{gamma} peroxisome proliferator-activated receptor-γ berger de moller month download article/chapter edwards ml slattery curtin ml slattery steroidal anti-inflammatory drug inhibits ppargamma-mediated adipogenesis anti-inflammatory drugs based nonsteroidal anti-inflammatory drugs bb/ss vdr genotypes growth factor-binding protein-3 obesity-related insulin sensitivity full article pdf article slattery gurnell jm wentworth pa/aa pparγ genotype pa/aa pro12ala pparγ dominant negative mutations fischer je cecil colon cancer cancer article cancer dr bette caan insulin-related genes evaluated tontonoz mc nelson colon epithelium cells privacy choices/manage cookies carol sweeney 971 population-based controls 001 population-based controls decreased receptor activity insulin receptor substrate-1 db/db mice colorectal cancer risk colon tumors int national cancer institute article log colon cancer cases insulin-related genes diabetes-related genes pa/aa genotypes utah cancer registry inflammatory genes interleukin human ppargamma gene inflammatory bowel disease specific tumor mutations maureen murtaugh check access instant access aa pparγ genotype

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         headline:PPARγ and Colon and Rectal Cancer: Associations with Specific Tumor Mutations, Aspirin, Ibuprofen and Insulin-Related Genes (United States)
         description:We hypothesize that the peroxisome proliferator-activated receptor-γ (PPARγ) is associated with colorectal cancer given its association with insulin, diabetes, obesity, and inflammation. In this study, we evaluated the association between colorectal cancer and specific tumor mutations and the Pro12Ala (P12A) PPARγ polymorphism. We also evaluated interactions between the PPARγ gene and other insulin-related genes and use of aspirin and non-steroidal anti-inflammatory drug use. Data were available from 1,577 cases of colon cancer that were matched to 1,971 population-based controls and 794 cases of rectal cancer that were matched to 1,001 population-based controls. Colon tumors from the case subjects were evaluated for p53 and Ki-ras mutations and microsatellite instability (MSI). Insulin-related genes evaluated were the Bsm1, polyA, and Fok1 polymorphisms of the VDR gene; the G972R IRS1 polymorphism; the G1057D IRS2 polymorphism; the 19CA repeat polymorphism of the IGF1 gene; and the –200A>C IGFBP3 polymorphism. The odds ratio (OR) between the PA/AA genotypes and proximal tumors was 0.83 (95% CI: 0.69–1.01); for distal tumors was 1.00 (95% CI: 0.83–1.21); and for rectal tumors was 1.04 (95% CI: 0.86–1.25). Evaluation of specific types of tumor mutations showed that colon cancer cases with the PA or AA genotypes were less likely to have p53 tumor mutations (OR 0.78; 95% CI: 0.62–0.99), specifically transition mutations (OR 0.74; 95% CI: 0.56–0.97). Colon cancer cases also were less likely to have a tumor with MSI if they had the PA or AA PPARγ genotype (OR 0.68; 95% CI: 0.47–0.98); differences in Ki-ras mutations were not seen in colon tumors by PPARγ genotype. Those who did not take ibuprofen-type drugs and had the PA or AA genotypes were at a significantly greater risk of rectal cancer (OR 2.11; 95% CI: 1.52–2.92; p interaction 0.03) than people with the PP genotype regardless of ibuprofen-type drug use. There was a significant interaction between the −200A>C IGFBP3 polymorphism and the Pro12Ala PPARγ polymorphism and risk of colon cancer (p for interaction = 0.02) with individuals being at significantly lower risk if they had both the CC IGFBP3 genotype and the PA/AA PPARγ genotype. For rectal cancer there was a significant interaction between the Bsm1/polyA polymorphisms (p = 0.001) of the VDR gene and the PA/AA Pro12Ala PPARγ polymorphism with the highest risk group being those with both the PA/AA Pro12Ala PPARγ and the BB/SS VDR genotypes. These data suggest that PPARγ may be associated with many aspects of colorectal cancer including insulin- and inflammation-related mechanisms.
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            Hematology
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      headline:PPARγ and Colon and Rectal Cancer: Associations with Specific Tumor Mutations, Aspirin, Ibuprofen and Insulin-Related Genes (United States)
      description:We hypothesize that the peroxisome proliferator-activated receptor-γ (PPARγ) is associated with colorectal cancer given its association with insulin, diabetes, obesity, and inflammation. In this study, we evaluated the association between colorectal cancer and specific tumor mutations and the Pro12Ala (P12A) PPARγ polymorphism. We also evaluated interactions between the PPARγ gene and other insulin-related genes and use of aspirin and non-steroidal anti-inflammatory drug use. Data were available from 1,577 cases of colon cancer that were matched to 1,971 population-based controls and 794 cases of rectal cancer that were matched to 1,001 population-based controls. Colon tumors from the case subjects were evaluated for p53 and Ki-ras mutations and microsatellite instability (MSI). Insulin-related genes evaluated were the Bsm1, polyA, and Fok1 polymorphisms of the VDR gene; the G972R IRS1 polymorphism; the G1057D IRS2 polymorphism; the 19CA repeat polymorphism of the IGF1 gene; and the –200A>C IGFBP3 polymorphism. The odds ratio (OR) between the PA/AA genotypes and proximal tumors was 0.83 (95% CI: 0.69–1.01); for distal tumors was 1.00 (95% CI: 0.83–1.21); and for rectal tumors was 1.04 (95% CI: 0.86–1.25). Evaluation of specific types of tumor mutations showed that colon cancer cases with the PA or AA genotypes were less likely to have p53 tumor mutations (OR 0.78; 95% CI: 0.62–0.99), specifically transition mutations (OR 0.74; 95% CI: 0.56–0.97). Colon cancer cases also were less likely to have a tumor with MSI if they had the PA or AA PPARγ genotype (OR 0.68; 95% CI: 0.47–0.98); differences in Ki-ras mutations were not seen in colon tumors by PPARγ genotype. Those who did not take ibuprofen-type drugs and had the PA or AA genotypes were at a significantly greater risk of rectal cancer (OR 2.11; 95% CI: 1.52–2.92; p interaction 0.03) than people with the PP genotype regardless of ibuprofen-type drug use. There was a significant interaction between the −200A>C IGFBP3 polymorphism and the Pro12Ala PPARγ polymorphism and risk of colon cancer (p for interaction = 0.02) with individuals being at significantly lower risk if they had both the CC IGFBP3 genotype and the PA/AA PPARγ genotype. For rectal cancer there was a significant interaction between the Bsm1/polyA polymorphisms (p = 0.001) of the VDR gene and the PA/AA Pro12Ala PPARγ polymorphism with the highest risk group being those with both the PA/AA Pro12Ala PPARγ and the BB/SS VDR genotypes. These data suggest that PPARγ may be associated with many aspects of colorectal cancer including insulin- and inflammation-related mechanisms.
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      pageEnd:249
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         Colorectal cancer
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         Public Health
         Epidemiology
         Hematology
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