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cancer, article, google, scholar, pubmed, cas, gdf, koniaris, zimmers, kim, sulindac, expression, colorectal, mice, min, nonsteroidal, antiinflammatory, colon, lee, gene, res, chemoprevention, intestinal, factor, apc, cell, research, mouse, gutierrez, injury, apoptosis, carcinogenesis, access, eling, growth, privacy, cookies, content, journal, model, member, superfamily, cells, gastric, induction, baek, cyclooxygenase, inhibitors, drugactivated, vogelstein,

Topics {✒️}

steroidal anti-inflammatory drugs tgf-beta superfamily member month download article/chapter mic-1/growth differentiation factor-15 tgf-beta superfamily akt/gsk3beta/nag-1 pathway growth-differentiation factor 15 growth differentiation factor-15 colon cancer prevention nsaid-mediated prevention full article pdf hereditary colon cancer heritable colon cancer anti-tumor effects familial adenomatous polyposis colorectal cancer formation heritable colorectal cancer sinonasal cancer cells hereditary colorectal cancer mediate sulindac chemoprevention sulindac suppresses tumorigenesis privacy choices/manage cookies related subjects cox-2 specific inhibitors hereditary poliposis coli sulindac chemoprotection activity cancer prevention casero ra jr malignant colorectal tumors human cdna encoding clinical oncology aims celecoxib induces apoptosis brown ta colon cancer cyclooxygenase-independent induction mic-1 serum level article zimmers apcmin/+ mouse model cyclooxygenase inhibitors regulate european economic area animal tumor models genetic mutation found significantly regulate heritable check access instant access article journal spontaneous intestinal adenomas colorectal cancer conditions privacy policy cancer research

Questions {❓}

• Zimmers TA, Gutierrez JC, Koniaris LG (2007) NAG-1/GDF-15: no evidence for an inhibitory role in colon cancer?

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         headline:Loss of GDF-15 abolishes Sulindac chemoprevention in the ApcMin/+ mouse model of intestinal cancer
         description:Growth-differentiation factor (GDF)-15, a member of the TGF-beta superfamily, is potently induced in the intestine following mechanical injury, genotoxic insult and following non-steroidal anti-inflammatory drugs (NSAIDs) exposure. GDF-15 expression correlates with apoptosis in intestinal cells and has been implicated in the pathogenesis of colorectal cancer formation and the anti-tumor effects of NSAIDs. We sought to determine the effect of loss of Gdf15 on animal tumor models of hereditary colon cancer and in the NSAID-mediated prevention of heritable colorectal cancer. GDF-15 null (Gdf15 −/−) mice and mice with the genetic mutation found in hereditary poliposis coli, Apc min/+ were bred. Gdf15 −/− , Apc min/+ and Gdf15 +/+ , Apc min/+ mice were generated. In Gdf15 −/− , Apc min/+ mice, intestinal neoplasia formation rate and size were indistinguishable from that in Gdf15 +/+ , Apc min/+ mice. Sulindac chemoprotection activity although potent in Gdf15 +/+ , Apc min/+ mice was abolished in Gdf15 −/− , Apc min/+ mice. These results demonstrate in a murine model that GDF-15 does not significantly regulate heritable in vivo intestinal carcinogenesis but does mediate sulindac chemoprevention in heritable colon cancer. These data suggest that the use of GDF-15 activated signaling pathways may allow improved chemoprevention and therapies for colorectal cancer.
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      headline:Loss of GDF-15 abolishes Sulindac chemoprevention in the ApcMin/+ mouse model of intestinal cancer
      description:Growth-differentiation factor (GDF)-15, a member of the TGF-beta superfamily, is potently induced in the intestine following mechanical injury, genotoxic insult and following non-steroidal anti-inflammatory drugs (NSAIDs) exposure. GDF-15 expression correlates with apoptosis in intestinal cells and has been implicated in the pathogenesis of colorectal cancer formation and the anti-tumor effects of NSAIDs. We sought to determine the effect of loss of Gdf15 on animal tumor models of hereditary colon cancer and in the NSAID-mediated prevention of heritable colorectal cancer. GDF-15 null (Gdf15 −/−) mice and mice with the genetic mutation found in hereditary poliposis coli, Apc min/+ were bred. Gdf15 −/− , Apc min/+ and Gdf15 +/+ , Apc min/+ mice were generated. In Gdf15 −/− , Apc min/+ mice, intestinal neoplasia formation rate and size were indistinguishable from that in Gdf15 +/+ , Apc min/+ mice. Sulindac chemoprotection activity although potent in Gdf15 +/+ , Apc min/+ mice was abolished in Gdf15 −/− , Apc min/+ mice. These results demonstrate in a murine model that GDF-15 does not significantly regulate heritable in vivo intestinal carcinogenesis but does mediate sulindac chemoprevention in heritable colon cancer. These data suggest that the use of GDF-15 activated signaling pathways may allow improved chemoprevention and therapies for colorectal cancer.
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