We are analyzing https://link.springer.com/article/10.1007/s00432-007-0336-4.

Title:
Effect of in vivo loss of GDF-15 on hepatocellular carcinogenesis | Journal of Cancer Research and Clinical Oncology
Description:
Background Growth/differentiation factor-15(GDF-15) is a divergent TGF-β family member that is expressed following liver injury and carcinogen exposure. GDF-15 expression is highly associated with gastrointestinal cancer stage, size, and metastasis and has been implicated in inhibition of tumor growth and increased tumor invasiveness. The current study sought to determine the effect of GDF-15 ablation on the development of hepatocellular carcinoma (HCC) in vivo. Materials and methods Male mice genetically deleted for the gene encoding GDF-15 (Gdf15 −/− mice) and wild-type controls were exposed to the hepatocarcinogen diethylnitrosamine (DEN). Mice were killed at 6 months of age and their livers dissected and processed for histology. Tumor number and size relative to total liver area examined were determined. Results At 6 months of age, tumors were identified in 16 of 20 (80%) Gdf15 −/− mice and 16 of 19 wild-type mice (84%). No significant difference in tumor-occupied area was observed in Gdf15 −/− mice versus wild-type mice. In addition, no difference in invasiveness was observed in HCC arising in Gdf15 −/− as compared to wild-type mice. In wild type mice strong immunohistochemical staining for GDF-15 was noted on small HCC foci, whereas a loss of GDF-15 expression was found in a number of advanced HCC tumors. Conclusions Although highly expressed in association with multiple gastrointestinal cancers, and lost in some advanced HCC, genetic ablation of GDF-15 has no apparent effect on HCC tumor formation rate, growth rate or invasiveness in diethylnitrosamine-induced HCC in vivo.
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google, scholar, pubmed, article, cas, cancer, growth, gdf, expression, factor, koniaris, gene, carcinoma, zimmers, liver, res, hepatocellular, jin, mice, transforming, tgfbeta, injury, tumor, hcc, cells, eling, carcinogenesis, access, cell, baek, human, growthdifferentiation, member, protein, nonsteroidal, antiinflammatory, nag, usa, privacy, cookies, content, journal, research, effect, vivo, pierce, family, cytokine, kim, superfamily,

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mic-1/growth differentiation factor-15 month download article/chapter growth/differentiation factor-15 growth-differentiation factor 15 growth differentiation factor-15 tgf-beta signaling pathway antitumorigenic nsaid-activated gene tgf-beta superfamily member tgf-beta signalling pathways long-term interleukin-6 exposure tgf-beta pathway gastric cancer cells related subjects 19 wild-type mice wild-type mice full article pdf hepatocellular carcinoma tgf-beta family wild-type controls lung carcinoma cells anti-gdf-15 antibody colorectal cancer cells privacy choices/manage cookies tgf β check access instant access gene expression regulated gastrointestinal cancer stage diethylnitrosamine-induced hcc mediated signaling pathways gene encoding gdf-15 p53 target gene bile duct injury extreme liver resection tumor growth clinical oncology aims kim jr tumor-occupied area growth rate small hcc foci glioblastoma cells independently european economic area colorectal carcinoma superfamily member hepatocellular carcinogenesis tumor suppressor activity cyclooxygenase inhibitors regulate midbrain dopaminergic neurons human cdna encoding article journal

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         description:Growth/differentiation factor-15(GDF-15) is a divergent TGF-β family member that is expressed following liver injury and carcinogen exposure. GDF-15 expression is highly associated with gastrointestinal cancer stage, size, and metastasis and has been implicated in inhibition of tumor growth and increased tumor invasiveness. The current study sought to determine the effect of GDF-15 ablation on the development of hepatocellular carcinoma (HCC) in vivo. Male mice genetically deleted for the gene encoding GDF-15 (Gdf15 −/− mice) and wild-type controls were exposed to the hepatocarcinogen diethylnitrosamine (DEN). Mice were killed at 6 months of age and their livers dissected and processed for histology. Tumor number and size relative to total liver area examined were determined. At 6 months of age, tumors were identified in 16 of 20 (80%) Gdf15 −/− mice and 16 of 19 wild-type mice (84%). No significant difference in tumor-occupied area was observed in Gdf15 −/− mice versus wild-type mice. In addition, no difference in invasiveness was observed in HCC arising in Gdf15 −/− as compared to wild-type mice. In wild type mice strong immunohistochemical staining for GDF-15 was noted on small HCC foci, whereas a loss of GDF-15 expression was found in a number of advanced HCC tumors. Although highly expressed in association with multiple gastrointestinal cancers, and lost in some advanced HCC, genetic ablation of GDF-15 has no apparent effect on HCC tumor formation rate, growth rate or invasiveness in diethylnitrosamine-induced HCC in vivo.
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      description:Growth/differentiation factor-15(GDF-15) is a divergent TGF-β family member that is expressed following liver injury and carcinogen exposure. GDF-15 expression is highly associated with gastrointestinal cancer stage, size, and metastasis and has been implicated in inhibition of tumor growth and increased tumor invasiveness. The current study sought to determine the effect of GDF-15 ablation on the development of hepatocellular carcinoma (HCC) in vivo. Male mice genetically deleted for the gene encoding GDF-15 (Gdf15 −/− mice) and wild-type controls were exposed to the hepatocarcinogen diethylnitrosamine (DEN). Mice were killed at 6 months of age and their livers dissected and processed for histology. Tumor number and size relative to total liver area examined were determined. At 6 months of age, tumors were identified in 16 of 20 (80%) Gdf15 −/− mice and 16 of 19 wild-type mice (84%). No significant difference in tumor-occupied area was observed in Gdf15 −/− mice versus wild-type mice. In addition, no difference in invasiveness was observed in HCC arising in Gdf15 −/− as compared to wild-type mice. In wild type mice strong immunohistochemical staining for GDF-15 was noted on small HCC foci, whereas a loss of GDF-15 expression was found in a number of advanced HCC tumors. Although highly expressed in association with multiple gastrointestinal cancers, and lost in some advanced HCC, genetic ablation of GDF-15 has no apparent effect on HCC tumor formation rate, growth rate or invasiveness in diethylnitrosamine-induced HCC in vivo.
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