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• W4252837233 abstract "As recently published in Gastroenterology,1Baek S.J. Okazaki R. Lee S.H. Martinez J. Kim J.S. Yamaguchi K. Mishina Y. Martin D.W. Shoieb A. McEntee M.F. Eling T.E. Nonsteroidal anti-inflammatory drug-activated gene-1 over expression in transgenic mice suppresses intestinal neoplasia.Gastroenterology. 2006; 131: 1553-1560Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholar we reported the reduction in AOM induced aberrant cryptic foci and colon tumors as well as the reduction in intestinal polyps in ApcMin/+ mice expressing the human NAG-1/GDF-15, as compared with littermate controls. We propose that NAG-1/GDF-15 may act as a tumor suppressor based on these data and other data we have reviewed.2Baek S.J. Eling T.E. Changes in gene expression contribute to cancer prevention by COX inhibitors.Prog Lipid Res. 2006; 45: 1-16Crossref PubMed Scopus (71) Google Scholar For example, the expression of this protein is up-regulated by 2 tumor suppressor pathways, p53 and GSK-3β. In a Letter to the Editor, Drs Zimmers, Gutierrez, and Koniaris have questioned this conclusion. Their comments are based on the speculation that, because the NAG-1/GDF-15 mice are smaller in weight (20% in males), the mice have a 20% smaller intestinal length and thus have 20% fewer mucosal cells. Based on an examination of only 1 section shown in Figure 3C, they conclude that the mucosal layer is 20% thinner with a 35% lower surface area. Hence, the reduction in tumor load in the ApcMin/+ mice depends only on the smaller intestinal mucosal area, rather than NAG-1/DGF-15 expression.The NAG-1/GDF-15 mice are essentially leaner mice with lower fat content, based on image analysis (Table 1). A greater difference in weight was observed in males (20%) compared with females (10%–12%), and we used more female than male mice in these experiments. Because it is not possible to determine the mucosal layer thickness from 1 section, we have had 8–10 sections from the NAG-1/GDF-15 transgenic mice and littermate controls used in this experiment examined by 2 independent pathologists. Both conclude there is no difference in the thickness of the intestinal mucosal layers. Thus, the speculation of smaller intestinal mucosal layers in the NAG/GDF-15 transgenic mouse is not supported by direct measurement and the conclusions of Zimmers et al are not correct.Zimmers et al have also ignored the data obtained from AOM-induced foci with a greater reduction in number of foci in the transgenic mice (65%; Figure 3A), and instead have chosen to focus on the results from the ApcMin/+ mice with a 40% reduction in polyps, which fits their hypothesis. In addition, the effect of NAG-1/GDF-15 is more dramatic with smaller sized polyps, a finding that is difficult to rationalize with their conclusions. We think the interpretations of our data by Zimmers et al are inappropriate conclusions, not based on the scientific data.We believe the data reported in our publication supports the hypothesis for suppression of tumors by NAG-1/GDF-15 in these intestinal models, and preliminary results with a mouse model of pulmonary tumors are supportive of this conclusion (manuscript in preparation). As recently published in Gastroenterology,1Baek S.J. Okazaki R. Lee S.H. Martinez J. Kim J.S. Yamaguchi K. Mishina Y. Martin D.W. Shoieb A. McEntee M.F. Eling T.E. Nonsteroidal anti-inflammatory drug-activated gene-1 over expression in transgenic mice suppresses intestinal neoplasia.Gastroenterology. 2006; 131: 1553-1560Abstract Full Text Full Text PDF PubMed Scopus (135) Google Scholar we reported the reduction in AOM induced aberrant cryptic foci and colon tumors as well as the reduction in intestinal polyps in ApcMin/+ mice expressing the human NAG-1/GDF-15, as compared with littermate controls. We propose that NAG-1/GDF-15 may act as a tumor suppressor based on these data and other data we have reviewed.2Baek S.J. Eling T.E. Changes in gene expression contribute to cancer prevention by COX inhibitors.Prog Lipid Res. 2006; 45: 1-16Crossref PubMed Scopus (71) Google Scholar For example, the expression of this protein is up-regulated by 2 tumor suppressor pathways, p53 and GSK-3β. In a Letter to the Editor, Drs Zimmers, Gutierrez, and Koniaris have questioned this conclusion. Their comments are based on the speculation that, because the NAG-1/GDF-15 mice are smaller in weight (20% in males), the mice have a 20% smaller intestinal length and thus have 20% fewer mucosal cells. Based on an examination of only 1 section shown in Figure 3C, they conclude that the mucosal layer is 20% thinner with a 35% lower surface area. Hence, the reduction in tumor load in the ApcMin/+ mice depends only on the smaller intestinal mucosal area, rather than NAG-1/DGF-15 expression. The NAG-1/GDF-15 mice are essentially leaner mice with lower fat content, based on image analysis (Table 1). A greater difference in weight was observed in males (20%) compared with females (10%–12%), and we used more female than male mice in these experiments. Because it is not possible to determine the mucosal layer thickness from 1 section, we have had 8–10 sections from the NAG-1/GDF-15 transgenic mice and littermate controls used in this experiment examined by 2 independent pathologists. Both conclude there is no difference in the thickness of the intestinal mucosal layers. Thus, the speculation of smaller intestinal mucosal layers in the NAG/GDF-15 transgenic mouse is not supported by direct measurement and the conclusions of Zimmers et al are not correct. Zimmers et al have also ignored the data obtained from AOM-induced foci with a greater reduction in number of foci in the transgenic mice (65%; Figure 3A), and instead have chosen to focus on the results from the ApcMin/+ mice with a 40% reduction in polyps, which fits their hypothesis. In addition, the effect of NAG-1/GDF-15 is more dramatic with smaller sized polyps, a finding that is difficult to rationalize with their conclusions. We think the interpretations of our data by Zimmers et al are inappropriate conclusions, not based on the scientific data. We believe the data reported in our publication supports the hypothesis for suppression of tumors by NAG-1/GDF-15 in these intestinal models, and preliminary results with a mouse model of pulmonary tumors are supportive of this conclusion (manuscript in preparation). NAG-1/GDF-15: No Evidence for an Inhibitory Role in Colon Cancer?GastroenterologyVol. 132Issue 3PreviewWe read with interest the recent article by Baek et al1 examining potential suppression of intestinal neoplasia in mice by overexpression of the human protein nonsteroidal anti-inflammatory drug-activated gene (NAG-1). NAG-1 is a transforming growth factor-β family member officially named growth differentiation factor-15 (GDF-15),2 but also termed MIC-1, PDF, PLAB, and PTGFB. Baek et al describe a reduction in AOM-induced aberrant crypt foci and colon tumors in NAG-1/GDF-15 transgenic mice versus nontransgenic littermates, along with reduced small intestine tumor number and tumor burden in ApcMin mice bearing the human NAG-1/GDF-15 transgene. Full-Text PDF" @default.
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