A Dominant Mutation That Predisposes to Multiple Intestinal Neoplasia in the Mouse

Moser, Amy R.; Pitot, Henry C.; Dove, William F.

doi:10.1126/science.2296722

Cited by 1,412 publications

(1,184 citation statements)

References 15 publications

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“…SirT1/Apc min mice SirT1 þ /À mice from the inbred 129/J genetic background (see above) were interbred with C57BL/6J-Apc min /J mice (Jax Mice; The Jackson Laboratory, Bar Harbor, ME, USA) (Moser et al, 1990). SirT1 þ /À of the first generation and bearing the Apc min allele were interbred with SirT1 þ /À mice of the inbred 129/J genetic background but no SirT1-null mice were obtained.…”

Section: Sirt1 Micementioning

confidence: 99%

SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrol

et al. 2009

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The function of the class III histone deacetylase, Sir2, in promoting lifespan extension is well established in small model organisms. By analogy, SirT1, the mammalian orthologue of Sir2, is a candidate gene to slow down aging and forestall the onset of age-associated diseases. We have used SirT1-null mice to study the function of SirT1 in susceptibility to tumorigenesis. The number of intestinal polyps induced in mice carrying the Apc min mutation was unaffected by the SirT1 genotype although the average polyp size was slightly smaller in the SirT1-null animals. Similarly, the presence or absence of SirT1 had no effect on incidence and tumor load of skin papillomas induced by the classical two-stage carcinogenesis protocol. We found that resveratrol topically applied to the skin profoundly reduced tumorigenesis. This chemoprotective effect was significantly reduced but not ablated in SirT1-null mice, suggesting that part of the protection afforded by resveratrol requires the SirT1-encoded protein. Thus, our results suggest that SirT1 does not behave like a classical tumor-suppressor gene but the antitumor activity of resveratrol is mediated at least in part by SirT1.

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Section: Sirt1 Micementioning

confidence: 99%

SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrol

et al. 2009

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“…Apc Min/ þ (Moser et al, 1990) and Apc 1638N/ þ (Fodde et al, 1994) mice on C57BL/6 background were treated according to animal protocols approved by the Animal Care and Use Committee at Montefiore Medical Center and the Albert Einstein College of Medicine. Small and large intestine were removed immediately after killing the mice at 5 or 8 months of age (Apc Min/ þ and Apc 1638N/ þ , respectively), flushed gently with cold phosphate-buffered saline, opened longitudinally and inspected with a dissection microscope.…”

Section: Animals and Tissue Preparationmentioning

confidence: 99%

Heterogeneity of Jagged1 expression in human and mouse intestinal tumors: implications for targeting Notch signaling

et al. 2009

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“…The resulting constitutive overexpression of beta-catenin is likely responsible for the activation of growthpromoting oncogenes, such as cyclin D1 or c-myc (14)(15)(16). In 1990, Moser and colleagues identified an APC mutant mouse, namely Apc Min/+ , which carries a mutation in the APC gene similar to that detected in FAP and sporadic colorectal cancers (17). Apc Min/+ mice do not survive beyond 120 days due to the occurrence of intestinal tumors that start from a rapid development of adenomatous polyps.…”

Section: Adenomatous Polyposis Coli (Apc) Tumor Suppressor Genementioning

confidence: 99%

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

Tassi

Wellstein

2006

Seminars in Oncology

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Tumor angiogenesis has been related to the initiation as well as progression toward more aggressive behavior of human tumors. We will discuss genetic events underlying the initiation and progression of colorectal and pancreatic adenocarcinoma with a particular focus on the modulation of angiogenesis. A secreted fibroblast growth factor (FGF) binding protein (FGF-BP), which is an extracellular chaperone molecule for FGFs, has been shown to enhance FGF-mediated biochemical and biologic events and to be a crucial rate-limiting factor for tumor-dependent angiogenesis. Histochemical and in situ hybridization studies with archival samples show that FGF-BP is induced early during the initiation of colorectal and pancreatic adenocarcinoma. We will discuss the potential of this secreted protein as a serum marker to identify at-risk subjects.

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A Dominant Mutation That Predisposes to Multiple Intestinal Neoplasia in the Mouse

Cited by 1,412 publications

References 15 publications

SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrol

SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrol

Heterogeneity of Jagged1 expression in human and mouse intestinal tumors: implications for targeting Notch signaling

The Angiogenic Switch Molecule, Secreted FGF-Binding Protein, an Indicator of Early Stages of Pancreatic and Colorectal Adenocarcinoma

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