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一种导致小鼠发生多发性肠道肿瘤的显性突变。

A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.

作者信息

Moser A R, Pitot H C, Dove W F

机构信息

McArdle Laboratory for Cancer Research, University of Wisconsin-Madison 53706.

出版信息

Science. 1990 Jan 19;247(4940):322-4. doi: 10.1126/science.2296722.

DOI:10.1126/science.2296722
PMID:2296722
Abstract

In a pedigree derived from a mouse treated with the mutagen ethylnitrosourea, a mutation has been identified that predisposes to spontaneous intestinal cancer. The mutant gene was found to be dominantly expressed and fully penetrant. Affected mice developed multiple adenomas throughout the entire intestinal tract at an early age.

摘要

在一个源自用诱变剂乙基亚硝基脲处理过的小鼠的家系中，已鉴定出一种易患自发性肠癌的突变。发现该突变基因呈显性表达且完全显性。受影响的小鼠在幼年时整个肠道会出现多个腺瘤。

相似文献

1
A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.一种导致小鼠发生多发性肠道肿瘤的显性突变。
Science. 1990 Jan 19;247(4940):322-4. doi: 10.1126/science.2296722.
2
The Min (multiple intestinal neoplasia) mutation: its effect on gut epithelial cell differentiation and interaction with a modifier system.Min（多发性肠道肿瘤）突变：其对肠道上皮细胞分化的影响以及与修饰系统的相互作用。
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A resistant genetic background leading to incomplete penetrance of intestinal neoplasia and reduced loss of heterozygosity in ApcMin/+ mice.一种导致肠道肿瘤不完全显性以及ApcMin/+小鼠杂合性缺失减少的抗性遗传背景。
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10826-31. doi: 10.1073/pnas.95.18.10826.
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Dnmt1N/+ reduces the net growth rate and multiplicity of intestinal adenomas in C57BL/6-multiple intestinal neoplasia (Min)/+ mice independently of p53 but demonstrates strong synergy with the modifier of Min 1(AKR) resistance allele.Dnmt1N/+降低了C57BL/6-多发性肠道肿瘤（Min）/+小鼠肠道腺瘤的净生长率和增殖倍数，这一作用不依赖于p53，但与Min 1（AKR）抗性等位基因的修饰因子表现出强烈的协同作用。
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Expression of guanylin is downregulated in mouse and human intestinal adenomas.鸟苷素在小鼠和人类肠道腺瘤中的表达下调。
Biochem Biophys Res Commun. 2000 Jun 24;273(1):225-30. doi: 10.1006/bbrc.2000.2917.
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Localized gene action controlling intestinal neoplasia in mice.控制小鼠肠道肿瘤形成的局部基因作用
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Intestinal tumours induced by the food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in multiple intestinal neoplasia mice have truncation mutations as well as loss of the wild-type Apc(+) allele.食物致癌物2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶在多发性肠道肿瘤小鼠中诱发的肠道肿瘤具有截短突变以及野生型Apc(+)等位基因的缺失。
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8
Mom1 is a semi-dominant modifier of intestinal adenoma size and multiplicity in Min/+ mice.Mom1是Min/+小鼠肠道腺瘤大小和数量的半显性修饰基因。
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Mapping of multiple intestinal neoplasia (Min) to proximal chromosome 18 of the mouse.小鼠多肠肿瘤（Min）基因定位于近端18号染色体。
Genomics. 1993 Jan;15(1):3-8. doi: 10.1006/geno.1993.1002.
10
Loss of Apc+ in intestinal adenomas from Min mice.Min小鼠肠道腺瘤中Apc+的缺失。
Cancer Res. 1994 Nov 15;54(22):5947-52.

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