Apc-L850X

Nomenclature

C57BL/6Smoc-Apcem1(L850X)Smoc

Cat. NO.

NM-KI-200001

Strain State

Repository Live

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Gene Summary

Gene Symbol
Apc

Synonyms

CC1， Min， mAPC， AI047805， AU020952， AW124434

NCBI ID

11789

MGI ID

88039

Ensembl ID

ENSMUSG00000005871

Pubmed

Apc

Human Ortholog

APC

Model Description

Familial adenomatous polyposis (FAP) is a heritable condition in which affected individuals develop benign intestinal polyps. Often, polyps progress to colorectal carcinomas later in life. The mutation of C57BL/6-Apcem1(L850X)Smoc(NM-KI-200001) strain of SMOC refers to the ApcMin model (Jax: 002020 ), a useful model to study intestinal adenomas. The C57BL/6-Apcem1(L850X)Smoc strain is highly susceptible to spontaneous intestinal adenoma formation and can be used as a research model for human FAP. These mice carry a p.L850X mutation of Apc gene.
Research Application：Heterozygotes of this strain are highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable.

Disease Connection

familial adenomatous polyposis

Phenotype(s)

MGI:4440863
Note：The expected phenotype(s) may be observed in the above-mentioned mice that bred with Rab25-KO(NM-KO-191148) mice.

Reference(s)

Nam KT, Lee HJ, Smith JJ, Lapierre LA, Kamath VP, Chen X, Aronow BJ, Yeatman TJ, Bhartur SG, Calhoun BC, Condie B, Manley NR, Beauchamp RD, Coffey RJ, Goldenring JR, Loss of Rab25 promotes the development of intestinal neoplasia in mice and is associated with human colorectal adenocarcinomas. J Clin Invest. 2010 Mar;120(3):840-9

Colorectal Cancer

Phenotype(s)

MGI:5636659
Note：The expected phenotype(s) may be observed in the above-mentioned mice that bred with Msh2-KO(NM-KO-2113943) mice.

Reference(s)

Reitmair AH, Cai JC, Bjerknes M, Redston M, Cheng H, Pind MT, Hay K, Mitri A, Bapat BV, Mak TW, Gallinger S, MSH2 deficiency contributes to accelerated APC-mediated intestinal tumorigenesis. Cancer Res. 1996 Jul 1;56(13):2922-6

Lynch Syndrome

Phenotype(s)

MGI:4412021
Note：The expected phenotype(s) may be observed in the above-mentioned mice that bred with Mlh1-KO(NM-KO-190626) mice.

Reference(s)

Edelmann W, Yang K, Kuraguchi M, Heyer J, Lia M, Kneitz B, Fan K, Brown AM, Lipkin M, Kucherlapati R, Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant mice. Cancer Res. 1999 Mar 15;59(6):1301-7

Colorectal Cancer

Phenotype(s)

MGI:5693797
Note：The expected phenotype(s) may be observed in the above-mentioned mice that bred with Ccdc80-KO(NM-KO-200795) mice.

Reference(s)

Grill JI, Neumann J, Herbst A, Hiltwein F, Ofner A, Marschall MK, Wolf E, Kirchner T, Goke B, Schneider MR, Kolligs FT, DRO1 inactivation drives colorectal carcinogenesis in ApcMin/+ mice. Mol Cancer Res. 2014 Nov;12(11):1655-62

Validation Data

Along with the development of intestinal adenoma, we found that most  of Apc-(L850X) mice heterozygous mice raised on a normal diet  died  by 160 days of age (Figure 1).

图片1.png

Figure 1. Survival Percent Of MT and WT Mouse(n=24).

The data of food intake and body weight analysis showed that Apc-(L850X) mice had reduced food intake and lighter body weights with the age(Figure 2-3).

apc-2-3.png


Most of the C57BL/6-Apcem1(L850X)Smoc heterozygous mice raised adenomas throughout the intestinal tract with the age (Figure 4-5 ).

apc-4.png

Figure 4. Intestinal Tract Tumour Numbers of MT and WT Mouse.

image.png

Figure 5. Mouse Intestinal Tract on day 109.

Pathologic results showed that adenomatous hyperplasia appeared in epithelium of intestinal type (Figure 6-8). Blue arrows indicate hyperplasia of gland, which is intestinal adenoma. Yellow arrows show inflammatory cells infiltrating the mucosal layer. Gray arrows show mesenteric lymph nodes.

图片1.png

Figure 6: Histological Result of WT and MT Mouse jejunum.

图片2.png 

Figure 7: Histological Result of WT and MT Mouse ileum.

图片3.png

Figure 8: Histological Result of WT and MT Mouse colon.

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