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Frequency and histological appearance of adenomas in multiple intestinal neoplasia mice are unaffected by severe combined immunodeficiency ( scid ) mutation
Author(s) -
Dudley Mark E.,
Sundberg John P.,
Roopenian Derry C.
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960117)65:2<249::aid-ijc20>3.0.co;2-7
Subject(s) - severe combined immunodeficiency , immunodeficiency , immunosurveillance , biology , carcinogenesis , adenomatous polyposis coli , mutation , phenotype , familial adenomatous polyposis , cancer research , immunology , cancer , genetics , colorectal cancer , immune system , gene
Well‐characterized murine mutations are powerful analytical tools for the genetic analysis of tumorigenesis. We crossed the multiple intestinal neoplasia ( Min ) allele of adenomatous polyposis coli ( Apc ), which produces a profound pre‐disposition to intestinal neoplasia, with the severe combined immunodeficiency ( scid ) mutation, which causes defective double‐strand DNA repair and severe immunodeficiency, on the common C57BL/6J genetic background to assay for any combined effect on intestinal tumorigenesis. Several phenotypic traits were exacerbated in an apparently additive manner in the double mutant mice, including reduced immunoglobulin levels, reduced body weight and increased morbidity. However, quantitation and histological evaluation of polyp phenotype indicated that these mutations did not interact to affect either polyp frequency or progression. Thus, neither genome instability nor lack of immunosurveillance conferred by scid contributes to intestinal polyps in this model. © 1996 Wiley‐Liss, Inc.