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A Potent Modifier of Liver Cancer Risk on Distal Mouse Chromosome 1This article is dedicated to the memory of our late colleague, Kristin M. Liss.
Author(s) -
Andrea Bilger,
Lee Bennett,
Rey A. Carabeo,
Teresa A. Chiaverotti,
Cecily Dvorak,
Kristin M Liss,
Susan A. Schadewald,
Henry C. Pitot,
Norman R. Drinkwater
Publication year - 2004
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1534/genetics.103.024521
Subject(s) - congenic , biology , chromosome , liver cancer , hepatocellular carcinoma , genetics , gene , microbiology and biotechnology , cancer , strain (injury) , ratón , immunology , anatomy
The C3H/HeJ (C3H) and CBA/J (CBA) mouse strains are classical mouse models of cancer susceptibility, exhibiting high risks for both spontaneous and chemically induced liver cancer. By analysis of backcrosses and intercrosses between C3H or CBA and resistant B6 mice, we have mapped a potent modifier of hepatocellular carcinoma development to distal chromosome 1, linked to the marker D1Mit33 with combined LOD(W) scores of approximately 5.9 (C3H) and 6.5 (CBA). We previously identified this region as one of two that modify susceptibility in the more distantly related C57BR/cdJ (BR) strain. Congenic B6.C3H(D1Mit5-D1Mit17) and B6.BR(D1Mit5-D1Mit17) mice developed significantly more liver tumors than B6 mice did (6- to 13-fold, P < 10(-11), in males; 3- to 4-fold, P < 10(-3), in females). Thus, distal chromosome 1 carries one or more genes that are sufficient to confer susceptibility to liver cancer.

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