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A locus that influences susceptibility to 1,2‐dimethylhydrazine–induced colon tumors maps to the distal end of mouse chromosome 3
Author(s) -
Angel Joe M.,
Popova Natasha,
Lanko N.,
Turusov Vladimir S.,
DiGiovanni John
Publication year - 2000
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(200001)27:1<47::aid-mc7>3.0.co;2-7
Subject(s) - biology , locus (genetics) , 1,2 dimethylhydrazine , genetics , chromosome , dimethylhydrazine , colorectal cancer , gene , cancer
While inheritance of mutated alleles of highly penetrant tumor suppressor genes such as retinoblastoma or p53 predisposes individuals to a greatly increased risk of developing cancer, epidemiological data indicate that the majority of sporadic tumors in humans result from interactions of environmental and host genetic factors. The host genetic factors are poorly penetrant tumor susceptibility genes that determine the likelihood that a cancer will arise from carcinogen exposure. The majority of colon tumors in humans are sporadic in nature. 1,2‐dimethylhydrazine (DMH)–induced colon tumors in mice provide a useful animal model to identify genes that influence susceptibility to carcinogen‐induced colon tumors in humans. A genome‐wide scan of genetic crosses of relatively sensitive C57BL/6J with relatively resistant CBA mice treated with DMH revealed a linkage of DMH susceptibility with the distal end of mouse chromosome 3, suggesting that one or more tumor susceptibility genes may map to this region. Mol. Carcinog. 27:47–54, 2000. © 2000 Wiley‐Liss, Inc.