<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Smith-Roe, Stephanie L</style></author><author><style face="normal" font="default" size="100%">Löhr, Christiane V</style></author><author><style face="normal" font="default" size="100%">Bildfell, Robert J</style></author><author><style face="normal" font="default" size="100%">Fischer, Kay A</style></author><author><style face="normal" font="default" size="100%">Hegan, Denise Campisi</style></author><author><style face="normal" font="default" size="100%">Glazer, Peter M</style></author><author><style face="normal" font="default" size="100%">Buermeyer, Andrew B</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Induction of aberrant crypt foci in DNA mismatch repair-deficient mice by the food-borne carcinogen 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP).</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer letters</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cancer Lett.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adaptor Proteins, Signal Transducing</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Carcinogens</style></keyword><keyword><style  face="normal" font="default" size="100%">Carrier Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Colon</style></keyword><keyword><style  face="normal" font="default" size="100%">Colonic Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mismatch Repair</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Neoplasm</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematologic Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Imidazoles</style></keyword><keyword><style  face="normal" font="default" size="100%">Incidence</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Nuclear Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Precancerous Conditions</style></keyword><keyword><style  face="normal" font="default" size="100%">Survival Rate</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2006 Nov 28</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">244</style></volume><pages><style face="normal" font="default" size="100%">79-85</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Disruption of the DNA mismatch repair (MMR) pathway results in elevated mutation rates, inappropriate survival of cells bearing DNA damage, and increased cancer risk. Relatively little is known about the impact of environmentally relevant carcinogens on cancer risk in individuals with MMR-deficiency. We evaluated the effect of MMR status (Mlh1(+/+) versus Mlh1(-/-)) on the carcinogenic potential of the cooked-meat mutagen, 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) in mice. PhIP exposure did not obviously increase lymphoma or small intestinal tumorigenesis in either Mlh1-deficient or -proficient mice. In contrast, the frequency of aberrant crypt foci (ACF), a preneoplastic biomarker for colon tumorigenesis, was increased by PhIP, and the increase due to PhIP was significantly greater in Mlh1(-/-) versus wild-type littermates. This apparent heightened susceptibility to induction of ACF parallels the previously reported hypermutability of Mlh1-deficient mice to PhIP and is consistent with the hypothesis that MMR-deficiency would increase the likelihood of PhIP-induced carcinogenic mutations. Further evaluation of the risk that consumption of heterocyclic amines may impart to MMR-deficient individuals therefore is warranted.</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16427736?dopt=Abstract</style></custom1></record></records></xml>