作者: Cora Reiss , Torsten Haneke , Hans-Ulrich Völker , Martin Spahn , Andreas Rosenwald
DOI: 10.3109/10428194.2010.510360
关键词:
摘要: Defects in the mismatch repair system (MMR) underlie hereditary non-polyposis colorectal cancer (HNPCC)/Lynch syndrome and also a significant number of sporadic cancers. Mice carrying null allele for MMR gene Mlh1 are preferentially prone to development lymphomas B- T-cell origin lesser extent gastrointestinal tumors. Consistent with these findings mice, defects have been observed hematological malignancies. To study role MLH1 lymphomagenesis more detail, we generated new mouse model conditional (Mlh1flox/flox). Mating mice EIIa-Cre recombinase transgenic allowed constitutive inactivation MLH1, resulting Mlh1Δex4/Δex4 line displays complete deficiency predisposition phenotype similar Mlh1−/− mice. For specific combined Mlh1flox/flox Lck-Cre transgene. In Mlh1TΔex4/TΔex4 ...