Novel Roles for MLH3 Deficiency and TLE6-Like Amplification in DNA Mismatch Repair-Deficient Gastrointestinal Tumorigenesis and Progression 英文参考文献.docVIP
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Novel Roles for MLH3 Deficiency and TLE6-Like Amplification in DNA Mismatch Repair-Deficient Gastrointestinal Tumorigenesis and Progression 英文参考文献
NovelRolesforMLH3DeficiencyandTLE6-Like
AmplificationinDNAMismatchRepair-Deficient
GastrointestinalTumorigenesisandProgression
Peng-ChiehChen1,2¤,MariKuraguchi3,4,JohnVelasquez2,YuxunWang5,KanYang6,RobertEdwards7,
DanGillen8,WinfriedEdelmann5,RajuKucherlapati3,4,StevenM.Lipkin1,2
*
1DepartmentofBiologicalChemistry,UniversityofCaliforniaIrvine,Irvine,California,UnitedStatesofAmerica,2DepartmentofMedicine,UniversityofCaliforniaIrvine,
Irvine,California,UnitedStatesofAmerica,3DepartmentofGenetics,HarvardMedicalSchool,HarvardPartnersCenterforGeneticsandGenomics,Boston,Massachusetts,
United States of America, 4Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America, 5Department of Molecular
Genetics,AlbertEinsteinCollegeofMedicine,NewYork,NewYork,UnitedStatesofAmerica,6StrangCancerResearchLaboratory,DepartmentofMedicine,WeillMedical
CollegeofCornellUniversity,NewYork,NewYork,UnitedStatesofAmerica,7DepartmentofPathology,UniversityofCaliforniaIrvine,Irvine,California,UnitedStatesof
America,8DepartmentofStatistics,UniversityofCaliforniaIrvine,Irvine,California,UnitedStatesofAmerica
Abstract
DNAmismatchrepairsuppressesgastrointestinaltumorgenesis.FourmammalianE.coliMutLhomologuesheterodimerize
toformthreedistinctcomplexes:MLH1/PMS2,MLH1/MLH3,andMLH1/PMS1.Tounderstandthemechanisticcontributions
ofMLH3andPMS2ingastrointestinaltumorsuppression,wegeneratedMlh32/2;Apc1638N andMlh32/2;Pms22/2;Apc1638N
(MPA) mice. Mlh3 nullizygosity significantly increased Apc frameshift mutations and tumor multiplicity. Combined
Mlh3;Pms2 nullizygosity further increased Apc base-substitution mutations. The spectrum of MPA tumor mutations was
distinct from that observed in Mlh12/2;Apc1638N mice, implicating the first potential role for MLH1/PMS1 in tumor
suppression.BecauseMlh3;Pms2deficiencyalsoincreasedgastrointestinaltumorprogression,weusedarray-CGHtoidentify
arecurrenttumoramplicon.ThisampliconcontainedapreviouslyuncharacterizedTransducinenh
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