Hepatotoxin-Induced Changes in the Adult Murine Liver Promote MYC-Induced Tumorigenesis 英文参考文献.docVIP
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Hepatotoxin-Induced Changes in the Adult Murine Liver Promote MYC-Induced Tumorigenesis 英文参考文献
Hepatotoxin-InducedChangesintheAdultMurineLiver
PromoteMYC-InducedTumorigenesis
ShellyBeer1,2,KimberlyKomatsubara1,2,DavidI.Bellovin1,2,MasashiKurobe3,KarlSylvester3.,DeanW.
Felsher1,2.
*
1Department of Medicine, Division of Oncology, School of Medicine, Center for Clinical Sciences Research, Stanford University, Stanford, California, United States of
America, 2Department of Pathology, Division of Oncology, School of Medicine, Center for Clinical Sciences Research, Stanford University, Stanford, California, United
StatesofAmerica,3DepartmentofSurgery,DivisionofPediatricSurgery,SchoolofMedicine,StanfordUniversity,Stanford,California,UnitedStatesofAmerica
Abstract
Background:Overexpressionofthehumanc-MYC(MYC)oncogeneisoneofthemostfrequentlyimplicatedeventsinthe
pathogenesisofhepatocellularcarcinoma(HCC).Previously,wehaveshowninaconditionaltransgenicmousemodelthat
MYCoverexpressionisrestrainedfrominducingmitoticcellulardivisionandtumorigenesisintheadultliver;whereas,in
markedcontrast,MYCinducesrobustproliferationassociatedwiththeveryrapidonsetoftumorigenesisinembryonicand
neonatalmice.
Methodology/Principal Findings: Here, we show that non-genotoxic hepatotoxins induce changes in the liver cellular
context associated with increased cellular proliferation and enhanced tumorigenesis. Both 5-diethoxycarbonyl-1,4-
dihydrocollidine(DDC)andcarbontetrachloride(CCl4)cooperatewithMYCtogreatlyacceleratetheonsetoflivercancerin
an adult host to less than 7 days versus a mean latency of onset of over 35 weeks for MYC alone. These hepatotoxin-
enhancedlivertumorsgrosslyandhistologicallyresembleembryonicandneonatallivertumors.Importantly,wefoundthat
MYCoverexpressionisonlycapableofinducingexpressionofthemitoticCyclinB1inembryonic/neonatalhostsoradult
hoststhatweretreatedwitheithercarcinogen.
Conclusion/Significance:Ourresultssuggestamodelwherebyoncogenescanremainlatentlyactivated,butexposureof
theadultlivertohepatotoxinsthatpromotehepatocyteproliferationcanrapidlyuncovertheirmalig
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