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Science (New York, N.Y.)|January 3, 2015
Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisionsCristian Tomasetti, Bert VogelsteinCell Cycle (Georgetown, Tex.)|May 1, 2004
HAUSP is required for p53 destabilizationJordan M Cummins, Bert VogelsteinThe New England Journal of Medicine|November 13, 2015
The Path to Cancer --Three Strikes and You're OutBert Vogelstein, Kenneth W KinzlerNature Medicine|August 3, 2004
Cancer genes and the pathways they controlBert Vogelstein, Kenneth W KinzlerProceedings of the National Academy of Sciences of the United States of America|January 25, 2013
Half or more of the somatic mutations in cancers of self-renewing tissues originate prior to tumor initiationCristian Tomasetti, Bert Vogelstein, Giovanni ParmigianiNature Protocols|November 17, 2007
Genetic knockouts and knockins in human somatic cellsCarlo Rago, Bert Vogelstein, Fred BunzScience (New York, N.Y.)|March 25, 2017
Stem cell divisions, somatic mutations, cancer etiology, and cancer preventionCristian Tomasetti, Lu Li, Bert VogelsteinNature Biotechnology|August 11, 2006
The role of companion diagnostics in the development and use of mutation-targeted cancer therapiesNickolas Papadopoulos, Kenneth W Kinzler, Bert VogelsteinCancer Research|September 23, 2003
Phosphorylation of beta-catenin at S33, S37, or T41 can occur in the absence of phosphorylation at T45 in colon cancer cellsZhenghe Wang, Bert Vogelstein, Kenneth W KinzlerPageof 41