Oncogene addiction: sometimes a temporary slavery.
Tumors induced in conditional oncomice can show remarkable different responses to subsequent oncogene deprivation. Complete sustained regression, concomitant with massive differentiation and/or apoptosis, and partial regression are both observed. In the latter case, tumor growth either resumes without being dependent any longer on the oncogene, or requires reactivation of the oncogene in cells that have become dormant. These models reflect many of the features we also witness in human cancer and can therefore assist us in understanding the underlying mechanisms and in designing more effective treatment protocols.
Jonkers
Jos
J
Division of Molecular Biology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.
Berns
Anton
A
D000818:Animals; D017209:Apoptosis; D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000235:genetics; D015870:Gene Expression; D020868:Gene Silencing; D016259:Genes, myc / Q000235:genetics; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000628:therapy; D011518:Proto-Oncogene Proteins / Q000235:genetics* / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D012008:Recurrence; D012074:Remission Induction
D011518:Proto-Oncogene Proteins; D016271:Proto-Oncogene Proteins c-myc