2010
DOI: 10.1016/j.cancergencyto.2010.04.008
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Transgenic oncogenes induce oncogene-independent cancers with individual karyotypes and phenotypes

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Cited by 29 publications
(41 citation statements)
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“…78 The lack of functional proof for somatic mutations that can generate autonomous growth remains an unmet obligation of the mutation theory to this very day. 17,[79][80][81] Nevertheless, the proponents of the mutation theory have singled out this very paper as the Achilles heel of Rous' scientific career. [82][83][84] Final answers to Rous' challenge would, however, depend on an experimental system that allows fast evolutions of new cancer karyotypes.…”
Section: 75mentioning
confidence: 99%
“…78 The lack of functional proof for somatic mutations that can generate autonomous growth remains an unmet obligation of the mutation theory to this very day. 17,[79][80][81] Nevertheless, the proponents of the mutation theory have singled out this very paper as the Achilles heel of Rous' scientific career. [82][83][84] Final answers to Rous' challenge would, however, depend on an experimental system that allows fast evolutions of new cancer karyotypes.…”
Section: 75mentioning
confidence: 99%
“…Furthermore, the formation of unique genomes in cancer is incredibly common; there is proclivity for chromosomal change during every cell division when the genome is highly unstable. The tradition of ignoring the non-specific changes in the cancer research field is the reason that these stochastic chromosomal aberrations have only recently been reconsidered as drivers of tumorigenesis and tumor growth (Castro-Gamero et al, 2013;Heng et al, 2004;Heng et al, 2006a;Heng et al, 2006b;Heng et al, 2006c;Heng et al, 2010a;Klein et al, 2010;McCormack et al, 2013;Podlaha et al, 2012;Valind and Gisselsson, 2014). The crucial realizations that have led to this reconsideration are: chromosome alterations change genome-defined systems; the high level of NCCAs is essential for cancer evolution (Heng et al, 2006a;Heng et al, 2013a); and massive and seemingly stochastic chromosomal alterations seem to be the only shared findings among many cancer types.…”
Section: Genome Theory Emphasizes the Ultimate Importance Of Chromosomentioning
confidence: 99%
“…DNA methyltransferase deficient cells are chromosomally unstable [154,155], and mice models have demonstrated that genomewide DNA hypomethylation can induce tumors [156][157][158]. Thus, a specific effect of oncoproteins is to cause aneuploidization [50] and the elevation of stochastic CIN [10].…”
Section: Cancer Genes Induce Promote and Licence Cinmentioning
confidence: 99%
“…However, many research groups monitoring long-term tumor response in diverse conditional mice models after oncoprotein withdrawal have repeatedly observed tumor relapses: H-RAS and p16 INK4A -/-(melanoma model), HER2/NEU (mammary carcinoma model), BCR-ABL (acute B-cell lymphoma model) (reviewed in [206]), MYC (lymphoma and mammary carcinoma models) [206,208,209], WNT1 (mammary carcinoma model) [206,208,210], MYC and K-RAS (mammary carcinoma model) [207], K-RAS and MAD2 (lung carcinoma model) [211], K-RAS (glioma model) [212] (see also [50] for additional examples), supporting the statement that "the nature of the initiating oncogene appears to be of little influence on the response of the resulting tumors to oncogene inactivation" [211]. In many cases tumor escape from oncogene dependence upon the primary oncogene inactivation was attributed to the acquired diverse novel genetic lesions [206,211].…”
Section: Egfr K-ras H-ras B-raf Metmentioning
confidence: 99%
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