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1 ad spectrum of drugs that target pathways of oncogene addiction.
2 ntenance and represents a novel mechanism of oncogene addiction.
3 rsely, its experimental inactivation elicits oncogene addiction.
4 ancer cell metabolism in the context of BRAF oncogene addiction.
5 nce, and/or apoptosis, a phenomenon known as oncogene addiction.
6 tion and survival, a phenomenon described as oncogene addiction.
7 teristic of solid tumours, has any effect on oncogene addiction.
8 ive tumour cell death, a phenomenon known as oncogene addiction.
9 the escape of cancers from a given state of oncogene addiction.
10 aintenance; this phenotype is referred to as oncogene addiction.
11 at angiogenesis is an essential component of oncogene addiction.
12 the transcription factor MYC generally show oncogene addiction.
13 s, making it possible to identify targetable oncogene addictions.
14 racterization of protein kinases that confer oncogene addiction and harbor a large number of disease-
16 , tumor angiogenesis, the Warburg effect and oncogene addiction and has been validated as a drug targ
17 nt transformation because they may result in oncogene addiction and represent promising targets for t
19 nt transformation because they may result in oncogene addiction and thus represent promising targets
20 s been increasingly used to understand such "oncogene addiction" and validate new therapeutic targets
21 s, in inducing proinflammatory cytokines, in oncogene addiction, and in overcoming cellular senescenc
22 e" analysis allows mechanistic dissection of oncogene addiction, and, when broadly applied, may provi
25 ctivated, serving as a critical mechanism of oncogene addiction associated with MYC inactivation.
27 together, our results show how blunting MYC oncogene addiction can leverage cancer cell sensitivity
28 conceptual framework of how oncogene and non-oncogene addictions contribute to these hallmarks and ho
29 oncogene, and therapeutically targeting this oncogene addiction has already proven to be an effective
30 nes during tumorigenesis underscores the non-oncogene addiction hypothesis in which a large class of
31 nd systems biology, to identify the state of oncogene addiction (i.e., the "Achilles heel") in specif
32 sults identify Myb as a critical mediator of oncogene addiction in AML, delineate relevant Myb target
36 of Cancer Cell, Sharma et al. reported that "oncogene addiction" may be mediated by differential rate
37 iological feedback mechanism that attenuates oncogene addiction-mediated cell death associated with t
38 this context, our findings suggest that the oncogene addiction model is not universally correct in i
42 vival depends on the drug target, so-called "oncogene addiction." Preclinical approaches to defining
43 ore, Taspase1 is better classified as a "non-oncogene addiction" protease, the inhibition of which ma
45 gnaling of the BCR-ABL oncogene, also termed oncogene addiction, reprogrammed cells lost this depende
47 molecularly targeted cancer therapies, with oncogene addiction serving to set the stage for tumor ce
48 weeks post-irradiation foster the concept of oncogene addiction signaling in radiogenic transformatio
49 nd driving resistance to therapies targeting oncogene-addiction.Significance: These important finding
50 single-driver mutations-a phenomenon dubbed "oncogene addiction." Such dependencies have been demonst
51 Following the discovery of BRD4 as a non-oncogene addiction target in acute myeloid leukaemia (AM
52 dings suggest that, much like the concept of oncogene addiction, targeted inhibition of SWI/SNF ATPas
55 pid growth and aneuploidy, can result in non-oncogene addiction to the proteostasis network that can
56 ls stems from an incomplete understanding of oncogene addiction, which nonetheless represents one of
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