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1 tion and survival, a phenomenon described as oncogene addiction.
2  the transcription factor MYC generally show oncogene addiction.
3 ad spectrum of drugs that target pathways of oncogene addiction.
4 ntenance and represents a novel mechanism of oncogene addiction.
5 rsely, its experimental inactivation elicits oncogene addiction.
6 ancer cell metabolism in the context of BRAF oncogene addiction.
7 nce, and/or apoptosis, a phenomenon known as oncogene addiction.
8 teristic of solid tumours, has any effect on oncogene addiction.
9 ive tumour cell death, a phenomenon known as oncogene addiction.
10  the escape of cancers from a given state of oncogene addiction.
11 aintenance; this phenotype is referred to as oncogene addiction.
12 at angiogenesis is an essential component of oncogene addiction.
13 on, a phenomenon that has been attributed to oncogene addiction.
14 ssion of cancers through a phenomenon called oncogene addiction.
15 s, making it possible to identify targetable oncogene addictions.
16 d therapeutics for cancer generally exploit "oncogene addiction," a phenomenon in which the growth an
17 racterization of protein kinases that confer oncogene addiction and harbor a large number of disease-
18             This phenotype is referred to as oncogene addiction and has been clinically validated by
19 , tumor angiogenesis, the Warburg effect and oncogene addiction and has been validated as a drug targ
20 bitor-based therapies, suggesting incomplete oncogene addiction and highlighting a need to elucidate
21 nt transformation because they may result in oncogene addiction and represent promising targets for t
22  been identified to exploit oncogene and non-oncogene addiction and synthetic lethality.
23                SIRT3 is thus a metabolic non-oncogene addiction and therapeutic target for DLBCLs.
24 nt transformation because they may result in oncogene addiction and thus represent promising targets
25 s been increasingly used to understand such "oncogene addiction" and validate new therapeutic targets
26 s, in inducing proinflammatory cytokines, in oncogene addiction, and in overcoming cellular senescenc
27 e" analysis allows mechanistic dissection of oncogene addiction, and, when broadly applied, may provi
28 sult in silencing of tumor-suppressor genes, oncogene addictions, and enhancement of immune responses
29 n, the mechanistic underpinnings that govern oncogene addiction are just beginning to emerge.
30                                        Known oncogene addictions are confirmed while surprising compl
31 ctivated, serving as a critical mechanism of oncogene addiction associated with MYC inactivation.
32                  YY1AP1 silencing eliminates oncogene addiction by altering the chromatin landscape a
33  together, our results show how blunting MYC oncogene addiction can leverage cancer cell sensitivity
34 conceptual framework of how oncogene and non-oncogene addictions contribute to these hallmarks and ho
35                                             "Oncogene addiction" describes the phenomenon that (1) we
36 of these interactions demonstrated that: (i) oncogene addiction effects are more robust than oncogene
37 oncogene, and therapeutically targeting this oncogene addiction has already proven to be an effective
38                                        While oncogene addiction has been experimentally validated in
39                          Therapies targeting oncogene addiction have had a tremendous impact on tumor
40 nes during tumorigenesis underscores the non-oncogene addiction hypothesis in which a large class of
41 nd systems biology, to identify the state of oncogene addiction (i.e., the "Achilles heel") in specif
42 sults identify Myb as a critical mediator of oncogene addiction in AML, delineate relevant Myb target
43 lly targetable mechanism of escape from NRAS oncogene addiction in AML.
44 rative example of the successes in targeting oncogene addiction in cancer and the role of tumor-speci
45             Loss of tumor suppressor gene or oncogene addiction in cancer cells can result in sustain
46 med cell death represents a critical form of oncogene addiction in cancer cells.
47 r of context-specific dependencies including oncogene addiction in cell lines with TCF3/ID3 or MYD88
48 , these data reveal a novel mechanism of ERG oncogene addiction in prostate cancer, whereby ERG facil
49 nd/or other downstream effectors may mediate oncogene addiction in urothelial hyperplasia.
50  establish a general approach for dissecting oncogene addiction in vivo.
51 R screens, we previously identified cellular oncogene addictions in PEL cell lines, including MCL1.
52 nic mutations drive cancer cell survival and oncogene addiction is deeper and broader, highlighting d
53                                              Oncogene addiction is mediated by cell-autonomous and im
54                                              Oncogene addiction is the description of the dramatic an
55 of Cancer Cell, Sharma et al. reported that "oncogene addiction" may be mediated by differential rate
56 iological feedback mechanism that attenuates oncogene addiction-mediated cell death associated with t
57  this context, our findings suggest that the oncogene addiction model is not universally correct in i
58 hat TGFbeta is a key factor that establishes oncogene addiction of T-cell lymphomas.
59 r-based evidence of molecular pathway and/or oncogene addiction of the tumour became mandatory for th
60   HSP27 is highly expressed in, and supports oncogene addiction of, many cancers.
61 able epigenetic factors that extend the BRAF oncogene addiction paradigm on the basis of tumor cell d
62                                      Classic oncogene addiction paradigms were modified by additional
63  implies that Hh signaling may represent an "oncogene addiction" pathway for HBV-associated HCC.
64 vival depends on the drug target, so-called "oncogene addiction." Preclinical approaches to defining
65 ore, Taspase1 is better classified as a "non-oncogene addiction" protease, the inhibition of which ma
66                     This phenomenon, called "oncogene addiction," provides a rationale for molecular
67 gnaling of the BCR-ABL oncogene, also termed oncogene addiction, reprogrammed cells lost this depende
68                           The phenomenon of 'oncogene addiction' reveals that despite the multistep n
69  molecularly targeted cancer therapies, with oncogene addiction serving to set the stage for tumor ce
70 weeks post-irradiation foster the concept of oncogene addiction signaling in radiogenic transformatio
71 nd driving resistance to therapies targeting oncogene-addiction.Significance: These important finding
72                  Thus, both oncogene and non-oncogene addiction stand out as promising targets to rob
73 single-driver mutations-a phenomenon dubbed "oncogene addiction." Such dependencies have been demonst
74     Following the discovery of BRD4 as a non-oncogene addiction target in acute myeloid leukaemia (AM
75 dings suggest that, much like the concept of oncogene addiction, targeted inhibition of SWI/SNF ATPas
76 eptor (EGFR) in lung cancer cells exhibiting oncogene addiction to EGFR.
77                     Our findings demonstrate oncogene addiction to GNAS in peritoneal models of GNAS(
78                          MT-125 also induces oncogene addiction to PDGFR signaling through a mechanis
79 itching off transgene expression, suggesting oncogene addiction to the c-Jun~Fra-2 transgene.
80                       As MCC cell lines show oncogene addiction to the MCV T antigens, pharmacologic
81 pid growth and aneuploidy, can result in non-oncogene addiction to the proteostasis network that can
82                           Viral cancers show oncogene addiction to viral oncoproteins, which are requ
83                       PEL cell lines exhibit oncogene addictions to both viral and cellular genes.
84 ls (a situation commonly referred to as 'non-oncogene addiction'), to support tumour progression not
85 ls stems from an incomplete understanding of oncogene addiction, which nonetheless represents one of
86 roliferation and survival, but also mediates oncogene addiction with significant implications for the