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1 umococci with high transformation capability are "addicted" to a "hypertransformable" state for optim
2 he "proneural" and "classical" subtypes that are addicted to aberrant signaling from integrin alphavb
3 been based on the assumption that PDAC cells are addicted to activated KRAS, but this assumption rema
4 into question the degree to which PDAC cells are addicted to activated KRAS, by illustrating adaptive
5 ent non-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellul
6  provide further evidence that myeloma cells are addicted to c-MYC activity and that c-MYC is a promi
7  amplified MYCC, indicating that these cells are addicted to continued MYCC overexpression.
8 icient cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was suf
9                                 Such cancers are "addicted" to EGFR, and treatment with a TKI invaria
10 h, suggesting that some FLT3/ITD AML may not be addicted to FLT3 signaling.
11 over, tumour cells expressing activated AKT1 are 'addicted' to FoxM1, as they require continuous pres
12 ent" kinases and the reason why some kinases are addicted to Hsp90 while closely related family membe
13     Here we show that ALCLs of both subtypes are addicted to IRF4 signaling, as knockdown of IRF4 by
14 r data demonstrate that miR-125a-induced MPN is addicted to its sustained overexpression, and highlig
15 stion the degree to which pancreatic cancers are addicted to KRAS by illustrating adaptive nongenetic
16 estingly, MYCN-amplified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its deplet
17                          Indeed, these cells are addicted to maintenance of low cAMP concentrations i
18           Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or
19 t tumors displaying c-MET gene amplification are "addicted" to MET signaling and therefore are very s
20  and recent findings suggest that tumors can be 'addicted' to miRNA overexpression, yielding a possib
21 nce, we demonstrated that MYC-induced tumors are addicted to mutant beta-catenin, and the combined in
22 a therapeutic strategy to manage tumors that are addicted to mutant p53 for survival.
23 al tumor, suggesting that tumors continue to be addicted to MYC.
24    These genetic aberrations cause tumors to be 'addicted' to NF-kappaB, which can be exploited thera
25 phoma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signaling through the CARD11-BC
26 tinoid in HCC1599 breast cancer cells, which are addicted to NOTCH1 for growth/viability.
27  a PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that p
28 ells including Bortezomib-resistant MM cells are addicted to RelB-p52 for survival.
29 ce, and fortunately a peculiar set of humans are addicted to solving the problems.
30                                  Our society is addicted to steel.
31 al, and CRC cells with BRAF(V600E) mutations are addicted to the ERK1/2 pathway for repression of BIM
32 use large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivat
33 howed that tumor cells carrying a mutant p53 are addicted to the mutant for cell survival and resista
34 480 carcinoma cells that carry a mutant p53, are addicted to the mutant for their survival and resist
35 loma (MM) cell lines and primary tumor cells are addicted to the MYC oncoprotein for survival.
36 phagy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate p
37                                          PDA is addicted to the activity of the mutated KRAS oncogene
38           Society, which likes to live well, is addicted to the products of science, and fortunately

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