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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
8 icient cells transformed by oncogenic RasV12 were addicted to DDX5, because reduction of DDX5 was suf
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
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
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
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
27 a PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that p
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
36 phagy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate p
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