ライフサイエンスコーパス: be addicted to

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 mple, HCC tumors with activated beta-catenin are addicted to fatty acid catabolism, whereas HCC tumor

11 h, suggesting that some FLT3/ITD AML may not be addicted to FLT3 signaling.

12 over, tumour cells expressing activated AKT1 are 'addicted' to FoxM1, as they require continuous pres

13 ead and neck squamous cell carcinoma (HNSCC) is addicted to glutaminolysis.

14 We report that HER2-amplified cancers are addicted to HER2 across different cancer types and t

15 ent" kinases and the reason why some kinases are addicted to Hsp90 while closely related family membe

16 MYC-driven B-cell lymphomas are addicted to increased levels of ribosome biogenesis

17 Here we show that ALCLs of both subtypes are addicted to IRF4 signaling, as knockdown of IRF4 by

18 r data demonstrate that miR-125a-induced MPN is addicted to its sustained overexpression, and highlig

19 stion the degree to which pancreatic cancers are addicted to KRAS by illustrating adaptive nongenetic

20 le pancreatic ductal adenocarcinomas (PDACs) are addicted to KRAS-activating mutations, inhibitors of

21 estingly, MYCN-amplified neuroblastoma cells are "addicted" to LDHA enzymatic activity, as its deplet

22 Indeed, these cells are addicted to maintenance of low cAMP concentrations i

23 Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or

24 Cells with BRAF(V600E) amplification are addicted to MEKi to maintain a precise level of ERK1

25 t tumors displaying c-MET gene amplification are "addicted" to MET signaling and therefore are very s

26 and recent findings suggest that tumors can be 'addicted' to miRNA overexpression, yielding a possib

27 indings demonstrate that MCCP and MCCN cells are addicted to MUC1-C and identify MUC1-C as a potentia

28 nce, we demonstrated that MYC-induced tumors are addicted to mutant beta-catenin, and the combined in

29 g option for treating pancreatic tumors that are addicted to mutant KRAS, thus offering opportunities

30 a therapeutic strategy to manage tumors that are addicted to mutant p53 for survival.

31 al tumor, suggesting that tumors continue to be addicted to MYC.

32 In ABC DLBCL cells, which are addicted to NF-kB and STAT3 survival signaling, DMF

33 These genetic aberrations cause tumors to be 'addicted' to NF-kappaB, which can be exploited thera

34 phoma (DLBCL) is an aggressive lymphoma that is addicted to NF-kappaB signaling through the CARD11-BC

35 tinoid in HCC1599 breast cancer cells, which are addicted to NOTCH1 for growth/viability.

36 ectious diseases in people who misuse and/or are addicted to opioids and to concurrently address the

37 a PI3K/AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that p

38 ells including Bortezomib-resistant MM cells are addicted to RelB-p52 for survival.

39 ce, and fortunately a peculiar set of humans are addicted to solving the problems.

40 Our society is addicted to steel.

41 al, and CRC cells with BRAF(V600E) mutations are addicted to the ERK1/2 pathway for repression of BIM

42 use large B-cell lymphoma (DLBCL) cell lines are addicted to the expression of OCT2 and its coactivat

43 howed that tumor cells carrying a mutant p53 are addicted to the mutant for cell survival and resista

44 480 carcinoma cells that carry a mutant p53, are addicted to the mutant for their survival and resist

45 loma (MM) cell lines and primary tumor cells are addicted to the MYC oncoprotein for survival.

46 y to selectively eliminate cancer cells that are addicted to the overexpression of the MeCP2 oncoprot

47 phagy enables melanomas that would otherwise be addicted to the Ras-Raf pathway to instead tolerate p

48 PDA is addicted to the activity of the mutated KRAS oncogene

49 Society, which likes to live well, is addicted to the products of science, and fortunately

50 th in low Zn(2+), suggesting these cells may be addicted to Zn(2+).