364 results on '"Cowley, Glenn S."'
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2. Preclinical efficacy of the potent, selective menin-KMT2A inhibitor JNJ-75276617 (bleximenib) in KMT2A- and NPM1-altered leukemias
3. SETDB1 suppresses NK cell-mediated immunosurveillance in acute myeloid leukemia with granulo-monocytic differentiation
4. The methyltransferase domain of DNMT1 is an essential domain in acute myeloid leukemia independent of DNMT3A mutation
5. Genetic barcoding systematically compares genes in del(5q) MDS and reveals a central role for CSNK1A1 in clonal expansion
6. CRISPR-Cas9 screen reveals a MYCN-amplified neuroblastoma dependency on EZH2
7. A Community Challenge for Inferring Genetic Predictors of Gene Essentialities through Analysis of a Functional Screen of Cancer Cell Lines
8. Supplementary Table S2 from Hyper-Dependence on NHEJ Enables Synergy between DNA-PK Inhibitors and Low-Dose Doxorubicin in Leiomyosarcoma
9. Supplementary Figure S7 from Hyper-Dependence on NHEJ Enables Synergy between DNA-PK Inhibitors and Low-Dose Doxorubicin in Leiomyosarcoma
10. Erratum: Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies
11. Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies.
12. Hyper-Dependence on NHEJ Enables Synergy Between DNA-PK Inhibitors and Low-Dose Doxorubicin in Leiomyosarcoma
13. REPLY TO HAFFNER ET AL. : DNA hypomethylation renders tumors more immunogenic
14. Epigenetic therapy activates type I interferon signaling in murine ovarian cancer to reduce immunosuppression and tumor burden
15. Genome-wide screen identifies cullin-RING ligase machinery required for lenalidomide-dependent CRL4CRBN activity
16. Small-molecule targeting of brachyury transcription factor addiction in chordoma
17. PIK3CA mutant tumors depend on oxoglutarate dehydrogenase
18. A genome-wide gain-of-function screen identifies CDKN2C as a HBV host factor
19. Supplementary Table S1.4 from Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a Target in LKB1-Mutant Lung Cancer
20. Supplementary Table 1 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
21. Supplementary Table S5 from Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival
22. Supplementary Figures S6 - S10 from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting
23. Supplementary Table S1 from Combined Pan-RAF and MEK Inhibition Overcomes Multiple Resistance Mechanisms to Selective RAF Inhibitors
24. Data from Combined Pan-RAF and MEK Inhibition Overcomes Multiple Resistance Mechanisms to Selective RAF Inhibitors
25. Supplementary Table S1 from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting
26. Data from Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a Target in LKB1-Mutant Lung Cancer
27. Supplementary Figures S1- S10 from Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a Target in LKB1-Mutant Lung Cancer
28. Supplementary Figure Legends from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting
29. Data from Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival
30. Supplementary Figures S1-S10 from Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival
31. Data from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
32. Supplementary Figure 3 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
33. Data from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting
34. Supplementary Figure 4 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
35. Supplementary Figure 1 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
36. Supplementary Figures S1 to S13 from Combined Pan-RAF and MEK Inhibition Overcomes Multiple Resistance Mechanisms to Selective RAF Inhibitors
37. Text for Supplementary Data from Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival
38. Supplementary Methods from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting
39. Supplementary Methods, Figure Legends from Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a Target in LKB1-Mutant Lung Cancer
40. Supplementary Figure 2 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
41. Supplementary Table 4 from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
42. Supplementary Table 2 from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
43. Supplementary Table 1 from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
44. Supplementary Table 5 from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
45. Supplementary method from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
46. Data from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
47. Supplementary Figures and Legends from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
48. Supplementary Table 3 from PRMT1-Mediated Translation Regulation Is a Crucial Vulnerability of Cancer
49. Rescue of a Drosophila NF1 Mutant Phenotype by Protein Kinase A
50. MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells
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