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1. Targeting TRIP13 in favorable histology Wilms tumor with nuclear export inhibitors synergizes with doxorubicin

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

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

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

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

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

33. Data from Genomic Copy Number Dictates a Gene-Independent Cell Response to CRISPR/Cas9 Targeting

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

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

50. MTAP deletion confers enhanced dependency on the PRMT5 arginine methyltransferase in cancer cells

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