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2. Cyclin-dependent kinases in cancer: Role, regulation, and therapeutic targeting

5. Correction: The Role of the Mammalian DNA End-processing Enzyme Polynucleotide Kinase 3’-Phosphatase in Spinocerebellar Ataxia Type 3 Pathogenesis

7. Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression

8. Abstract 335: Ubiquitin Specific Peptidase 37promotes Osteosarcoma oncogenesis by interacting with PCNA and impacting constitutive replication fork movement.

13. Supplemental Figures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

14. Supplementary Table 1-3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

15. Data from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

16. Supplemental table S1 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

17. Supplemental table S1 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

18. Figure S5 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

19. Figure S4 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

20. Extended supplementary procedures from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

21. Figure S5 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

22. Supplemental experimental Procedures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

23. Supplemental Table S2 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

25. Supplemental Figures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

26. Figure S3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

27. Figure S2 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

28. Supplemental experimental Procedures from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

29. Data from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

30. Figure S1 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

31. Figure S4 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

32. Extended supplementary procedures from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

33. Supplementary Table 1-3 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

34. Figure S1 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

35. Data from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

36. Data from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

37. Supplemental Table S2 from Histone Acetyltransferase Activity of MOF Is Required for MLL-AF9 Leukemogenesis

38. Figure S2 from CDKN2A/p16 Deletion in Head and Neck Cancer Cells Is Associated with CDK2 Activation, Replication Stress, and Vulnerability to CHK1 Inhibition

41. Supplementary Figures 1-5 from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

43. Data from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

47. Data from Single-Strand DNA-Binding Protein SSB1 Facilitates TERT Recruitment to Telomeres and Maintains Telomere G-Overhangs

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