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1. IFITM proteins assist cellular uptake of diverse linked chemotypes

2. A landscape of response to drug combinations in non-small cell lung cancer

3. EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

4. SULT1A1-dependent sulfonation of alkylators is a lineage-dependent vulnerability of liver cancers

5. Genome-wide prediction of synthetic rescue mediators of resistance to targeted and immunotherapy.

7. Catastrophic ATP loss underlies a metabolic combination therapy tailored for MYCN -amplified neuroblastoma

8. Differential Effector Engagement by Oncogenic KRAS

9. Screening and Validation of Molecular Targeted Radiosensitizers

10. Pharmacological Targeting of Vacuolar H+-ATPase via Subunit V1G Combats Multidrug-Resistant Cancer

11. Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

12. Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

13. Figure S5 from Pharmacologic Inhibition of SHP2 Blocks Both PI3K and MEK Signaling in Low-epiregulin HNSCC via GAB1

14. Table S1 from Pharmacologic Inhibition of SHP2 Blocks Both PI3K and MEK Signaling in Low-epiregulin HNSCC via GAB1

15. Data from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

16. Supplementary Table from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

17. Supplementary Figure from EGFR Inhibition Potentiates FGFR Inhibitor Therapy and Overcomes Resistance in FGFR2 Fusion–Positive Cholangiocarcinoma

18. Data from Pharmacologic Inhibition of SHP2 Blocks Both PI3K and MEK Signaling in Low-epiregulin HNSCC via GAB1

21. Data from Potent Dual BET Bromodomain-Kinase Inhibitors as Value-Added Multitargeted Chemical Probes and Cancer Therapeutics

23. Supplementary Table S1 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

25. Supplementary Figure 1 from Venetoclax-based Rational Combinations are Effective in Models of MYCN-amplified Neuroblastoma

26. Data from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

28. Supplementary Tables S4, S5 from Potent Dual BET Bromodomain-Kinase Inhibitors as Value-Added Multitargeted Chemical Probes and Cancer Therapeutics

33. Supplementary Tables S1-S3 and Figures S1-S11 from Potent Dual BET Bromodomain-Kinase Inhibitors as Value-Added Multitargeted Chemical Probes and Cancer Therapeutics

35. Supplementary Figure 4 from Venetoclax-based Rational Combinations are Effective in Models of MYCN-amplified Neuroblastoma

36. Supplementary Tables 1 - 9 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

37. Supplementary Figure Legends, Figures S1 - S6 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

43. Supplementary Figure 2 from Venetoclax-based Rational Combinations are Effective in Models of MYCN-amplified Neuroblastoma

44. Supplementary Figures 1 -11 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

45. Data from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

48. Supplementary Figure Legend from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

49. Supplementary Figure 3 from Venetoclax-based Rational Combinations are Effective in Models of MYCN-amplified Neuroblastoma

50. Figure S2 from KRAS G12C NSCLC Models Are Sensitive to Direct Targeting of KRAS in Combination with PI3K Inhibition

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