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1. An allosteric pan-TEAD inhibitor blocks oncogenic YAP/TAZ signaling and overcomes KRAS G12C inhibitor resistance

3. TEAD Proteins Associate With DNA Repair Proteins to Facilitate Cellular Recovery From DNA Damage

4. CRAF dimerization with ARAF regulates KRAS-driven tumor growth

6. AKT mutant allele-specific activation dictates pharmacologic sensitivities

7. Integrative Analysis Identifies Four Molecular and Clinical Subsets in Uveal Melanoma

8. ARAF mutations confer resistance to the RAF inhibitor belvarafenib in melanoma

11. Targeting the Hippo pathway in cancers via ubiquitination dependent TEAD degradation

12. The Molecular Taxonomy of Primary Prostate Cancer

13. The Genomic Landscape of Endocrine-Resistant Advanced Breast Cancers

14. Integrative Analysis Identifies Four Molecular and Clinical Subsets in Uveal Melanoma

15. Genome doubling shapes the evolution and prognosis of advanced cancers

16. Data from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

17. Table S7 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

18. Supplementary Figure 5 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

19. Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

20. Figure S1-7 from Accelerating Discovery of Functional Mutant Alleles in Cancer

21. Figure S1 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

22. Data from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

23. Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

24. Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

25. Supplementary Figure 3 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

26. Figure S1-S5 from Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties

27. Supplementary Figure 1 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

28. Supplementary Figure 7 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

29. Supplementary Figure 4 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

30. Supplementary tables S1-4 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

31. Data from Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties

32. Table S1-4 from Accelerating Discovery of Functional Mutant Alleles in Cancer

33. Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

34. Supplementary Figure 2 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

35. Table S1 from Allele-Specific Mechanisms of Activation of MEK1 Mutants Determine Their Properties

36. Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

37. Data from Accelerating Discovery of Functional Mutant Alleles in Cancer

38. Supplementary Figure 6 from Prospective Comprehensive Molecular Characterization of Lung Adenocarcinomas for Efficient Patient Matching to Approved and Emerging Therapies

39. Table S1-S7 from Small-Cell Carcinomas of the Bladder and Lung Are Characterized by a Convergent but Distinct Pathogenesis

40. Supplementary Tables S1-S11 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

41. Supplementary Figure S7 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

42. Supplementary Figures from Phase I Basket Study of Taselisib, an Isoform-Selective PI3K Inhibitor, in Patients with PIK3CA-Mutant Cancers

43. Supplementary Figures S1-S6 from Combined Inhibition of Gαq and MEK Enhances Therapeutic Efficacy in Uveal Melanoma

44. Supplementary Data from Leveraging Systematic Functional Analysis to Benchmark an In Silico Framework Distinguishes Driver from Passenger MEK Mutants in Cancer

45. Supplementary Table and Figure Legends from Clinical Utility of Prospective Molecular Characterization in Advanced Endometrial Cancer

46. Figure S1 from Clinical Utility of Prospective Molecular Characterization in Advanced Endometrial Cancer

47. Figure S5 from Small-Cell Carcinomas of the Bladder and Lung Are Characterized by a Convergent but Distinct Pathogenesis

48. Table S1 from Clinical Utility of Prospective Molecular Characterization in Advanced Endometrial Cancer

49. Abstract P4-08-02: LOXO-783: A potent, highly mutant selective and brain-penetrant allosteric PI3Kα H1047R inhibitor in combination with standard of care (SOC) treatments in preclinical PI3Kα H1047R-mutant breast cancer models

50. Targeting MCL‐1 and BCL‐2 with polatuzumab vedotin and venetoclax overcomes treatment resistance in R/R non‐Hodgkin lymphoma: Results from preclinical models and a Phase Ib study

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