288 results on '"Chang, Matthew T"'
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2. Nucleation and dissolution mechanism underlying amyotrophic lateral sclerosis/frontotemporal lobar dementia-linked fused in sarcoma condensates
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
5. Identifying transcriptional programs underlying cancer drug response with TraCe-seq
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
9. The Hippo Pathway as a Driver of Select Human Cancers
10. An integrated molecular profile of endometrioid ovarian cancer
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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