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3. Profound MEK inhibitor response in a cutaneous melanoma harboring a GOLGA4-RAF1 fusion

4. Supplementary Table 18 from Nonequivalent Gene Expression and Copy Number Alterations in High-Grade Serous Ovarian Cancers with BRCA1 and BRCA2 Mutations

5. Supplementary Data from Integrated Genome-Wide DNA Copy Number and Expression Analysis Identifies Distinct Mechanisms of Primary Chemoresistance in Ovarian Carcinomas

6. Data from EIF1AX and NRAS Mutations Co-occur and Cooperate in Low-Grade Serous Ovarian Carcinomas

7. Table S4 from Homologous Recombination DNA Repair Pathway Disruption and Retinoblastoma Protein Loss Are Associated with Exceptional Survival in High-Grade Serous Ovarian Cancer

8. Supplementary Figures 1 - 15 from Nonequivalent Gene Expression and Copy Number Alterations in High-Grade Serous Ovarian Cancers with BRCA1 and BRCA2 Mutations

9. Supplementary Methods, Figures 1-5 from Genomic Classification of Serous Ovarian Cancer with Adjacent Borderline Differentiates RAS Pathway and TP53-Mutant Tumors and Identifies NRAS as an Oncogenic Driver

10. Supplementary Figures S1 - S6 from Selective Targeting of Cyclin E1-Amplified High-Grade Serous Ovarian Cancer by Cyclin-Dependent Kinase 2 and AKT Inhibition

11. Supplementary Data from Survival Following Chemotherapy in Ovarian Clear Cell Carcinoma Is Not Associated with Pathological Misclassification of Tumor Histotype

12. Supplementary Figures S1-S9 from Resistance to CDK2 Inhibitors Is Associated with Selection of Polyploid Cells in CCNE1-Amplified Ovarian Cancer

13. Supplementary Data from Homologous Recombination DNA Repair Pathway Disruption and Retinoblastoma Protein Loss Are Associated with Exceptional Survival in High-Grade Serous Ovarian Cancer

14. Supplementary Highlighted Methods from Genomic Classification of Serous Ovarian Cancer with Adjacent Borderline Differentiates RAS Pathway and TP53-Mutant Tumors and Identifies NRAS as an Oncogenic Driver

15. Supplementary Figures 1 - 9 from Profiles of Genomic Instability in High-Grade Serous Ovarian Cancer Predict Treatment Outcome

16. Data from Integrated Genome-Wide DNA Copy Number and Expression Analysis Identifies Distinct Mechanisms of Primary Chemoresistance in Ovarian Carcinomas

17. Supplemental Material - Group Authorship from EIF1AX and NRAS Mutations Co-occur and Cooperate in Low-Grade Serous Ovarian Carcinomas

18. Supplementary Data from Novel Molecular Subtypes of Serous and Endometrioid Ovarian Cancer Linked to Clinical Outcome

19. Supplementary Tables 4 - 8 from Profiles of Genomic Instability in High-Grade Serous Ovarian Cancer Predict Treatment Outcome

20. Supplementary Methods and Figure legends from Selective Targeting of Cyclin E1-Amplified High-Grade Serous Ovarian Cancer by Cyclin-Dependent Kinase 2 and AKT Inhibition

21. Supplementary Tables S1-S8 from Selective Targeting of Cyclin E1-Amplified High-Grade Serous Ovarian Cancer by Cyclin-Dependent Kinase 2 and AKT Inhibition

22. Supplementary Methods and Tables 1 - 15, 19 from Nonequivalent Gene Expression and Copy Number Alterations in High-Grade Serous Ovarian Cancers with BRCA1 and BRCA2 Mutations

23. Supplemental Materials and Methods from EIF1AX and NRAS Mutations Co-occur and Cooperate in Low-Grade Serous Ovarian Carcinomas

24. Supplementary Data from Resistance to CDK2 Inhibitors Is Associated with Selection of Polyploid Cells in CCNE1-Amplified Ovarian Cancer

25. Supplementary Tables S1-5 from Resistance to CDK2 Inhibitors Is Associated with Selection of Polyploid Cells in CCNE1-Amplified Ovarian Cancer

26. Supplementary Tables from EIF1AX and NRAS Mutations Co-occur and Cooperate in Low-Grade Serous Ovarian Carcinomas

27. Supplementary Tables 1 - 3 from Profiles of Genomic Instability in High-Grade Serous Ovarian Cancer Predict Treatment Outcome

28. Supplementary Figures from EIF1AX and NRAS Mutations Co-occur and Cooperate in Low-Grade Serous Ovarian Carcinomas

29. Supplementary Methods from Resistance to CDK2 Inhibitors Is Associated with Selection of Polyploid Cells in CCNE1-Amplified Ovarian Cancer

30. Supplementary Tables 1-7 from Genomic Classification of Serous Ovarian Cancer with Adjacent Borderline Differentiates RAS Pathway and TP53-Mutant Tumors and Identifies NRAS as an Oncogenic Driver

34. Data from LRP1B Deletion in High-Grade Serous Ovarian Cancers Is Associated with Acquired Chemotherapy Resistance to Liposomal Doxorubicin

37. Supplementary Figures 1-10 from LRP1B Deletion in High-Grade Serous Ovarian Cancers Is Associated with Acquired Chemotherapy Resistance to Liposomal Doxorubicin

38. Supplementary Methods from LRP1B Deletion in High-Grade Serous Ovarian Cancers Is Associated with Acquired Chemotherapy Resistance to Liposomal Doxorubicin

39. Supplementary Tables 1-6 from LRP1B Deletion in High-Grade Serous Ovarian Cancers Is Associated with Acquired Chemotherapy Resistance to Liposomal Doxorubicin

40. The Colorectal cancer RISk Prediction (CRISP) trial: a randomised controlled trial of a decision support tool for risk-stratified colorectal cancer screening

41. Immune and genomic biomarkers of immunotherapy response in cancer of unknown primary

42. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns

43. Combined burden and functional impact tests for cancer driver discovery using DriverPower

44. Integrative pathway enrichment analysis of multivariate omics data

45. Pathway and network analysis of more than 2500 whole cancer genomes

46. Divergent mutational processes distinguish hypoxic and normoxic tumours

47. Genomic footprints of activated telomere maintenance mechanisms in cancer

48. Synthetic lethality between CCNE1 amplification and loss of BRCA1

49. Whole–genome characterization of chemoresistant ovarian cancer

50. SIK2 Is a Centrosome Kinase Required for Bipolar Mitotic Spindle Formation that Provides a Potential Target for Therapy in Ovarian Cancer

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