103 results on '"Dongre, Anushka"'
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2. Abstract B022: Targeting epithelial-mesenchymal plasticity and CD73 to enhance responses of breast cancers to immune checkpoint blockade therapies
3. Immuno-PET identifies the myeloid compartment as a key contributor to the outcome of the antitumor response under PD-1 blockade
4. Leveraging immunochemotherapy for treating pancreatic cancer
5. New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer
6. IL-1β inflammatory response driven by primary breast cancer prevents metastasis-initiating cell colonization
7. Supplementary Data from Direct and Indirect Regulators of Epithelial–Mesenchymal Transition–Mediated Immunosuppression in Breast Carcinomas
8. Data from Direct and Indirect Regulators of Epithelial–Mesenchymal Transition–Mediated Immunosuppression in Breast Carcinomas
9. Supplementary Figure 4 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
10. Data from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
11. Supplementary Figure Legends from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
12. Supplementary Figure 6 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
13. Data from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
14. Supplementary Figure 5 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
15. Supplementary Table 2- Incidence of orthotopic tumor formation and spontaneous metastasis in D2A1-d & parental D2A1 cells from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
16. Supplementary Figure 3 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
17. Supplementary Table 4- Orthotopic tumor incidence of Zeb1 knockdown cells from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
18. Supplementary Table 1- Incidence of lung metastases in D2A1-d & parental D2A1 cells from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
19. Supplementary Figure 1 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
20. Supplementary Figure legends from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
21. Supplementary Figure 1- Extended characterization of D2A1-d and parental D2A1 from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
22. Supplementary Table 3- Tumor incidence of CD24 negative & CD24 positive cell populations from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
23. Supplementary Figure 7 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
24. Supplementary Figure 3- LPS effects on the immune system are not restricted to D2A1-d cells from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
25. Supplementary Figure 2- Prolonged EMT induction causes modest metastatic outgrowth from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
26. Supplementary Figure 2 from Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
27. Direct and Indirect Regulators of Epithelial–Mesenchymal Transition–Mediated Immunosuppression in Breast Carcinomas
28. Immune Checkpoint Blockade Therapy for Breast Cancer: Lessons from Epithelial–Mesenchymal Transition.
29. Epithelial-to-mesenchymal transition promotes immune escape by inducing CD70 in non-small cell lung cancer
30. Editorial: The Role of the EMT Program in Regulating the Immune Response in Carcinoma
31. Targeting Hypoxia‐Adenosinergic Signaling to Enable Effective Anti‐Tumor Responses by Reprogramming the Immunosuppressive Tumor Microenvironment
32. Abstract PR010: Potentiating the efficacy of immune checkpoint blockade by targeting the epithelial-to-mesenchymal transition (EMT) in breast carcinomas
33. Direct and Indirect Regulators of Epithelial–Mesenchymal Transition–Mediated Immunosuppression in Breast Carcinomas
34. 232 The epithelial-to-mesenchymal transition (EMT) contributes to immunosuppression in breast carcinomas and regulates their response to immune checkpoint blockade
35. Abstract A82: Direct and indirect regulators of epithelial-to-mesenchymal transition mediated immunosuppression in breast carcinomas
36. Inadequate DNA Damage Repair Promotes Mammary Transdifferentiation, Leading to BRCA1 Breast Cancer
37. Inadequate DNA Damage Repair Promotes Mammary Transdifferentiation, Leading to BRCA1 Breast Cancer
38. New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer
39. Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
40. Predicting the response to CTLA-4 blockade by longitudinal noninvasive monitoring of CD8 T cells
41. Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
42. Epithelial-to-Mesenchymal Transition Contributes to Immunosuppression in Breast Carcinomas
43. Predicting the response to CTLA-4 blockade by longitudinal noninvasive monitoring of CD8 T cells
44. Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency
45. NON-CANONICAL NOTCH SIGNALING REGULATES ACTIVATION AND DIFFERENTIATION OF PERIPHERAL CD4+ T CELLS
46. Non-Canonical Notch Signaling Drives Activation and Differentiation of Peripheral CD4+ T Cells
47. Therapeutic targeting of NOTCH signaling ameliorates immune-mediated bone marrow failure of aplastic anemia
48. Low energy electron induced damage to plasmid DNA pQE30
49. Identifying the function of Notch1 in T-cell activation (121.1)
50. Non-canonical Notch signaling drives activation and differentiation of peripheral CD4+ T cells.
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