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2. Safety and anti-tumour activity of the IgE antibody MOv18 in patients with advanced solid tumours expressing folate receptor-alpha: a phase I trial

3. LYVE-1+ macrophages form a collaborative CCR5-dependent perivascular niche that influences chemotherapy responses in murine breast cancer

4. Folate receptor alpha in ovarian cancer tissue and patient serum is associated with disease burden and treatment outcomes

6. Development of a deep‐learning model tailored for HER2 detection in breast cancer to aid pathologists in interpreting HER2‐low cases.

8. A cohort profile of the Graham Roberts study cohort

10. Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

11. Genetic predisposition to in situ and invasive lobular carcinoma of the breast.

12. An optimized five-gene multi-platform predictor of hormone receptor negative and triple negative breast cancer metastatic risk

13. Dynamics of breast-cancer relapse reveal late-recurring ER-positive genomic subgroups

14. Risk estimation of distant metastasis in node-negative, estrogen receptor-positive breast cancer patients using an RT-PCR based prognostic expression signature

16. Cohort profile: King’s Health Partners bladder cancer biobank

17. Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial

19. Multiscale deep learning framework captures systemic immune features in lymph nodes predictive of triple negative breast cancer outcome in large‐scale studies

20. Data from Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

21. Supplementary Tables S1 - S4 from Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

22. Supplementary File from Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

23. Supplementary Figures S1 - S16 from Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

24. Supplementary Methods, Figure Legends, Table Legends from Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers

25. Supplementary Data from Dynamic Changes in the NK-, Neutrophil-, and B-cell Immunophenotypes Relevant in High Metastatic Risk Post Neoadjuvant Chemotherapy–Resistant Early Breast Cancers

26. Supplementary Figure from Dynamic Changes in the NK-, Neutrophil-, and B-cell Immunophenotypes Relevant in High Metastatic Risk Post Neoadjuvant Chemotherapy–Resistant Early Breast Cancers

28. Data from RORγt+ Innate Lymphoid Cells Promote Lymph Node Metastasis of Breast Cancers

29. Supplementary figures from Anti-Folate Receptor Alpha–Directed Antibody Therapies Restrict the Growth of Triple-negative Breast Cancer

30. Video S2, Related to Figure 2 from RORγt+ Innate Lymphoid Cells Promote Lymph Node Metastasis of Breast Cancers

31. Supplementary Figures 1-10, Supplementary Materials and Methods, Supplementary References from Repurposing Tin Mesoporphyrin as an Immune Checkpoint Inhibitor Shows Therapeutic Efficacy in Preclinical Models of Cancer

32. Supplementary Table from Repurposing Tin Mesoporphyrin as an Immune Checkpoint Inhibitor Shows Therapeutic Efficacy in Preclinical Models of Cancer

33. Supplementary Figures & Tables from RORγt+ Innate Lymphoid Cells Promote Lymph Node Metastasis of Breast Cancers

34. Supplementary Movie Legends 1-2 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

35. Supplementary Figures 1-7 from FGFR1 Amplification Drives Endocrine Therapy Resistance and Is a Therapeutic Target in Breast Cancer

36. Data from FGFR1 Amplification Drives Endocrine Therapy Resistance and Is a Therapeutic Target in Breast Cancer

37. Supplementary Figure 1 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

38. Supplementary Methods and Results from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

39. Supplementary Tables 1-3 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

40. Supplementary Figure 5 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

41. Supplementary Figure 3 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

42. Supplementary Methods, Figure Legends 1-7 from FGFR1 Amplification Drives Endocrine Therapy Resistance and Is a Therapeutic Target in Breast Cancer

43. Data from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

44. Supplementary Figure 2 from Selectin Ligand Sialyl-Lewis x Antigen Drives Metastasis of Hormone-Dependent Breast Cancers

45. Supplementary materials and methods and Supplementary figure legends revised from Tumor-Infiltrating B Lymphocyte Profiling Identifies IgG-Biased, Clonally Expanded Prognostic Phenotypes in Triple-Negative Breast Cancer

46. Supplementary tables and figures from Tumor-Infiltrating B Lymphocyte Profiling Identifies IgG-Biased, Clonally Expanded Prognostic Phenotypes in Triple-Negative Breast Cancer

47. Abstract P5-01-01: Multiscale Deep Learning framework to capture systemic immune features in lymph nodes predictive of triple negative breast cancer outcome

48. LYVE-1+ macrophages form a collaborative CCR5-dependent perivascular niche that influences chemotherapy responses in murine breast cancer.

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