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1. Tumor-informed ctDNA as an objective marker for postoperative residual disease in epithelial ovarian cancer.

2. Monitoring ctDNA dynamics in early breast cancer using a novel ultra-sensitive tumor-informed structural variant approach combining whole-genome sequencing and multiplex dPCR.

5. Matched analysis of circulating selenium with the breast cancer selenotranscriptome: a multicentre prospective study

10. Supplementary Spreadsheet S5 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

11. Supplementary Spreadsheet S1 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

12. Supplementary Data for Article from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

13. Supplementary Spreadsheet S4 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

14. Supplementary Spreadsheet S3 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

15. Supplementary Spreadsheet S2 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

16. Supplementary Spreadsheet S2 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

17. Supplementary Spreadsheet S1 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

18. Supplementary Spreadsheet S4 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

19. Data from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

20. Data from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

21. Supplementary Data for Article from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

22. Supplementary Spreadsheet S5 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

23. Supplementary Spreadsheet S3 from p53 Maintains Baseline Expression of Multiple Tumor Suppressor Genes

24. Figure S1 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

25. Figure S3 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

26. Figure S2 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

27. Figure S3 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

28. Appendix S1 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

29. Figure S2 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

30. Figure S1 from Prediction of Lymph Node Metastasis in Breast Cancer by Gene Expression and Clinicopathological Models: Development and Validation within a Population-Based Cohort

33. Data from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

34. Supplementary Table 1 from The Retinoblastoma Gene Undergoes Rearrangements in BRCA1-Deficient Basal-like Breast Cancer

35. Data from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

36. Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

37. Supplementary Table 1 from The Retinoblastoma Gene Undergoes Rearrangements in BRCA1-Deficient Basal-like Breast Cancer

38. Supplementary Figure 1 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

39. Supplementary Figure 2 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

40. Supplementary Figure 2 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

41. Data from The Retinoblastoma Gene Undergoes Rearrangements in BRCA1-Deficient Basal-like Breast Cancer

42. Data from The Retinoblastoma Gene Undergoes Rearrangements in BRCA1-Deficient Basal-like Breast Cancer

43. Supplementary Material from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

44. Supplementary Figure 1 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

45. Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

49. Duplex Sequencing Uncovers Recurrent Low-frequency Cancer-associated Mutations in Infant and Childhood KMT2A-rearranged Acute Leukemia

50. How Reliable Are Gene Expression-Based and Immunohistochemical Biomarkers Assessed on a Core-Needle Biopsy? A Study of Paired Core-Needle Biopsies and Surgical Specimens in Early Breast Cancer

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