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  1. ERα/PR crosstalk is altered in the context of the ERα Y537S mutation and contributes to endocrine therapy-resistant tumor proliferation
  2. Glucocorticoid Receptor Activation in Lobular Breast Cancer Is Associated with Reduced Cell Proliferation and Promotion of Metastases
  3. Supplemental Materials and Methods and Figure Legends from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  4. Supplemental Materials and Methods and Figure Legends from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  5. Supplemental Table 1 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  6. Supplemental Table 1 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  7. Supplemental Table 2 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  8. Supplemental Table 2 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  9. Supplemental Table 3 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  10. Supplemental Table 3 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  11. Supplementary Figures 1-6 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  12. Supplementary Figures 1-6 from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  13. Data from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  14. Data from The NF-κB Pathway Promotes Tamoxifen Tolerance and Disease Recurrence in Estrogen Receptor–Positive Breast Cancers
  15. Unconventional isoquinoline-based SERMs elicit fulvestrant-like transcriptional programs in ER+ breast cancer cells
  16. Targeting MYC with modular synthetic transcriptional repressors derived from bHLH DNA-binding domains
  17. Unconventional Isoquinoline-Based SERMs Elicit Fulvestrant-Like Transcriptional Programs in ER+ Breast Cancer Cells
  18. Labeling of a Mutant Estrogen Receptor with an Affimer in a Breast Cancer Cell Line
  19. Endocrine Therapy-Resistant Breast Cancer Cells Are More Sensitive to Ceramide Kinase Inhibition and Elevated Ceramide Levels Than Therapy-Sensitive Breast Cancer Cells
  20. Defining the Energetic Basis for a Conformational Switch Mediating Ligand-Independent Activation of Mutant Estrogen Receptors in Breast Cancer
  21. Lasofoxifene as a potential treatment for therapy-resistant ER-positive metastatic breast cancer
  22. Reinvestigating the acyl cyclization to the precursor of diptoindonesin G
  23. Facilitating Drug Discovery in Breast Cancer by Virtually Screening Patients Using In Vitro Drug Response Modeling
  24. The NFκB pathway promotes tamoxifen tolerance and disease recurrence in estrogen receptor positive breast cancers
  25. Next Generation ERα Inhibitors for Endocrine-Resistant ER+ Breast Cancers
  26. Specific stereochemistry of OP-1074 disrupts estrogen receptor alpha helix 12 and confers pure antiestrogenic activity
  27. Structural underpinnings of oestrogen receptor mutations in endocrine therapy resistance
  28. A “cross-stitched” peptide with improved helicity and proteolytic stability
  29. Metabolism of megestrol acetate in vitro and the role of oxidative metabolites
  30. Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer
  31. Estrogen receptor alpha somatic mutations Y537S and D538G confer breast cancer endocrine resistance by stabilizing the activating function-2 binding conformation
  32. In Memoriam: Elwood Jensen (1920–2012)
  33. Overcoming mutation-based resistance to antiandrogens with rational drug design