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53. Combinatorial inhibition of PTPN12-regulated receptors leads to a broadly effective therapeutic strategy in triple-negative breast cancer

55. A Multiparameter Molecular Classifier to Predict Response to Neoadjuvant Lapatinib plus Trastuzumab without Chemotherapy in HER2+ Breast Cancer

59. Supplementary table 3 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

60. Data from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

63. Supplementary Figure 1 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

64. Supplementary Figure 2 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

65. Supplementary table 4 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

66. Supplementary table 2 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

67. Supplementary table 1 from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

70. Legend for supplementay figures from Blockade of AP-1 Potentiates Endocrine Therapy and Overcomes Resistance

72. FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer

73. The Signaling Pathways Project, an integrated ‘omics knowledgebase for mammalian cellular signaling pathways

74. Supplementary Table 1 from TBCRC023: A Randomized Phase II Neoadjuvant Trial of Lapatinib Plus Trastuzumab Without Chemotherapy for 12 versus 24 Weeks in Patients with HER2-Positive Breast Cancer

75. Data from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes

76. Supplementary Tables from HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

77. Supplementary information from HER2 Reactivation through Acquisition of the HER2 L755S Mutation as a Mechanism of Acquired Resistance to HER2-targeted Therapy in HER2+ Breast Cancer

78. Data from TBCRC023: A Randomized Phase II Neoadjuvant Trial of Lapatinib Plus Trastuzumab Without Chemotherapy for 12 versus 24 Weeks in Patients with HER2-Positive Breast Cancer

79. Supplementary Figure 2 from Upregulation of ER Signaling as an Adaptive Mechanism of Cell Survival in HER2-Positive Breast Tumors Treated with Anti-HER2 Therapy

80. Supplementary Data from Evaluation of the Predictive Role of Tumor Immune Infiltrate in Patients with HER2-Positive Breast Cancer Treated with Neoadjuvant Anti-HER2 Therapy without Chemotherapy

83. Supplementary Figures from Activation of the IFN Signaling Pathway is Associated with Resistance to CDK4/6 Inhibitors and Immune Checkpoint Activation in ER-Positive Breast Cancer

84. Supplementary Figure 1 from Upregulation of ER Signaling as an Adaptive Mechanism of Cell Survival in HER2-Positive Breast Tumors Treated with Anti-HER2 Therapy

87. Supplementary Table 2 from TBCRC023: A Randomized Phase II Neoadjuvant Trial of Lapatinib Plus Trastuzumab Without Chemotherapy for 12 versus 24 Weeks in Patients with HER2-Positive Breast Cancer

89. Figure S8 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes

90. Data from Comprehensive Genomic Analysis Identifies Novel Subtypes and Targets of Triple-Negative Breast Cancer

91. Data from Activation of the IFN Signaling Pathway is Associated with Resistance to CDK4/6 Inhibitors and Immune Checkpoint Activation in ER-Positive Breast Cancer

94. Supplementary Table Set S11-S18 from Comprehensive Genomic Analysis Identifies Novel Subtypes and Targets of Triple-Negative Breast Cancer

97. Supplementary Figures S1-S4 from High IGF-IR Activity in Triple-Negative Breast Cancer Cell Lines and Tumorgrafts Correlates with Sensitivity to Anti–IGF-IR Therapy

98. Auxiliary Supplementary File from Therapeutic Targeting of Nemo-like Kinase in Primary and Acquired Endocrine-resistant Breast Cancer

99. Data from A Wnt-Independent LGR4–EGFR Signaling Axis in Cancer Metastasis

100. Data from High IGF-IR Activity in Triple-Negative Breast Cancer Cell Lines and Tumorgrafts Correlates with Sensitivity to Anti–IGF-IR Therapy

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