Henry W. Long
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View article: Supplementary Fig. S1 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Fig. S1 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Supplementary Fig. S1. Comprehensive analysis of protein expression data in immune and invasive cancer epithelial regions from in various patient cohorts.
View article: Supplementary Table S9 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S9 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S9
View article: Supplementary Table S8 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S8 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S8
View article: Supplementary Tables S2-13 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Tables S2-13 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Supplementary Tables S2-13
View article: Supplementary Table S1 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S1 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S1
View article: Supplementary Fig. S4 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Fig. S4 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Supplementary Fig. S4. Schematic of flow cytometry experiments and differential impact of IFNg stimulation on HR+ breast cancer cells.
View article: Supplementary Table S3 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S3 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S3
View article: Supplementary Figures from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Figures from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Figures
View article: Supplementary Fig. S2 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Fig. S2 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Supplementary Fig. S2. Comprehensive analysis of protein expression changes before and after endocrine treatment
View article: Supplementary Table S7 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S7 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S7
View article: Supplementary Table S5 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S5 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S5
View article: Supplementary Table S4 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States
Supplementary Table S4 from JAK–STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States Open
Supplementary Table S4
View article: Supplementary Fig. S7 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Fig. S7 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Supplementary Fig. S7. Impact of treatment with fulvestrant, birinapant, and their combination on a PDX model of HR+ breast cancer.
View article: Supplementary Table S1 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer
Supplementary Table S1 from Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor–Positive Breast Cancer Open
Table S1
View article: A multiomics resource of B cell activation helps decipher disease pathogenesis 4355
A multiomics resource of B cell activation helps decipher disease pathogenesis 4355 Open
Description Most genetic variants that confer risk of complex immune-mediated diseases (IMD) affect gene regulation in specific cell types. Their target genes and focus cell types are often unknown, partially because some effects are hidde…
View article: 119 Endogenous retroviruses as tumor-specific antigens in clear cell renal cell carcinoma: A new avenue for immunotherapy
119 Endogenous retroviruses as tumor-specific antigens in clear cell renal cell carcinoma: A new avenue for immunotherapy Open
View article: EZH2-TTP-mTORC1 Axis Drives Phenotypic Plasticity and Therapeutic Vulnerability in Lethal Prostate Cancer
EZH2-TTP-mTORC1 Axis Drives Phenotypic Plasticity and Therapeutic Vulnerability in Lethal Prostate Cancer Open
View article: EZH2-TTP-mTORC1 Axis Drives Phenotypic Plasticity and Therapeutic Vulnerability in Lethal Prostate Cancer
EZH2-TTP-mTORC1 Axis Drives Phenotypic Plasticity and Therapeutic Vulnerability in Lethal Prostate Cancer Open
Phenotypic plasticity is a recognized mechanism of therapeutic resistance in prostate cancer (PCa), however current knowledge of driver mechanisms and therapeutic interventions are limited. Using genetically engineered mouse models (GEMMs)…
View article: EED Maintains the Small Cell Lung Cancer Neuroendocrine Phenotype and Drives Lung Cancer Histological Transformation
EED Maintains the Small Cell Lung Cancer Neuroendocrine Phenotype and Drives Lung Cancer Histological Transformation Open
Lung cancer histological subtypes include lung adenocarcinoma (LUAD) and small cell lung cancer (SCLC). While typically distinct, combined LUAD/SCLC histology tumors occur, and LUAD can transform into SCLC as a resistance mechanism to targ…
View article: Table S7 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Table S7 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Table S7. Sequences of Alt-R CRISPR-Cas9 sgRNAs
View article: Table S6 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Table S6 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Table S6. Sequence of the Alt-R CRISPR-Cas9 sgRNA That targets N-terminus of EPAS1 and the Sequence of the Homology Directed Repair Template
View article: Table S3 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Table S3 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Table S3. Sequences of Oligonucleotides Used for the Cloning of CRISPRa and CRISPRko sgRNAs
View article: Shirole Fig. S15 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S15 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S15: High Cyclin D2 Expression as a Potential Cause of In Vitro HIF2-independence
View article: Shirole Fig. S12 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S12 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S12: Loss of All 3 pRB Paralogs is Required to Confer Resistance to CDK4/6 Inhibitor
View article: Shirole Fig. S5 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S5 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S5: Failure to Downregulate CCND1 Confers Resistance to HIF2alpha Inhibition
View article: Table S1 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Table S1 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Table S1. Genes Targeted by sgRNAs in HIF2⍺ Subpool CRISPRa sgRNA Library (CP1904)
View article: Shirole Fig. S7 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S7 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S7: The HIF2 Inhibitor PT2399 Impairs G1/S Traversal by ccRCC Cells
View article: Shirole Fig. S8 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S8 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S8: HIF2alpha Inhibitor PT2399 Does Not Induce Apoptosis in ccRCC Cell Lines
View article: Shirole Fig. S3 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S3 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S3: HIF2alpha Subpool CRISPRa Screen for Modulators of 786-O Cell Sensitivity to HIF2alpha Inhibition
View article: Shirole Fig. S14 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer
Shirole Fig. S14 from Requirement for Cyclin D1 Underlies Cell-Autonomous HIF2 Dependence in Kidney Cancer Open
Fig. S14: Failure to Downregulate VEGFA and CCND1 Confers Resistance to PT2399 In Vivo