Jake R. Conway
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View article: Dissecting tumor cell programs through group biology estimation in clinical single-cell transcriptomics
Dissecting tumor cell programs through group biology estimation in clinical single-cell transcriptomics Open
With the growth of clinical cancer single-cell RNA sequencing studies, robust differential expression methods for case/control analyses (e.g., treatment responders vs. non-responders) using gene signatures are pivotal to nominate hypothese…
View article: Somatic structural variants drive distinct modes of oncogenesis in melanoma
Somatic structural variants drive distinct modes of oncogenesis in melanoma Open
The diversity of structural variants (SVs) in melanoma and how they impact oncogenesis are incompletely known. We performed harmonized analysis of SVs across melanoma histologic and genomic subtypes, and we identified distinct global prope…
View article: Somatic structural variants driving distinct modes of oncogenesis in melanoma
Somatic structural variants driving distinct modes of oncogenesis in melanoma Open
The diversity of structural variants (SVs) in melanoma and how they impact oncogenesis are incompletely known. We performed harmonized analysis of SVs across melanoma histological and genomic subtypes, and we identified distinct global pro…
View article: 110 Deep learning models identify key tumor microenvironment features associated with genetic signatures of UV mutagenesis and alkylating agent treatment in melanoma
110 Deep learning models identify key tumor microenvironment features associated with genetic signatures of UV mutagenesis and alkylating agent treatment in melanoma Open
Background Melanoma is the most aggressive type of skin cancer and often exhibits therapeutic resistance.1 2 Different types of mutagenesis, for example UV exposure,3 4 have been shown to result in distinct genetic si…
View article: Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Traf3-knockout signature derived from RNA-seq
View article: Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
MAGeCK analysis of CRISPR screen results to identify the regulators of MHC-I/PD-L1
View article: Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
MAGeCK analysis of CRISPR screen results to identify the regulators of MHC-I/PD-L1
View article: Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and H3K27ac ChIP-seq of MHC-I-high and MHC-I-low primary melanoma samples
View article: Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Information on the ICB treatment clinical cohorts used in this study
View article: Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Effect of different drug treatment on the expression of genes encoding MHC-I, TAP1, PD-L1, and PD-L2
View article: Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Information on the ICB treatment clinical cohorts used in this study
View article: Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq of bulk B16F10 tumors that underwent different treatments
View article: Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq of bulk B16F10 tumors that underwent different treatments
View article: Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and ATAC-seq of TRAF3-normal and -deficient B16F10 cells treated with vehicle control or IFNγ
View article: Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and H3K27ac ChIP-seq of MHC-I-high and MHC-I-low primary melanoma samples
View article: Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and ATAC-seq of TRAF3-normal and -deficient B16F10 cells treated with vehicle control or IFNγ
View article: Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Traf3-knockout signature derived from RNA-seq
View article: Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Effect of different drug treatment on the expression of genes encoding MHC-I, TAP1, PD-L1, and PD-L2
View article: Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Supplementary Figures S1-S8
View article: Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Supplementary Figures S1-S8
View article: Integration of deep learning-based histopathology and transcriptomics reveals key genes associated with fibrogenesis in patients with advanced NASH
Integration of deep learning-based histopathology and transcriptomics reveals key genes associated with fibrogenesis in patients with advanced NASH Open
View article: Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival Open
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
View article: Supplementary Data from Clinical Efficacy and Molecular Response Correlates of the WEE1 Inhibitor Adavosertib Combined with Cisplatin in Patients with Metastatic Triple-Negative Breast Cancer
Supplementary Data from Clinical Efficacy and Molecular Response Correlates of the WEE1 Inhibitor Adavosertib Combined with Cisplatin in Patients with Metastatic Triple-Negative Breast Cancer Open
Supplemental methods, results, figures, tables, and references
View article: Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival Open
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
View article: Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival Open
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
View article: Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival Open
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
View article: Data from Clinical Efficacy and Molecular Response Correlates of the WEE1 Inhibitor Adavosertib Combined with Cisplatin in Patients with Metastatic Triple-Negative Breast Cancer
Data from Clinical Efficacy and Molecular Response Correlates of the WEE1 Inhibitor Adavosertib Combined with Cisplatin in Patients with Metastatic Triple-Negative Breast Cancer Open
Purpose:We report results from a phase II study assessing the efficacy of the WEE1 inhibitor adavosertib with cisplatin in metastatic triple-negative breast cancer (mTNBC).Patients and Methods:Patients with mTNBC treated with 0–1 prior lin…
View article: Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival Open
Supplementary Data from Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival