Jason E. Long
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View article: Data from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Data from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Purpose:Lung adenocarcinomas comprise the largest fraction of non–small cell lung cancer, which is the leading cause of cancer-related deaths. Seventy-five percent of adenocarcinomas lack targeted therapies because of scarcity of druggable…
View article: Figures S1-S14, Tables S1-S2 from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment
Figures S1-S14, Tables S1-S2 from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment Open
Supplementary methods, supplementary figures and tables
View article: Data from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment
Data from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment Open
Purpose: The tumor microenvironment presents with altered extracellular matrix (ECM) and stroma composition, which may affect treatment efficacy and contribute to tissue stiffness. Ultrasound (US) elastography can visualize and quantify ti…
View article: Figure S4 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S4 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 4. Prognostic value of STK11 status relative to transcriptional subtype.
View article: Figure S3 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S3 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 3. Subtype characteristics in early/advanced LUAD.
View article: Supplementary File from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Supplementary File from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplementary Methods, Figure legends and Table legends
View article: Figure S3 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S3 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 3. Subtype characteristics in early/advanced LUAD.
View article: Supplementary Tables from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Supplementary Tables from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Tables S1-S9
View article: Figure S6 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S6 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 6. Subtype-specific response to MAPK inhibition.
View article: Figure S6 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S6 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 6. Subtype-specific response to MAPK inhibition.
View article: Figure S2 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S2 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 2. Biological characterization of the three subtypes in human LUAD.
View article: Data from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment
Data from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment Open
Purpose: The tumor microenvironment presents with altered extracellular matrix (ECM) and stroma composition, which may affect treatment efficacy and contribute to tissue stiffness. Ultrasound (US) elastography can visualize and quantify ti…
View article: Figure S5 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S5 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 5. Identification of subtypes across preclinical models.
View article: Figure S4 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S4 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 4. Prognostic value of STK11 status relative to transcriptional subtype.
View article: Figure S1 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S1 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 1. Subtype identification in early/advanced LUAD.
View article: Data from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Data from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Purpose:Lung adenocarcinomas comprise the largest fraction of non–small cell lung cancer, which is the leading cause of cancer-related deaths. Seventy-five percent of adenocarcinomas lack targeted therapies because of scarcity of druggable…
View article: Figures S1-S14, Tables S1-S2 from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment
Figures S1-S14, Tables S1-S2 from Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment Open
Supplementary methods, supplementary figures and tables
View article: Figure S5 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S5 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 5. Identification of subtypes across preclinical models.
View article: Supplementary Tables from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Supplementary Tables from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Tables S1-S9
View article: Supplementary File from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Supplementary File from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplementary Methods, Figure legends and Table legends
View article: Figure S2 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S2 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 2. Biological characterization of the three subtypes in human LUAD.
View article: Figure S1 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Figure S1 from Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Supplemental Figure 1. Subtype identification in early/advanced LUAD.
View article: Drug Discovery Oncology in a Mouse: concepts, Models and Limitations
Drug Discovery Oncology in a Mouse: concepts, Models and Limitations Open
The utilization of suitable mouse models is a critical step in the drug discovery oncology workflow as their generation and use are important for target identification and validation as well as toxicity and efficacy assessments. Current mu…
View article: Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma
Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma Open
Purpose: Lung adenocarcinomas comprise the largest fraction of non–small cell lung cancer, which is the leading cause of cancer-related deaths. Seventy-five percent of adenocarcinomas lack targeted therapies because of scarcity of druggabl…
View article: Therapeutic resistance and susceptibility is shaped by cooperative multi-compartment tumor adaptation
Therapeutic resistance and susceptibility is shaped by cooperative multi-compartment tumor adaptation Open
Emerging research suggests that multiple tumor compartments can influence treatment responsiveness and relapse, yet the search for therapeutic resistance mechanisms remains largely focused on acquired genomic alterations in cancer cells. H…
View article: Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment
Tumor Elastography and Its Association with Collagen and the Tumor Microenvironment Open
Purpose: The tumor microenvironment presents with altered extracellular matrix (ECM) and stroma composition, which may affect treatment efficacy and contribute to tissue stiffness. Ultrasound (US) elastography can visualize and quantify ti…
View article: <i>Kras</i> mutant genetically engineered mouse models of human cancers are genomically heterogeneous
<i>Kras</i> mutant genetically engineered mouse models of human cancers are genomically heterogeneous Open
Significance RAS mutant cancers represent a large unmet clinical need. Kras mutant genetically engineered mouse models (GEMMs) of cancer recapitulate disease characteristics and are relied upon preclinically to validate targets and test th…