Joshua J. Lingo
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Joshua J. Lingo has a total of 57 co-authors. Here are the top co-authors by number of shared publications:
- Dawn E. Quelle
Cancer Biology Graduate Program, University of Iowa, Iowa City, IA 52242, USA
68 shared publications - Patrick Breheny
Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, IA
67 shared publications - Akshaya Warrier
Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa
66 shared publications - Amanda Scherer
Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, IA 52240, USA
66 shared publications - Amy Tang
Department of Microbiology and Molecular Cell Biology, Leroy T. Canoles Jr. Cancer Research Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA
66 shared publications - Ana Calizo
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland
66 shared publications
Latest Publications
- Open Access
- 1 August 2026
- Published by Elsevier in EBioMedicine
- Vol. 131
Intratumoural plasma cells mediate a pro-inflammatory response to kinase inhibition and successful immune checkpoint blockade therapy in malignant peripheral nerve sheath tumours
- 1 August 2026
- Published by Elsevier in EBioMedicine
- Vol. 131
Open AccessIntratumoural plasma cells mediate a pro-inflammatory response to kinase inhibition and successful immune checkpoint blockade therapy in malignant peripheral nerve sheath tumours
- Open Access
Perturb-seq resolves physiologic programs and bidirectional regulation of non-canonical NF-κB signaling in epidermal organoids
Regulated keratinocyte differentiation is required for formation of the stratified epidermis and a functional barrier. Understanding genetic drivers of keratinocyte differentiation is crucial for understanding several skin diseases. Perturb-seq is a single-cell CRISPR screen that measures transcriptomic responses to perturbations. To date, Perturb-seq experiments have principally focused on 2-dimensional cell culture models lacking hallmarks of skin development – physiological desmosome formation and barrier function. Here, we leverage Perturb-seq in an epidermal organoid model that recapitulates physiologically relevant differentiation programs. We demonstrate that our perturbations significantly impact diverse differentiation programs and reveal bidirectional function of non-canonical NF-κB signaling in late keratinocyte differentiation.
Open AccessPerturb-seq resolves physiologic programs and bidirectional regulation of non-canonical NF-κB signaling in epidermal organoids
Regulated keratinocyte differentiation is required for formation of the stratified epidermis and a functional barrier. Understanding genetic drivers of keratinocyte differentiation is crucial for understanding several skin diseases. Perturb-seq is a single-cell CRISPR screen that measures transcriptomic responses to perturbations. To date, Perturb-seq experiments have principally focused on 2-dimensional cell culture models lacking hallmarks of skin development – physiological desmosome formation and barrier function. Here, we leverage Perturb-seq in an epidermal organoid model that recapitulates physiologically relevant differentiation programs. We demonstrate that our perturbations significantly impact diverse differentiation programs and reveal bidirectional function of non-canonical NF-κB signaling in late keratinocyte differentiation.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S5. Abbreviated list of top kinase inhibitory compounds predicted to be effective against MPNSTs from C-Map analyses of the MPNST transcriptome from NF1 patients.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S5. Abbreviated list of top kinase inhibitory compounds predicted to be effective against MPNSTs from C-Map analyses of the MPNST transcriptome from NF1 patients.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S6. Analysis of helper (CD4) and pan (CD3) T cells in combination therapysensitive versus combination therapy-resistant MPNSTs
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S6. Analysis of helper (CD4) and pan (CD3) T cells in combination therapysensitive versus combination therapy-resistant MPNSTs
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S4. Primers for qRT-PCR analyses
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S4. Primers for qRT-PCR analyses
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S5 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S5. Evaluation of differentially expressed genes (DEGs) and tumor infiltrating immune cells (plasma cells and B cells) in drug-treated de novo MPNSTs.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S5 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S5. Evaluation of differentially expressed genes (DEGs) and tumor infiltrating immune cells (plasma cells and B cells) in drug-treated de novo MPNSTs.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S3. Cluster of differentiation (CD) markers used to delineate immune cell populations after gating on CD45+ live cells.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S3. Cluster of differentiation (CD) markers used to delineate immune cell populations after gating on CD45+ live cells.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S1. Antibody sources and conditions for western blotting, IF, and IHC
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Table S1. Antibody sources and conditions for western blotting, IF, and IHC
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S7 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S7. Analyses of p-RB1, Ki67, and PD-L1 in combination therapy-sensitive and - resistant MPNSTs and PD-L1 in NF1 patient tumors.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S7 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S7. Analyses of p-RB1, Ki67, and PD-L1 in combination therapy-sensitive and - resistant MPNSTs and PD-L1 in NF1 patient tumors.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S3. Tumor growth kinetics of individual de novo MPNSTs during therapy
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from CDK4/6-MEK Inhibition in MPNSTs Causes Plasma Cell Infiltration, Sensitization to PD-L1 Blockade, and Tumor Regression
Supplementary Figure S3. Tumor growth kinetics of individual de novo MPNSTs during therapy