Andrew Stiff
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Andrew Stiff has a total of 18 co-authors. Here are the top co-authors by number of shared publications:
- Alexander Abreo
Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio
31 shared publications - Bradley W. Blaser
Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
31 shared publications - Carter Allen
Biomedical Sciences Graduate Program, The Ohio State University, Columbus, Ohio
31 shared publications - Dionisia Quiroga
Division of Medical Oncology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH
31 shared publications - Dongjun Chung
Department of Biomedical Informatics, The Ohio State University, Columbus, OH, USA
31 shared publications - Emily Schwarz
The James Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio
31 shared publications
Latest Publications
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 6 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Expression thresholds for CD14 gene expression.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 6 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Expression thresholds for CD14 gene expression.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 3 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Head & Neck baseline MDSC gene expression.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 3 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Head & Neck baseline MDSC gene expression.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Comparison of melanoma MDSC to breast MDSC (A-B) and to head and neck MDSC (C-D).
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Comparison of melanoma MDSC to breast MDSC (A-B) and to head and neck MDSC (C-D).
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 5 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Melanoma MDSC baseline gene expression.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 5 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Melanoma MDSC baseline gene expression.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Individual UMAP plots melanoma MDSC treated with DMSO control or 5 µM ibrutinib for 4h.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Individual UMAP plots melanoma MDSC treated with DMSO control or 5 µM ibrutinib for 4h.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Table listing patient characteristics of 5 patients from which 7 MDSC samples were processed for single cell RNA-seq.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Table listing patient characteristics of 5 patients from which 7 MDSC samples were processed for single cell RNA-seq.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Data from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Myeloid-derived suppressor cell (MDSC) levels are elevated in patients with cancer and contribute to reduced efficacy of immune checkpoint therapy. MDSC express Bruton's tyrosine kinase (BTK) and BTK inhibition with ibrutinib, an FDA-approved irreversible inhibitor of BTK, leads to reduced MDSC expansion/function in mice and significantly improves the antitumor activity of anti-PD-1 antibody treatments. Single-cell RNA sequencing (scRNA-seq) was used to characterize the effect of ibrutinib on gene expression of fluorescence-activated cell sorting-enriched MDSC from patients with different cancer types [breast, melanoma, head and neck squamous cell cancer (HNSCC)]. Melanoma patient MDSC were treated in vitro for 4 hours with 5 μmol/L ibrutinib or DMSO, processed for scRNA-seq using the Chromium 10× Genomics platform, and analyzed via the Seurat v4 standard integrative workflow. Baseline gene expression of MDSC from patients with breast, melanoma, and HNSCC cancer revealed similarities among the top expressed genes. In vitro ibrutinib treatment of MDSC from patients with melanoma resulted in significant changes in gene expression. GBP1, IL-1β, and CXCL8 were among the top downregulated genes whereas RGS2 and ABHD5 were among the top upregulated genes (P < 0.001). Double positive CD14+CD15+ MDSC and PMN-MDSC responded similarly to BTK inhibition and exhibited more pronounced gene changes compared with early MDSC and M-MDSC. Pathway analysis revealed significantly downregulated pathways including TREM1, nitric oxide signaling, and IL-6 signaling (P < 0.004).Implications:scRNA-seq revealed characteristic gene expression patterns for MDSC from different patients with cancer and BTK inhibition led to the downregulation of multiple genes and pathways important to MDSC function and migration.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessData from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Myeloid-derived suppressor cell (MDSC) levels are elevated in patients with cancer and contribute to reduced efficacy of immune checkpoint therapy. MDSC express Bruton's tyrosine kinase (BTK) and BTK inhibition with ibrutinib, an FDA-approved irreversible inhibitor of BTK, leads to reduced MDSC expansion/function in mice and significantly improves the antitumor activity of anti-PD-1 antibody treatments. Single-cell RNA sequencing (scRNA-seq) was used to characterize the effect of ibrutinib on gene expression of fluorescence-activated cell sorting-enriched MDSC from patients with different cancer types [breast, melanoma, head and neck squamous cell cancer (HNSCC)]. Melanoma patient MDSC were treated in vitro for 4 hours with 5 μmol/L ibrutinib or DMSO, processed for scRNA-seq using the Chromium 10× Genomics platform, and analyzed via the Seurat v4 standard integrative workflow. Baseline gene expression of MDSC from patients with breast, melanoma, and HNSCC cancer revealed similarities among the top expressed genes. In vitro ibrutinib treatment of MDSC from patients with melanoma resulted in significant changes in gene expression. GBP1, IL-1β, and CXCL8 were among the top downregulated genes whereas RGS2 and ABHD5 were among the top upregulated genes (P < 0.001). Double positive CD14+CD15+ MDSC and PMN-MDSC responded similarly to BTK inhibition and exhibited more pronounced gene changes compared with early MDSC and M-MDSC. Pathway analysis revealed significantly downregulated pathways including TREM1, nitric oxide signaling, and IL-6 signaling (P < 0.004).Implications:scRNA-seq revealed characteristic gene expression patterns for MDSC from different patients with cancer and BTK inhibition led to the downregulation of multiple genes and pathways important to MDSC function and migration.
- Open Access
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Individual UMAP plots melanoma MDSC treated with DMSO control or 5 µM ibrutinib for 4h.
- 1 March 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from Single-Cell RNA-Seq Analysis of Patient Myeloid-Derived Suppressor Cells and the Response to Inhibition of Bruton's Tyrosine Kinase
Individual UMAP plots melanoma MDSC treated with DMSO control or 5 µM ibrutinib for 4h.