Jacquelyn W. Zimmerman
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Jacquelyn W. Zimmerman has a total of 284 co-authors. Here are the top co-authors by number of shared publications:
- Elizabeth M. Jaffee
Sidney Kimmel Comprehensive Cancer Center 1 Department of Oncology Johns Hopkins University School of Medicine, Baltimore, Maryland
190 shared publications - Samantha Guinn
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland
164 shared publications - Todd D. Armstrong
Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland
132 shared publications - Daniel J. Zabransky
Sidney Kimmel Comprehensive Cancer Center 1 Department of Oncology Johns Hopkins University School of Medicine, Baltimore, Maryland
120 shared publications - Emma Kartalia
Sidney Kimmel Comprehensive Cancer Center 1 Department of Oncology Johns Hopkins University School of Medicine, Baltimore, Maryland
120 shared publications - Richard Andrew Burkhart
Convergence Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland
111 shared publications
Latest Publications
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 5 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Cells analyzed per patient and subset nearest neighbor analysis by treatment status and at increased radii
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 5 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Cells analyzed per patient and subset nearest neighbor analysis by treatment status and at increased radii
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Data from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, in part resulting from cellular heterogeneity that supports overall tumorigenicity. Cancer-associated fibroblasts (CAF) are key determinants of PDAC biology and response to systemic therapy, and multiple CAF subtypes have been defined. However, defining the effects of patient-specific CAF heterogeneity and plasticity on tumor cell behavior is required to better characterize the role of CAFs in PDAC. In this study, we used multiomic analyses to characterize the tumor microenvironment (TME) in tumors from patients undergoing curative-intent surgery for PDAC. In these same patients, matched tumor organoid and CAF lines were established to functionally validate the impact of CAFs on the tumor cells. CAFs promoted epithelial–mesenchymal transition and a switch in tumor cell classification from classical to basal subtype. Furthermore, CAF-specific interleukin 8 functioned as a modulator of tumor cell subtype. Finally, neighborhood relationships between tumor cells and T cell subsets were defined, demonstrating a distinct spatial coordination among CAF and tumor cell subtypes. Overall, this study provides data supporting CAF signaling as a regulator of the cellular and behavioral heterogeneity in the PDAC TME. These findings can be used to explore rational approaches to improve therapies for this difficult-to-treat disease.Significance:Multidimensional analyses highlight the diverse role of cancer-associated fibroblasts in influencing cells in the tumor microenvironment and provide a platform for evaluating emerging therapeutic approaches and studying mechanisms dictating tumor behavior.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessData from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis, in part resulting from cellular heterogeneity that supports overall tumorigenicity. Cancer-associated fibroblasts (CAF) are key determinants of PDAC biology and response to systemic therapy, and multiple CAF subtypes have been defined. However, defining the effects of patient-specific CAF heterogeneity and plasticity on tumor cell behavior is required to better characterize the role of CAFs in PDAC. In this study, we used multiomic analyses to characterize the tumor microenvironment (TME) in tumors from patients undergoing curative-intent surgery for PDAC. In these same patients, matched tumor organoid and CAF lines were established to functionally validate the impact of CAFs on the tumor cells. CAFs promoted epithelial–mesenchymal transition and a switch in tumor cell classification from classical to basal subtype. Furthermore, CAF-specific interleukin 8 functioned as a modulator of tumor cell subtype. Finally, neighborhood relationships between tumor cells and T cell subsets were defined, demonstrating a distinct spatial coordination among CAF and tumor cell subtypes. Overall, this study provides data supporting CAF signaling as a regulator of the cellular and behavioral heterogeneity in the PDAC TME. These findings can be used to explore rational approaches to improve therapies for this difficult-to-treat disease.Significance:Multidimensional analyses highlight the diverse role of cancer-associated fibroblasts in influencing cells in the tumor microenvironment and provide a platform for evaluating emerging therapeutic approaches and studying mechanisms dictating tumor behavior.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 6 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Quantification of N-cadherin and Krt17 surface expression on organoids with and without coculture
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 6 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Quantification of N-cadherin and Krt17 surface expression on organoids with and without coculture
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 10 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Wound healing assay with CAF conditioned media
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 10 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Wound healing assay with CAF conditioned media
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 3 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Coculture setup and deconstruction.
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 3 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
Coculture setup and deconstruction.
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 7 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
RNAscope of classical and basal tumor cell markers
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 7 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
RNAscope of classical and basal tumor cell markers
- Open Access
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Supplemental Figure 4 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
IMC workflow and quality control
- 15 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplemental Figure 4 from Cancer-Associated Fibroblasts Promote Epithelial–Mesenchymal Transition and Classical to Basal Subtype Shift in Pancreatic Cancer
IMC workflow and quality control