Julia Freeman
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Julia Freeman has a total of 45 co-authors. Here are the top co-authors by number of shared publications:
- Ahmed M. Elhossiny
Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan
48 shared publications - Eileen S. Carpenter
Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan
48 shared publications - Filip Bednar
Department of Surgery, University of Michigan, Ann Arbor, Michigan
48 shared publications - Henry Dai
10Department of Surgery, University of Michigan, Ann Arbor, Michigan
48 shared publications - Marina Pasca di Magliano
Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA
48 shared publications - Padma Kadiyala
Immunology Graduate Program, University of Michigan, Ann Arbor, Michigan
48 shared publications
Latest Publications
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 7 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Longitudinal Single Cell Sequencing PBMC Differentially Expressed Genes
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 7 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Longitudinal Single Cell Sequencing PBMC Differentially Expressed Genes
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig 8 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
PDAC Organoids chemoattract myeloid cells in a CXCL8-dependent manner.
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig 8 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
PDAC Organoids chemoattract myeloid cells in a CXCL8-dependent manner.
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 9 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical Table of patients whose longitudinally matched plasma samples were subject to CXCL8 chemokine profiling
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 9 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical Table of patients whose longitudinally matched plasma samples were subject to CXCL8 chemokine profiling
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 6 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical table of PDAC patients who underwent longitudinal collection of PBMCS for single cell RNA sequencing
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 6 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical table of PDAC patients who underwent longitudinal collection of PBMCS for single cell RNA sequencing
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig 1 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Supplementary epithelial analysis of human PDAC single cell RNA sequencing.
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig 1 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Supplementary epithelial analysis of human PDAC single cell RNA sequencing.
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig 9 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
CXCL8-high tumor infiltrating granulocytes are marked by a pro-tumor gene signature.
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig 9 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
CXCL8-high tumor infiltrating granulocytes are marked by a pro-tumor gene signature.
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 8 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical Table of University of Michigan patients that were utilized for survival analysis with corresponding CXCL8 and CA19-9 plasma values
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 8 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Clinical Table of University of Michigan patients that were utilized for survival analysis with corresponding CXCL8 and CA19-9 plasma values
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Supplementary Table 2 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
Supplementary Table 2 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig 11 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
CXCL8 levels in patient plasma correlate with abundance of KRT17high; CXCL8+ cancer cells in treatment naïve patients.
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig 11 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
CXCL8 levels in patient plasma correlate with abundance of KRT17high; CXCL8+ cancer cells in treatment naïve patients.
- Open Access
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Fig 3 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
KRT17 and CLDN18 are co-expressed in a unique subpopulation of tumor epithelial cells.
- 3 June 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Fig 3 from KRT17high/CXCL8+ Tumor Cells Display Both Classical and Basal Features and Regulate Myeloid Infiltration in the Pancreatic Cancer Microenvironment
KRT17 and CLDN18 are co-expressed in a unique subpopulation of tumor epithelial cells.