Nature Communications (May 2022)
Rapid acceleration of KRAS-mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ
- Yi Liu,
- Yasunori Deguchi,
- Daoyan Wei,
- Fuyao Liu,
- Micheline J. Moussalli,
- Eriko Deguchi,
- Donghui Li,
- Huamin Wang,
- Lovie Ann Valentin,
- Jennifer K. Colby,
- Jing Wang,
- Xiaofeng Zheng,
- Haoqiang Ying,
- Mihai Gagea,
- Baoan Ji,
- Jiaqi Shi,
- James C. Yao,
- Xiangsheng Zuo,
- Imad Shureiqi
Affiliations
- Yi Liu
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Yasunori Deguchi
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Daoyan Wei
- Department of Gastroenterology, Hepatology, and Nutrition, The University of Texas MD Anderson Cancer Center
- Fuyao Liu
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Micheline J. Moussalli
- Department of Palliative, Rehabilitation, and Integrative Medicine, The University of Texas MD Anderson Cancer Center
- Eriko Deguchi
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Donghui Li
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Huamin Wang
- Department of Pathology, The University of Texas MD Anderson Cancer Center
- Lovie Ann Valentin
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Jennifer K. Colby
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Jing Wang
- Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center
- Xiaofeng Zheng
- Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center
- Haoqiang Ying
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Mihai Gagea
- Department of Veterinary Medicine and Surgery, The University of Texas MD Anderson Cancer Center
- Baoan Ji
- Department of Cancer Biology, Mayo Clinic
- Jiaqi Shi
- Department of Pathology, University of Michigan
- James C. Yao
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Xiangsheng Zuo
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- Imad Shureiqi
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center
- DOI
- https://doi.org/10.1038/s41467-022-30392-7
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 18
Abstract
Pancreatic intraepithelial neoplasia (PanIN) can develop into pancreatic ductal adenocarcinoma (PDAC), however, the factors which determine how this occurs are unknown. Here, the authors illustrate the role of PPARδ in the upregulation of CCL2, resulting in an immunosuppressive microenvironment, and driving the progression of PanIN to PDAC.
