Rapid acceleration of KRAS-mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ - Liu, Yi; Deguchi, Yasunori; Wei, Daoyan; Liu, Fuyao; Moussalli, Micheline J.; Deguchi, Eriko; Li, Donghui; Wang, Huamin; Valentin, Lovie Ann; Colby, Jennifer K.; Wang, Jing; Zheng, Xiaofeng; et al. (Nature communications, 2022)
Keywords: 13; 13/106; 13/44; 14/1; 14/105; 14/63; 42/89; 49; 49/91; 631/67/1504/1713; 631/67/2327; 631/67/327; 631/67/69; 631/67/70; 64/60; Adenocarcinoma; Aging; Animals; Cancer; Carcinogenesis; Carcinogenesis - genetics; Carcinogenesis - pathology; Carcinogens; Carcinoma in Situ - pathology; Carcinoma, Pancreatic Ductal - pathology; CC chemokine receptors; CCR2 protein; Epithelial cells; Epithelium; High fat diet; Humanities and Social Sciences; Humans; K-Ras protein; Ligands; Lipids; Macrophages; Mice; Monocyte chemoattractant protein 1; multidisciplinary; Mutants; Mutation; Pancreas; Pancreas - pathology; Pancreatic cancer; Pancreatic Neoplasms; Pancreatic Neoplasms - pathology; PPAR delta - genetics; Proto-Oncogene Proteins p21(ras) - genetics; Receptors; Science; Science (multidisciplinary); Suppressor cells; Tumor microenvironment; Tumor Microenvironment - genetics; Tumorigenesis; Tumors