The interplay between natural killer cells and pancreatic stellate cells in pancreatic ductal adenocarcinoma  

作　　者：Rachel Elizabeth Ann Fincham Parthiban Periasamy Craig Ryan Joseph Jia Meng Jeffrey Chun Tatt Lim Felicia Wee Konstantinos Stasinos Michelle Rodrigues Goulart Jiangfeng Ye Li Yen Chong Bijin Veonice Au Denise Goh Joe Poh Sheng Yeong Hemant Mahendrakumar Kocher 

机构地区：[1]Centre for Tumour Biology,Barts Cancer Institute-a Cancer Research United Kingdom(CRUK)Centre of Excellence,Queen Mary University of London,London,UK [2]Institute of Molecular and Cell Biology(IMCB),Agency of Science,Technology and Research(A*STAR),Singapore,Singapore [3]Centre for Quantitative Medicine,Duke-National University of Singapore(NUS)Medical School,Singapore,Singapore [4]Department of Anatomical Pathology,Singapore General Hospital,Singapore,Singapore [5]Cancer Science Institute of Singapore,National University of Singapore,Singapore,Singapore [6]Barts and the London Hepato-Pancreato-Biliary(HPB)Centre,The Royal London Hospital,Barts Health National Health Service Trust,London,UK

出　　处：《Cancer Communications》2025年第2期172-177,共6页癌症通讯(英文)

摘　　要：Pancreatic ductal adenocarcinoma(PDAC)remains one of medicine’s most urgent areas of unmet need.With 5-year survival rates of∼11%,PDAC is set to become the second leading cause of cancer related deaths by 2040[1].The complex tumour microenvironment(TME)in PDAC,responsible for poor prognosis,is comprised of extracellular matrix(ECM)proteins and multiple cell types;with pancreatic stellate cells(PSCs),which become activated cancer associated fibroblasts(CAFs),being regarded as key orchestrators of the TME.We have demonstrated that treatment with all-trans retinoic acid(ATRA)can render activated PSCs(aPSC)to a quiescent(qPSC)phenotype(shift to G1 phase of cell cycle and other features[2]),resulting in stromal remodelling and thus,influencing cancer cell co-targeting with chemotherapy in patients[3].This has resulted in the use of ATRA along with standard-of-care chemotherapy in the Stromal TARgeting for PAncreatic Cancer(STARPAC)clinical trial,with promising results[4].These clinically relevant[5],exciting potential therapeutic benefits of stromal co-targeting through rendering PSCs quiescent[6],along with predictive inflammation-related biomarkers[7],and increased focus on cellular therapeutics such as NK cells,led us to postulate potential targetable PSC-immune cell interactions which may uncover a comprehensive therapeutic strategy for treating hitherto,incurable PDAC.

关 键 词：ADENOCARCINOMA CHEMOTHERAPY KILLER 

分 类 号：R73[医药卫生—肿瘤]