| Literature DB >> 32451460 |
Hae-Ock Lee1,2, Yourae Hong1,3, Hakki Emre Etlioglu4, Yong Beom Cho3,5, Valentina Pomella4, Ben Van den Bosch4, Jasper Vanhecke4, Sara Verbandt4, Hyekyung Hong5, Jae-Woong Min1, Nayoung Kim1,2, Hye Hyeon Eum1,2, Junbin Qian6,7, Bram Boeckx6,7, Diether Lambrechts6,7, Petros Tsantoulis8,9,10, Gert De Hertogh11,12, Woosung Chung1, Taeseob Lee1,13, Minae An1,3, Hyun-Tae Shin1, Je-Gun Joung1, Min-Hyeok Jung14, Gunhwan Ko15, Pratyaksha Wirapati16, Seok Hyung Kim17, Hee Cheol Kim5, Seong Hyeon Yun5, Iain Bee Huat Tan18,19,20, Bobby Ranjan21, Woo Yong Lee5, Tae-You Kim22, Jung Kyoon Choi23, Young-Joon Kim14,24, Shyam Prabhakar21, Sabine Tejpar25, Woong-Yang Park26,27,28.
Abstract
Immunotherapy for metastatic colorectal cancer is effective only for mismatch repair-deficient tumors with high microsatellite instability that demonstrate immune infiltration, suggesting that tumor cells can determine their immune microenvironment. To understand this cross-talk, we analyzed the transcriptome of 91,103 unsorted single cells from 23 Korean and 6 Belgian patients. Cancer cells displayed transcriptional features reminiscent of normal differentiation programs, and genetic alterations that apparently fostered immunosuppressive microenvironments directed by regulatory T cells, myofibroblasts and myeloid cells. Intercellular network reconstruction supported the association between cancer cell signatures and specific stromal or immune cell populations. Our collective view of the cellular landscape and intercellular interactions in colorectal cancer provide mechanistic information for the design of efficient immuno-oncology treatment strategies.Entities:
Mesh：
Year: 2020 PMID： 32451460 DOI： 10.1038/s41588-020-0636-z
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330