한빛사논문
Hee Chul Chung1,2, Eun Jeong Cho1,3, Hyeonjin Lee1,2, Won-Kyung Kim1,3, Ji-Hye Oh1,3, Seok-Hyung Kim4,*, Dakeun Lee5,*, Chang Ohk Sung1,2,3,*
1Center for Cancer Genome Discovery, Asan Institute for Life Sciences, Asan Medical Center, Songpa-gu, Seoul, Republic of Korea
2Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Songpa-gu, Seoul, Republic of Korea
3Department of Medical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
4Department of Pathology and Translational Genomics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
5Department of Pathology, Ajou University School of Medicine, Suwon, Republic of Korea
*Correspondence :
Chang Ohk Sung, MD, PhD, Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Republic of Korea.
Dakeun Lee, MD, PhD, Department of Pathology, Ajou University School of Medicine, 164, Worldcup-ro, Yeongtong-gu, Suwon-si, Gyeonggi-do 16499, Republic of Korea.
Seok-Hyung Kim, MD, PhD, Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Republic of Korea
Abstract
Dear Editor,
The origin and the phenotypic heterogeneity of cancer-associated fibroblasts (CAFs) are suggested by various models, but not completely understood.1-3 We used six publicly available single-cell RNA sequencing (scRNA-seq) datasets of five cancer types (except breast cancer) on CAFs and corresponding normal fibroblasts (NFs) (Figure 1A)4-6 and established a comprehensive model for CAF development and gene expression dynamics over time. The fibroblast fraction constituted less than 10% of all cellular components in each dataset (Figure 1B). This relatively low fraction may be ascribed to our two-step, strict procedure for defining fibroblasts.
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