Supporting data on enhanced reprogramming of human CD34+ hematopoietic stem cells to induced pluripotent stem cells using human placenta-derived cell conditioned medium
- Authors
- Lee, Seung-Jin; Kim, Ji-Hea; Kang, Ka-Won; Park, Young; Kim, Byung-Soo
- Issue Date
- 10월-2020
- Publisher
- ELSEVIER
- Keywords
- Reprogramming; Human induced pluripotent stem cells; Human placenta-derived cell conditioned medium; Hematopoietic stem cells; Acute lymphoblastic leukemia
- Citation
- DATA IN BRIEF, v.32
- Indexed
- SCOPUS
- Journal Title
- DATA IN BRIEF
- Volume
- 32
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/53052
- DOI
- 10.1016/j.dib.2020.106140
- ISSN
- 2352-3409
- Abstract
- The data presented herein support "Generation of an induced pluripotent stem cell line KUMCi001-A from CD34+ bone marrow cells of a patient with acute lymphoblastic leukemia using human placenta-derived cell conditioned medium." The supplementary data were as follows. (1) Comparison of reprogramming efficiency of human placenta-derived cell conditioned medium with defined medium (mTeSR(TM) 1) and the generation of induced pluripotent stem cells (iPSCs) from a patient with acute lymphoblastic leukemia (ALL) with significantly higher reprogramming efficiency than that of the defined medium (P <= 0.05). (2) Evaluation of differentiation capability of the generated ALL_iPSCs into hematopoietic stem cells (HSCs) and comparison with normal iPSCs using the colony-forming unit (CFU) assay. ALL_iPSCs manifested all lineages for hematopoiesis in their colonies similar to normal iPSCs. (3) ALL_iPSCs showed a considerably higher number of burst-forming unit-erythroid colonies indicating the presence of more erythroid progenitors than normal iPSCs; this tendency was confirmed in the CFU assay of ALL_CD34+ cells. This has been previously reported as a feature of ALL. Thus, the hematopoietic characteristics of the donor patient with ALL appear to be maintained in our ALL_hiPSC line although the karyotype was normalized during reprogramming. (C) 2020 The Authors. Published by Elsevier Inc.
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