Evidence map›Paper›PMID 31305260›Full record

ArticleThe Journal of clinical investigation2019

CDKN2B upregulation prevents teratoma formation in multipotent fibromodulin-reprogrammed cells.

Zhong Zheng, Chenshuang Li, Pin Ha, Grace X Chang, Pu Yang, Xinli Zhang, Jong Kil Kim, Wenlu Jiang, Xiaoxiao Pang, Emily A Berthiaume and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Zhong ZhengDivision of Growth and Development, School of Dentistry, and.
Chenshuang LiDivision of Growth and Development, School of Dentistry, and.
Pin HaDivision of Growth and Development, School of Dentistry, and.
Grace X ChangDavid Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Pu YangState Key Laboratory of Oral Diseases, Department of Orthodontics, West China School of Stomatology, Sichuan University, Chengdu, China.
Xinli ZhangDivision of Growth and Development, School of Dentistry, and.
Jong Kil KimDivision of Growth and Development, School of Dentistry, and.
Wenlu JiangDivision of Growth and Development, School of Dentistry, and.
Xiaoxiao PangDivision of Growth and Development, School of Dentistry, and.
Emily A BerthiaumeDavid Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Zane MillsDepartment of Ecology and Evolutionary Biology, and.
Christos S HavelesDavid Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Eric ChenDivision of Growth and Development, School of Dentistry, and.
Kang TingDivision of Growth and Development, School of Dentistry, and.
Chia SooDivision of Plastic and Reconstructive Surgery and Department of Orthopaedic Surgery and the Orthopaedic Hospital Research Center, UCLA, Los Angeles, California, USA.
University of California, Los Angeles · USOrthopaedic Hospital · USSichuan University · CNStomatological Hospital of Chongqing Medical University · CN

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
NCATS NIH HHS UL1 TR001881
6 · The paper itself

Abstract

Tumorigenicity is a well-documented risk to overcome for pluripotent or multipotent cell applications in regenerative medicine. To address the emerging demand for safe cell sources in tissue regeneration, we established a novel, protein-based reprogramming method that does not require genome integration or oncogene activation to yield multipotent fibromodulin (FMOD)-reprogrammed (FReP) cells from dermal fibroblasts. When compared with induced pluripotent stem cells (iPSCs), FReP cells exhibited a superior capability for bone and skeletal muscle regeneration with markedly less tumorigenic risk. Moreover, we showed that the decreased tumorigenicity of FReP cells was directly related to an upregulation of cyclin-dependent kinase inhibitor 2B (CDKN2B) expression during the FMOD reprogramming process. Indeed, sustained suppression of CDKN2B resulted in tumorigenic, pluripotent FReP cells that formed teratomas in vivo that were indistinguishable from iPSC-derived teratomas. These results highlight the pivotal role of CDKN2B in cell fate determination and tumorigenic regulation and reveal an alternative pluripotent/multipotent cell reprogramming strategy that solely uses FMOD protein.

Indexed as

Cellular ReprogrammingGene Expression Regulation, NeoplasticUp-RegulationCell LineCyclin-Dependent Kinase Inhibitor p15FibromodulinHumansMultipotent Stem CellsTeratomaCDKN2B protein, humanCyclin-Dependent Kinase Inhibitor p15FibromodulinFMOD protein, humanAdult stem cellsCell BiologyStem cellsStem cell transplantationTumor suppressors

Identifiers

PMID31305260
PMCPMC6668700
OpenAlexW2957373822

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.