Evidence map›Paper›PMID 34413299›Full record

ArticleNature communications2021

DMRT1-mediated reprogramming drives development of cancer resembling human germ cell tumors with features of totipotency.

Jumpei Taguchi, Hirofumi Shibata, Mio Kabata, Masaki Kato, Kei Fukuda, Akito Tanaka, Sho Ohta, Tomoyo Ukai, Kanae Mitsunaga, Yosuke Yamada and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. A cross-talk between p16High senescence and cellular reprogramming.Clinical science (London, England : 1979) · 2026
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  5. Research ofRegenerative therapy · 2025
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  8. Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 2024
    Review
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  18. Review
  19. Article
  20. Transcription factorZoological research · 2023
    Article
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

20 authors at 4 institutions in 1 country.

Jumpei TaguchiDivision of Stem Cell Pathology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Minoto-ku, Tokyo, Japan.
Hirofumi ShibataDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Mio KabataDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Masaki KatoCellular Memory Laboratory, RIKEN Cluster for Pioneering Research, Wako-shi, Saitama, Japan.
Kei FukudaCellular Memory Laboratory, RIKEN Cluster for Pioneering Research, Wako-shi, Saitama, Japan.ORCID 0000-0002-4111-9409
Akito TanakaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Sho OhtaDivision of Stem Cell Pathology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Minoto-ku, Tokyo, Japan.
Tomoyo UkaiDivision of Stem Cell Pathology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Minoto-ku, Tokyo, Japan.
Kanae MitsunagaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Yosuke YamadaDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
So I NagaokaDepartment of Anatomy and Cell Biology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan.
Sho YamazawaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kotaro OhnishiDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Knut WoltjenDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.ORCID 0000-0003-2293-1183
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-1763-8380
Manabu OzawaLaboratory of Reproductive Systems Biology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Mitinori SaitouDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Yoichi ShinkaiCellular Memory Laboratory, RIKEN Cluster for Pioneering Research, Wako-shi, Saitama, Japan.ORCID 0000-0002-6051-2484
Takuya YamamotoDepartment of Life Science Frontiers, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.ORCID 0000-0002-0022-3947
Yasuhiro YamadaDivision of Stem Cell Pathology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Minoto-ku, Tokyo, Japan. yasu@ims.u-tokyo.ac.jp.ORCID 0000-0002-2463-1478
Kyoto University · JPSystems Biology Institute · JPRIKEN · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In vivo reprogramming provokes a wide range of cell fate conversion. Here, we discover that in vivo induction of higher levels of OSKM in mouse somatic cells leads to increased expression of primordial germ cell (PGC)-related genes and provokes genome-wide erasure of genomic imprinting, which takes place exclusively in PGCs. Moreover, the in vivo OSKM reprogramming results in development of cancer that resembles human germ cell tumors. Like a subgroup of germ cell tumors, propagated tumor cells can differentiate into trophoblasts. Moreover, these tumor cells give rise to induced pluripotent stem cells (iPSCs) with expanded differentiation potential into trophoblasts. Remarkably, the tumor-derived iPSCs are able to contribute to non-neoplastic somatic cells in adult mice. Mechanistically, DMRT1, which is expressed in PGCs, drives the reprogramming and propagation of the tumor cells in vivo. Furthermore, the DMRT1-related epigenetic landscape is associated with trophoblast competence of the reprogrammed cells and provides a therapeutic target for germ cell tumors. These results reveal an unappreciated route for somatic cell reprogramming and underscore the impact of reprogramming in development of germ cell tumors.

Indexed as

AnimalsAnimals, Genetically ModifiedCell DifferentiationCell Line, TumorCells, CulturedCellular ReprogrammingEpigenesis, GeneticFemaleGenomic ImprintingHumansInduced Pluripotent Stem CellsMiceMice, Inbred ICRNeoplasmsNeoplasms, Germ Cell and EmbryonalTranscription FactorsDMRT1 proteinTranscription Factors

Identifiers

PMID34413299
PMCPMC8377058
OpenAlexW3194092796

What OpenQuestion holds

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Registered trials

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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.