Evidence map›Paper›PMID 27161380›Full record

ArticleNature communications2016

Tumour resistance in induced pluripotent stem cells derived from naked mole-rats.

Shingo Miyawaki, Yoshimi Kawamura, Yuki Oiwa, Atsushi Shimizu, Tsuyoshi Hachiya, Hidemasa Bono, Ikuko Koya, Yohei Okada, Tokuhiro Kimura, Yoshihiro Tsuchiya and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.0field-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

57 citing papers in PubMed, 99 citations in OpenAlex.

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  12. The evolution of aging and lifespan.Trends in genetics : TIG · 2023
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  17. Hyaluronic Acid as a Modern Approach in Anticancer Therapy-Review.International journal of molecular sciences · 2022
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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

21 authors at 9 institutions in 1 country.

Shingo MiyawakiBiomedical Animal Research Laboratory, Institute for Genetic Medicine, Hokkaido University, Hokkaido 060-0815, Japan.
Yoshimi KawamuraBiomedical Animal Research Laboratory, Institute for Genetic Medicine, Hokkaido University, Hokkaido 060-0815, Japan.
Yuki OiwaBiomedical Animal Research Laboratory, Institute for Genetic Medicine, Hokkaido University, Hokkaido 060-0815, Japan.
Atsushi ShimizuDivision of Biomedical Information Analysis, Iwate Tohoku Medical Megabank Organization, Disaster Reconstruction Center, Iwate Medical University, Iwate 028-3694, Japan.
Tsuyoshi HachiyaDivision of Biomedical Information Analysis, Iwate Tohoku Medical Megabank Organization, Disaster Reconstruction Center, Iwate Medical University, Iwate 028-3694, Japan.
Hidemasa BonoDatabase Center for Life Science, Research Organization of Information and Systems, Mishima 411-8540, Japan.ORCID 0000-0003-4413-0651
Ikuko KoyaDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yohei OkadaDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Tokuhiro KimuraDepartment of Pathology, Yamaguchi University Graduate School of Medicine, Yamaguchi 755-8505, Japan.
Yoshihiro TsuchiyaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Tokyo 142-8501, Japan.
Sadafumi SuzukiDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Nobuyuki OnishiDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Naoko KuzumakiDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yumi MatsuzakiDepartment of Life Science, Shimane University Faculty of Medicine, Shimane 693-8501, Japan.
Minoru NaritaDepartment of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Tokyo 142-8501, Japan.
Eiji IkedaDepartment of Pathology, Yamaguchi University Graduate School of Medicine, Yamaguchi 755-8505, Japan.
Kazuo OkanoyaGraduate School of Arts and Science, The University of Tokyo, Tokyo 153-8902, Japan.
Ken-Ichiro SeinoDivision of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Hokkaido 060-0815, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo 160-8582, Japan.ORCID 0000-0001-6610-1902
Hideyuki OkanoDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Kyoko MiuraBiomedical Animal Research Laboratory, Institute for Genetic Medicine, Hokkaido University, Hokkaido 060-0815, Japan.
Keio University · JPHokkaido University · JPHoshi University · JPIwate Medical University · JPYamaguchi University · JPAichi Medical University · JPResearch Organization of Information and Systems · JPShimane University · JPTokyo University of the Arts · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The naked mole-rat (NMR, Heterocephalus glaber), which is the longest-lived rodent species, exhibits extraordinary resistance to cancer. Here we report that NMR somatic cells exhibit a unique tumour-suppressor response to reprogramming induction. In this study, we generate NMR-induced pluripotent stem cells (NMR-iPSCs) and find that NMR-iPSCs do not exhibit teratoma-forming tumorigenicity due to the species-specific activation of tumour-suppressor alternative reading frame (ARF) and a disruption mutation of the oncogene ES cell-expressed Ras (ERAS). The forced expression of Arf in mouse iPSCs markedly reduces tumorigenicity. Furthermore, we identify an NMR-specific tumour-suppression phenotype-ARF suppression-induced senescence (ASIS)-that may protect iPSCs and somatic cells from ARF suppression and, as a consequence, tumorigenicity. Thus, NMR-specific ARF regulation and the disruption of ERAS regulate tumour resistance in NMR-iPSCs. Our findings obtained from studies of NMR-iPSCs provide new insight into the mechanisms of tumorigenicity in iPSCs and cancer resistance in the NMR.

Indexed as

Genes, Tumor SuppressorAnimalsCell Transformation, NeoplasticCellular ReprogrammingInduced Pluripotent Stem CellsMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, NudeMice, SCIDMole RatsMutationOncogene Protein p21(ras)Reading FramesOncogene Protein p21(ras)

Identifiers

PMID27161380
PMCPMC4866046
OpenAlexW2394034390

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.