Evidence map›Paper›PMID 27722205›Full record

ReviewTrends in cancer2016

Modeling Cancer with Pluripotent Stem Cells.

Julian Gingold, Ruoji Zhou, Ihor R Lemischka, Dung-Fang Lee

Abstract readReview
In one paragraph

Review in Trends in cancer, 2016. 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
–field-weighted citation impact
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.

  1. Review
  2. Decoding cancer etiology with cellular reprogramming.Current opinion in genetics & development · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Rewired mNature communications · 2023
    Article
  7. Merits and challenges of iPSC-derived organoids for clinical applications.Frontiers in cell and developmental biology · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. OncogenicProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Oncogenic role of SFRP2 in p53-mutant osteosarcoma development via autocrine and paracrine mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Article
  20. 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

4 authors.

Julian GingoldWomen's Health Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Ruoji ZhouDepartment of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA.
Ihor R LemischkaDepartment of Developmental and Regenerative Biology, Department of Pharmacology and System Therapeutics, The Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Dung-Fang LeeDepartment of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; Center for Stem Cell and Regenerative Medicine, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.

Funding

Programming HematopoiesisR01HL119404 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEMISCHKA, IHOR R, MOORE, KATERI A. · 2014 to 2017
$1.7M
Modeling p53 Mutant-Associated Cancer With LFS Patient-Derived iPSCsR00CA181496 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LEE, DUNG-FANG · 2016 to 2018
$729k
Modeling p53 Mutant-Associated Cancer With LFS Patient-Derived iPSCsK99CA181496 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEE, DUNG-FANG · 2014 to 2015
$203k
NCI NIH HHS K99 CA181496NCI NIH HHS R00 CA181496NHLBI NIH HHS R01 HL119404United States NCIUnited States NHLBI
6 · The paper itself

Abstract

The elucidation of cancer pathogenesis has been hindered by limited access to patient samples, tumor heterogeneity and the lack of reliable model organisms. Characterized by their ability to self-renew indefinitely and differentiate into all cell lineages of an organism, pluripotent stem cells (PSCs), including embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), provide a powerful and unlimited source to generate differentiated cells that can be used to study disease biology, facilitate drug discovery and development, and provide key insights for developing personalized therapies. This article reviews the recent developments and technologies converting PSCs into clinically relevant model systems for cancer research.

Indexed as

Models, BiologicalNeoplasmsPluripotent Stem CellsAnimalsCell DifferentiationHumansOrganoidsCancer Disease ModelingDifferentiationGenome EditingPluripotent Stem Cells

Identifiers

PMID27722205
PMCPMC5050918

What OpenQuestion holds

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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.