Evidence map›Paper›PMID 21779433›Full record

ArticleGenes & cancer2010

Tinkering with transcription factors uncovers plasticity of somatic cells.

Judi L Azevedo, Ricardo A Feldman

Open access · bronzeAbstract read
In one paragraph

Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.1field-weighted citation impact, top 45% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
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

2 authors at 2 institutions in 1 country.

Judi L AzevedoDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
Ricardo A Feldman
U-M Rogel Cancer CenterUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The advent of induced pluripotent stem cells (iPSCs) has brought the goal of using patient-derived cells for tissue repair closer to reality. However, the mechanisms involved in reprogramming to a pluripotent state are still not clear. It is understood that reprogramming to pluripotency involves epigenetic remodeling and the reactivation of "core" pluripotency factors. However, little is known about the mechanisms involved in overcoming senescence while avoiding oncogenesis, the maintenance of self-renewal, and the regulation of the balance between pluripotency and differentiation. Here, we review recent advances in reprogramming technology and what is currently known about the mechanism of reprogramming to pluripotency. Work with patient-derived iPSCs is already providing new insights into the cellular and molecular mechanisms involved in human disease. Further advances in reprogramming technology should result in efficient methods to reprogram patient-derived cells into iPSCs for use in regenerative medicine.

Indexed as

epigenetic mechanismsinduced pluripotent stem cells (iPSCs)reprogrammingsenescencetranscriptional regulation

Identifiers

PMID21779433
PMCPMC3092276
OpenAlexW2110449372

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.