Evidence map›Paper›PMID 22704268›Full record

ArticleClinical epigenetics2011

Molecular marks for epigenetic identification of developmental and cancer stem cells.

Samir Kumar Patra, Moonmoon Deb, Aditi Patra

Open access · hybridAbstract read
In one paragraph

Article in Clinical epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. The role of epigenetics in cancer: From pathways to the clinic.Journal of family medicine and primary care · 2025
    Review
  3. KLF4 is an epigenetically modulated, context-dependent tumor suppressor.Frontiers in cell and developmental biology · 2024
    Review
  4. Observational
  5. SOX2 and BCL-2 Expressions in Odontogenic Keratocyst and Ameloblastoma.Medicina oral, patologia oral y cirugia bucal · 2020
    Article
  6. Article
  7. Review
  8. Silencing of ZRF1 impedes survival of estrogen receptor positive MCF-7 cells and potentiates the effect of curcumin.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Epigenetic alterations in patients with type 2 diabetes mellitus.Balkan journal of medical genetics : BJMG · 2015
    Article
  10. Review
  11. Review
  12. Article
  13. Histone deacetylases: a saga of perturbed acetylation homeostasis in cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

3 authors at 2 institutions in 1 country.

Samir Kumar Patra
Moonmoon Deb
Aditi Patra
National Institute of Technology Rourkela · INBidhan Chandra Krishi Viswavidyalaya · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledEpigenetic regulations of genes by reversible methylation of DNA (at the carbon-5 of cytosine) and numerous reversible modifications of histones play important roles in normal physiology and development, and epigenetic deregulations are associated with developmental disorders and various disease states, including cancer. Stem cells have the capacity to self-renew indefinitely. Similar to stem cells, some malignant cells have the capacity to divide indefinitely and are referred to as cancer stem cells. In recent times, direct correlation between epigenetic modifications and reprogramming of stem cell and cancer stem cell is emerging. Major discoveries were made with investigations on reprogramming gene products, also known as master regulators of totipotency and inducer of pluoripotency, namely, OCT4, NANOG, cMYC, SOX2, Klf4, and LIN28. The challenge to induce pluripotency is the insertion of four reprogramming genes (Oct4, Sox2, Klf4, and c-Myc) into the genome. There are always risks of silencing of these genes by epigenetic modifications in the host cells, particularly, when introduced through retroviral techniques. In this contribution, we will discuss some of the major discoveries on epigenetic modifications within the chromatin of various genes associated with cancer progression and cancer stem cells in comparison to normal development of stem cell. These modifications may be considered as molecular signatures for predicting disorders of development and for identifying disease states. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s13148-010-0016-0) contains supplementary material, which is available to authorized users.

Identifiers

PMID22704268
PMCPMC3365374
OpenAlexW2068922733

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.