Evidence map›Paper›PMID 21943668›Full record

ReviewSeminars in oncology2011

Molecular dissection of the 5q deletion in myelodysplastic syndrome.

Benjamin L Ebert

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Targeting Casein Kinase 1 (CK1) in Hematological Cancers.International journal of molecular sciences · 2020
    Review
  10. Review
  11. International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. The molecular mechanism of thalidomide analogs in hematologic malignancies.Journal of molecular medicine (Berlin, Germany) · 2016
    Review
  19. The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016
    Review
  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

1 author at 1 institution in 1 country.

Benjamin L EbertBrigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. bebert@partners.org
Brigham and Women's Hospital · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI JEROME RITZ · 1996 to 2026
$52.5M
Tyrosine Kinases, Serine-Threonine Kinases,&Phosophatases in PathogenesisP01CA108631 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ESTEY, ELIHU · 2005 to 2009
$9.7M
Functional Genomic Dissection of Refractory AnemiaR01HL082945 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI EBERT, BENJAMIN LEVINE · 2005 to 2022
$6.8M
NCI NIH HHS P01 CA066996NCI NIH HHS P01 CA108631NHLBI NIH HHS R01 HL082945Wellcome Trust
6 · The paper itself

Abstract

The 5q-syndrome is a subtype of myelodysplastic syndrome (MDS) with a defined clinical phenotype associated with heterozygous deletions of chromosome 5q. While no genes have been identified that undergo recurrent homozygous inactivation, functional studies have revealed individual genes that contribute to the clinical phenotype of MDS through haplo-insufficient gene expression. Heterozygous loss of the RPS14 gene on 5q leads to activation of p53 in the erythroid lineage and the macrocytic anemia characteristic of the 5q-syndrome. The megakaryocytic and platelet phenotype of the 5q-syndrome has been attributed to heterozygous deletion of miR145 and miR146a. Murine models have implicated heterozygous loss of APC, EGR1, DIAPH1, and NPM1 in the pathophysiology of del(5q) MDS. These findings indicate that the phenotype of MDS patients with deletions of chromosome 5q is due to haplo-insufficiency of multiple genes.

Indexed as

Anemia, MacrocyticChromosome DeletionChromosomes, Human, Pair 5Disease ProgressionHaploinsufficiencyHumansMyelodysplastic SyndromesNucleophosminPhenotypeNucleophosmin

Identifiers

PMID21943668
PMCPMC3183434
OpenAlexW2005405628

What OpenQuestion holds

Textmetadata
LicenceTDM
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.