Evidence map›Paper›PMID 19710397›Full record

ReviewThe Journal of molecular diagnostics : JMD2009

Down syndrome and malignancies: a unique clinical relationship: a paper from the 2008 william beaumont hospital symposium on molecular pathology.

Ana C Xavier, Yubin Ge, Jeffrey W Taub

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of molecular diagnostics : JMD, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.

  1. Sex differences in cardiovascular disease and dysregulation in Down syndrome.American journal of physiology. Heart and circulatory physiology · 2023
    Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Observational
  8. Genetic Predisposition to Hematologic Malignancies.Cold Spring Harbor perspectives in medicine · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Omnipresence of DYRK1A in Human Diseases.International journal of molecular sciences · 2022
    Review
  16. Selective Macrocyclic Inhibitors of DYRK1A/B.ACS medicinal chemistry letters · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Ana C XavierDivision of Hematology/Oncology, Children's Hospital of Michigan, Department of Pediatrics, Wayne State University School of Medicine, 3901 Beaubien Blvd., Detroit, Michigan 48201, USA.
Yubin Ge
Jeffrey W Taub
Wayne State University · USChildren's Hospital of Michigan · US

Funding

Molecular and Pharmacologic Correletes of Acute Myeloid Leukemia in Down SyndromeR01CA120772 · NCI · WAYNE STATE UNIVERSITY · PI TAUB, JEFFREY WARREN · 2007 to 2011
$2.1M
NCI NIH HHS R01 CA120772
6 · The paper itself

Abstract

The patterns of malignancies in Down syndrome (DS) are unique and highlight the relationship between chromosome 21 and cancer. DS children have a approximately 10- to 20-fold higher risk for developing acute lymphoblastic leukemia and acute myeloid leukemia (AML), as compared with non-DS children, although they do not have a uniformly increased risk of developing solid tumors. DS children with acute lymphoblastic leukemia frequently experience higher levels of treatment-related toxicity and inferior event-free survival rates, as compared with non-DS children. DS children also develop AML with unique features and have a 500-fold increased risk of developing the AML subtype, acute megakaryocytic leukemia (AMkL; M7). Nearly 10% of DS newborns are diagnosed with a variant of AMkL, the transient myeloproliferative disorder, which can resolve spontaneously without treatment; event-free survival rates for DS patients with AMkL ranges from 80% to 100%, in comparison with <30% for non-DS children with AMkL. In addition, somatic mutations of the GATA1 gene have been detected in nearly all DS TMD and AMkL cases and not in leukemia cases in non-DS children. GATA1 mutations are key factors linked to both leukemogenesis and the high cure rates of DS AMkL patients. Identifying the mechanisms that account for the high event-free survival rates of DS AMkL patients may ultimately improve AML treatment as well. Examining leukemogenesis in DS children may identify factors linked to the general development of childhood leukemia and lead to potential new therapeutic strategies to fight this disease.

Indexed as

AnimalsDisease-Free SurvivalDown SyndromeGATA1 Transcription FactorHumansLeukemia, Megakaryoblastic, AcuteLeukemia, Myeloid, AcutePrecursor Cell Lymphoblastic Leukemia-LymphomaGATA1 protein, humanGATA1 Transcription Factor

Identifiers

PMID19710397
PMCPMC2729834
OpenAlexW1591723496

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.