Evidence map›Paper›PMID 21274003›Full record

ArticleLeukemia2011

Comprehensive array CGH of normal karyotype myelodysplastic syndromes reveals hidden recurrent and individual genomic copy number alterations with prognostic relevance.

A Thiel, M Beier, D Ingenhag, K Servan, M Hein, V Moeller, B Betz, B Hildebrandt, C Evers, U Germing and 1 more

Abstract read
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In one paragraph

Article in Leukemia, 2011. 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

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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. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. TET2 mutation in diffuse large B-cell lymphoma.Journal of clinical and experimental hematopathology : JCEH · 2017
    Article
  9. Article
  10. Article
  11. The progress of early growth response factor 1 and leukemia.Intractable & rare diseases research · 2016
    Review
  12. Article
  13. Relapse after Allogeneic Hematopoietic Cell Transplantation for Myelodysplastic Syndromes: Analysis of Late Relapse Using Comparative Karyotype and Chromosome Genome Array Testing.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2015
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Standardizing the initial evaluation for myelodysplastic syndromes.Current hematologic malignancy reports · 2013
    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

11 authors.

A ThielInstitute of Human Genetics and Anthropology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany.
M Beier
D Ingenhag
K Servan
M Hein
V Moeller
B Betz
B Hildebrandt
C Evers
U Germing
B Royer-Pokora

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

About 40% of patients with myelodysplastic syndromes (MDSs) present with a normal karyotype, and they are facing different courses of disease. To advance the biological understanding and to find molecular prognostic markers, we performed a high-resolution oligonucleotide array study of 107 MDS patients (French American British) with a normal karyotype and clinical follow-up through the Duesseldorf MDS registry. Recurrent hidden deletions overlapping with known cytogenetic aberrations or sites of known tumor-associated genes were identified in 4q24 (TET2, 2x), 5q31.2 (2x), 7q22.1 (3x) and 21q22.12 (RUNX1, 2x). One patient with a 7q22.1 deletion had an additional 5q31.2 deletion of the acute myeloid leukemia/MDS region, the smallest deletion identified so far and including the putative tumor suppressor (ts) genes, EGR1 and CTNNA1. One TET2 deletion was homozygous and one heterozygous, with a missense mutation in the remaining allele, further supporting its role as a ts gene. Besides these recurrent alterations, additional individual imbalances were found in 34 cases; in total, 42/107 (39%) cases had genomic imbalances. These patients had an inferior survival as compared with the rest of the patients (P=0.002). This study emphasizes the heterogeneity of MDS, but points to interesting genes that may have diagnostic and prognostic impact.

Indexed as

Chromosome AberrationsComparative Genomic HybridizationGene DosageAgedCore Binding Factor Alpha 2 SubunitDioxygenasesDNA-Binding ProteinsFemaleHumansKaryotypingMaleMiddle AgedMyelodysplastic SyndromesPrognosisProto-Oncogene ProteinsRecurrenceCore Binding Factor Alpha 2 SubunitDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsRUNX1 protein, humanTET2 protein, human

Identifiers

PMID21274003

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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.