Evidence map›Paper›PMID 27834397›Full record

ReviewNature reviews. Cancer2017

The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia.

Adam S Sperling, Christopher J Gibson, Benjamin L Ebert

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03217903 (High Risk Myelodysplasia Treated by Azacytidine), which is not on this map. Cited by 303 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
303citing papers in PubMed, 1 pooled it
46.4field-weighted citation impact, top 1% 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.

NCT03217903 naunknown statusnot on this map

High Risk Myelodysplasia Treated by Azacytidine : Genetic and Epigenetic (MYRAGE)

TypeinterventionalSponsorCentral Hospital, Nancy, FranceRan2017 to 2022Enrolled32ConditionsHigh-risk Myelodysplastic Syndromes With Excess BlastsArmsMyelogram
3 · Its place in the literature

Who cites it

303 citing papers in PubMed, 1 synthesis or guideline pooled it, 654 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  7. Review
  8. Review
  9. Article
  10. Pseudouridine synthase 7 as a context-specific therapeutic target in cancer.The Journal of pharmacology and experimental therapeutics · 2026
    Review
  11. Cancer risk in adults with pathogenic germline variants in RAS/MAPK genes using genomic ascertainment.Genetics in medicine : official journal of the American College of Medical Genetics · 2026
    Article
  12. Molecular and therapeutic frontiers in anemia therapy.The Journal of clinical investigation · 2026
    Review
  13. Article
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  15. Article
  16. Article
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  19. Article
  20. Review

243 more citing papers are in PubMed but not listed here.

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.

Adam S SperlingDepartment of Medical Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Christopher J GibsonDepartment of Medical Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Benjamin L EbertDepartment of Medical Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Dana-Farber Brigham Cancer Center · USDana-Farber Cancer Institute · US

Funding

Translational Studies of Inherited Marrow Failure and Myelodysplastic SyndromesR24DK099808 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ABKOWITZ, JANIS L, EBERT, BENJAMIN LEVINE · 2013 to 2017
$8.2M
Training Program in Molecular HematologyT32HL116324 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI NANCY BERLINER · 2013 to 2026
$7.4M
Functional Genomic Dissection of Refractory AnemiaR01HL082945 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI EBERT, BENJAMIN LEVINE · 2005 to 2022
$6.8M
NHLBI NIH HHS R01 HL082945NHLBI NIH HHS T32 HL116324NIDDK NIH HHS R24 DK099808
6 · The paper itself

Abstract

Myelodysplastic syndrome (MDS) is a clonal disease that arises from the expansion of mutated haematopoietic stem cells. In a spectrum of myeloid disorders ranging from clonal haematopoiesis of indeterminate potential (CHIP) to secondary acute myeloid leukaemia (sAML), MDS is distinguished by the presence of peripheral blood cytopenias, dysplastic haematopoietic differentiation and the absence of features that define acute leukaemia. More than 50 recurrently mutated genes are involved in the pathogenesis of MDS, including genes that encode proteins involved in pre-mRNA splicing, epigenetic regulation and transcription. In this Review we discuss the molecular processes that lead to CHIP and further clonal evolution to MDS and sAML. We also highlight the ways in which these insights are shaping the clinical management of MDS, including classification schemata, prognostic scoring systems and therapeutic approaches.

Indexed as

Clonal EvolutionClone CellsHematopoiesisHumansLeukemia, Myeloid, AcuteMyelodysplastic Syndromes

Identifiers

PMID27834397
PMCPMC5470392
OpenAlexW2551607099

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.