Evidence map›Paper›PMID 32439724›Full record

ReviewHaematologica2020

Myelodysplastic syndromes: moving towards personalized management.

Eva Hellström-Lindberg, Magnus Tobiasson, Peter Greenberg

Open access · goldAbstract readReview
In one paragraph

Review in Haematologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
12.8field-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.

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

44 citing papers in PubMed, 115 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. The Circular RNA Circ-ANAPC7 as a Biomarker for the Risk Stratification of Myelodysplastic Syndrome.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. High Co-Expression ofJournal of oncology · 2023
    Article
  19. Impact of single versus multiple spliceosome mutations on myelodysplastic syndrome.Journal of clinical and experimental hematopathology : JCEH · 2023
    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 2 countries.

Eva Hellström-LindbergKarolinska Institutet, Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska University Hospital, Stockholm, Sweden.
Magnus TobiassonKarolinska Institutet, Center for Hematology and Regenerative Medicine, Department of Medicine Huddinge, Karolinska University Hospital, Stockholm, Sweden magnus.tobiasson@ki.se.
Peter GreenbergStanford Cancer Institute, Division of Hematology, Stanford University School of Medicine, Stanford, CA, USA.
Karolinska University Hospital · SEStanford Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The myelodysplastic syndromes (MDS) share their origin in the hematopoietic stem cell but have otherwise very heterogeneous biological and genetic characteristics. Clinical features are dominated by cytopenia and a substantial risk for progression to acute myeloid leukemia. According to the World Health Organization, MDS is defined by cytopenia, bone marrow dysplasia and certain karyotypic abnormalities. The understanding of disease pathogenesis has undergone major development with the implementation of next-generation sequencing and a closer integration of morphology, cytogenetics and molecular genetics is currently paving the way for improved classification and prognostication. True precision medicine is still in the future for MDS and the development of novel therapeutic compounds with a propensity to markedly change patients' outcome lags behind that for many other blood cancers. Treatment of higher-risk MDS is dominated by monotherapy with hypomethylating agents but novel combinations are currently being evaluated in clinical trials. Agents that stimulate erythropoiesis continue to be first-line treatment for the anemia of lower-risk MDS but luspatercept has shown promise as second-line therapy for sideroblastic MDS and lenalidomide is an established second-line treatment for del(5q) lower-risk MDS. The only potentially curative option for MDS is hematopoietic stem cell transplantation, until recently associated with a relatively high risk of transplant-related mortality and relapse. However, recent studies show increased cure rates due to better tools to target the malignant clone with less toxicity. This review provides a comprehensive overview of the current status of the clinical evaluation, biology and therapeutic interventions for this spectrum of disorders.

Indexed as

AnemiaLeukemia, Myeloid, AcuteMyelodysplastic SyndromesErythropoiesisHumansLenalidomideLenalidomide

Identifiers

PMID32439724
PMCPMC7327628
OpenAlexW3026493820

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.