Evidence map›Paper›PMID 28642604›Full record

ReviewNature reviews. Cancer2017

Turning the tide in myelodysplastic/myeloproliferative neoplasms.

Michael W N Deininger, Jeffrey W Tyner, Eric Solary

Abstract readReview
PubMed Publisher
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. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

48 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. IsolatedHaematologica · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Proposals for Clinical Trials in Chronic Myelomonocytic Leukemia.Current treatment options in oncology · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Chronic Myelomonocytic Leukemia: Hematopathology Perspective.Journal of immunotherapy and precision oncology · 2021
    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.

Michael W N DeiningerDivision of Hematology and Hematologic Malignancies, Department of Internal Medicine, University of Utah.
Jeffrey W TynerKnight Cancer Institute, Oregon Health and Science University.
Eric SolaryINSERM U1170, Gustave Roussy, Faculté de médecine Paris-Sud, Université Paris-Saclay, F-94805 Villejuif, France.

Funding

Mechanisms of resistance to ponatinib therapy in chronic myeloid leukemiaR01CA178397 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W., O'HARE, THOMAS J. · 2014 to 2018
$2.6M
UV and p21 DegradationR01CA108947 · NCI · SIDNEY KIMMEL CANCER CENTER · PI FOTEDAR, RATI · 2005 to 2009
$1.7M
ROR1 as a Therapeutic Target in Acute Lymphoblastic LeukemiaR00CA151457 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI TYNER, JEFFREY WALLACE · 2012 to 2014
$723k
SIRT5 as a Therapeutic Target in Acute Myeloid LeukemiaR21CA205936 · NCI · UNIVERSITY OF UTAH · PI DEININGER, MICHAEL W. · 2016 to 2017
$361k
NCI NIH HHS R00 CA151457NCI NIH HHS R01 CA108947NCI NIH HHS R01 CA178397NCI NIH HHS R21 CA205936
6 · The paper itself

Abstract

Myelodysplastic syndromes/myeloproliferative neoplasms (MDS/MPN) are aggressive myeloid malignancies recognized as a distinct category owing to their unique combination of dysplastic and proliferative features. Although current classification schemes still emphasize morphology and exclusionary criteria, disease-defining somatic mutations and/or germline predisposition alleles are increasingly incorporated into diagnostic algorithms. The developing picture suggests that phenotypes are driven mostly by epigenetic mechanisms that reflect a complex interplay between genotype, physiological processes such as ageing and interactions between malignant haematopoietic cells and the stromal microenvironment of the bone marrow. Despite the rapid accumulation of genetic knowledge, therapies have remained nonspecific and largely inefficient. In this Review, we discuss the pathogenesis of MDS/MPN, focusing on the relationship between genotype and phenotype and the molecular underpinnings of epigenetic dysregulation. Starting with the limitations of current therapies, we also explore how the available mechanistic data may be harnessed to inform strategies to develop rational and more effective treatments, and which gaps in our knowledge need to be filled to translate biological understanding into clinical progress.

Indexed as

Epigenesis, GeneticAdultAntineoplastic AgentsChildDNA MethylationGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenotypeHematopoietic Stem Cell TransplantationHumansInflammationMolecular Targeted TherapyMutationMyelodysplastic-Myeloproliferative DiseasesPhenotypePrognosisAntineoplastic Agents

Identifiers

PMID28642604

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.