Evidence map›Paper›PMID 20008300›Full record

ArticleBlood2010

Two routes to leukemic transformation after a JAK2 mutation-positive myeloproliferative neoplasm.

Philip A Beer, François Delhommeau, Jean-Pierre LeCouédic, Mark A Dawson, Edwin Chen, David Bareford, Rajko Kusec, Mary Frances McMullin, Claire N Harrison, Alessandro M Vannucchi and 2 more

Registry-linked trialOpen access · bronzeAbstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03558607 (Concomitant Ruxolitinib Induction and Maintenance With Cytarabine Based Chemotherapy in Secondary Acute Myelogenous Leukemia Evolving From Myeloproliferative Neoplasm), which is not on this map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
14.6field-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.

NCT03558607 phase1 / phase2unknown statusnot on this mapstarted 2018, after this paper: background citation

Concomitant Ruxolitinib Induction and Maintenance With Cytarabine Based Chemotherapy in Secondary Acute Myelogenous Leukemia Evolving From Myeloproliferative Neoplasm

TypeinterventionalSponsorSeoul National University HospitalRan2018 to 2024Enrolled17ConditionsSecondary Acute Myelogenous Leukemia Evolving From Myeloproliferative DisorderArmsRuxolitinib
3 · Its place in the literature

Who cites it

148 citing papers in PubMed, 299 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Unraveling the role ofHemaSphere · 2026
    Review
  5. Article
  6. Article
  7. The molecular management of classic myeloproliferative neoplasm.Journal of the Egyptian National Cancer Institute · 2025
    Review
  8. bioRxiv : the preprint server for biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Myeloproliferative Neoplasms: Challenging Dogma.Journal of clinical medicine · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 4 countries.

Philip A BeerDepartment of Haematology, Cambridge Institute for Medical Research, Cambridge, UK.
François Delhommeau
Jean-Pierre LeCouédic
Mark A Dawson
Edwin Chen
David Bareford
Rajko Kusec
Mary Frances McMullin
Claire N Harrison
Alessandro M Vannucchi
William Vainchenker
Anthony R Green
Institut Gustave Roussy · FRQueen's University Belfast · GBRussells Hall Hospital · GBSt Thomas' Hospital · GBUniversity Hospital Dubrava · HRUniversity of Florence · IT

Funding

Cancer Research UK 8961Medical Research Council G0300497
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) may follow a JAK2-positive myeloproliferative neoplasm (MPN), although the mechanisms of disease evolution, often involving loss of mutant JAK2, remain obscure. We studied 16 patients with JAK2-mutant (7 of 16) or JAK2 wild-type (9 of 16) AML after a JAK2-mutant MPN. Primary myelofibrosis or myelofibrotic transformation preceded all 7 JAK2-mutant but only 1 of 9 JAK2 wild-type AMLs (P = .001), implying that JAK2-mutant AML is preceded by mutation(s) that give rise to a "myelofibrosis" phenotype. Loss of the JAK2 mutation by mitotic recombination, gene conversion, or deletion was excluded in all wild-type AMLs. A search for additional mutations identified alterations of RUNX1, WT1, TP53, CBL, NRAS, and TET2, without significant differences between JAK2-mutant and wild-type leukemias. In 4 patients, mutations in TP53, CBL, or TET2 were present in JAK2 wild-type leukemic blasts but absent from the JAK2-mutant MPN. By contrast in a chronic-phase patient, clones harboring mutations in JAK2 or MPL represented the progeny of a shared TET2-mutant ancestral clone. These results indicate that different pathogenetic mechanisms underlie transformation to JAK2 wild-type and JAK2-mutant AML, show that TET2 mutations may be present in a clone distinct from that harboring a JAK2 mutation, and emphasize the clonal heterogeneity of the MPNs.

Indexed as

MutationAgedBlast CrisisDioxygenasesDNA-Binding ProteinsFemaleHematologic NeoplasmsHumansJanus Kinase 2Leukemia, Myeloid, AcuteMaleMiddle AgedNeoplasms, Second PrimaryPrimary MyelofibrosisProto-Oncogene ProteinsProto-Oncogene Proteins c-cblCBL protein, humanDioxygenasesDNA-Binding ProteinsJAK2 protein, humanJanus Kinase 2Proto-Oncogene ProteinsProto-Oncogene Proteins c-cblTET2 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID20008300
OpenAlexW1977590248

What OpenQuestion holds

Textmetadata
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.