Evidence map›Paper›PMID 20428194›Full record

ReviewLeukemia2010

Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1.

A Tefferi

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 2 pooled it
30.2field-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

244 citing papers in PubMed, 2 syntheses or guidelines pooled it, 521 citations in OpenAlex.

  1. Guideline
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  6. TET2, ASXL1, IDH1, and IDH2 Single Nucleotide Polymorphisms in Turkish Patients with Chronic Myeloproliferative Neoplasms.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2017
    Trial
  7. Trial
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  9. Review
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  11. The molecular management of classic myeloproliferative neoplasm.Journal of the Egyptian National Cancer Institute · 2025
    Review
  12. Article
  13. Article
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  16. Article
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  20. Article

184 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

1 author at 1 institution in 1 country.

A TefferiDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA. tefferi.ayalew@mayo.edu
Mayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloproliferative neoplasms (MPNs) originate from genetically transformed hematopoietic stem cells that retain the capacity for multilineage differentiation and effective myelopoiesis. Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs. However, none of these mutations were MPN specific, displayed mutual exclusivity or could be traced back to a common ancestral clone. JAK2 and MPL mutations appear to exert a phenotype-modifying effect and are distinctly associated with polycythemia vera, essential thrombocythemia and primary myelofibrosis; the corresponding mutational frequencies are approximately 99, 55 and 65% for JAK2 and 0, 3 and 10% for MPL mutations. The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1). The functional consequences of MPN-associated mutations include unregulated JAK-STAT (Janus kinase/signal transducer and activator of transcription) signaling, epigenetic modulation of transcription and abnormal accumulation of oncoproteins. However, it is not clear as to whether and how these abnormalities contribute to disease initiation, clonal evolution or blastic transformation.

Indexed as

Biomarkers, TumorDioxygenasesDNA-Binding ProteinsHumansIkaros Transcription FactorIsocitrate DehydrogenaseJanus Kinase 2MutationMyeloproliferative DisordersNeoplasm ProteinsPrognosisProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-cblReceptors, ThrombopoietinRepressor ProteinsASXL1 protein, humanBiomarkers, TumorCBL protein, humanDioxygenasesDNA-Binding ProteinsIDH1 protein, humanIkaros Transcription FactorIKZF1 protein, humanIsocitrate DehydrogenaseJAK2 protein, humanJanus Kinase 2MAS1 protein, humanMPL protein, humanNeoplasm ProteinsProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-cblReceptors, ThrombopoietinRepressor ProteinsTET2 protein, human

Identifiers

PMID20428194
PMCPMC3035972
OpenAlexW2028803880

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.