Evidence map›Paper›PMID 19262599›Full record

ArticleLeukemia2009

Frequent TET2 mutations in systemic mastocytosis: clinical, KITD816V and FIP1L1-PDGFRA correlates.

A Tefferi, R L Levine, K-H Lim, O Abdel-Wahab, T L Lasho, J Patel, C M Finke, A Mullally, C-Y Li, A Pardanani and 1 more

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
14.1field-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

109 citing papers in PubMed, 245 citations in OpenAlex.

  1. Trial
  2. TET2 mutations improve the new European LeukemiaNet risk classification of acute myeloid leukemia: a Cancer and Leukemia Group B study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011
    Trial
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Detection ofInternational journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Structure and Function of TET Enzymes.Advances in experimental medicine and biology · 2022
    Article
  16. Review
  17. Article
  18. Review
  19. The Prevalence ofCancers · 2021
    Review
  20. TETology: Epigenetic Mastermind in Action.Applied biochemistry and biotechnology · 2021
    Review

49 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

11 authors at 6 institutions in 2 countries.

A TefferiDivisions of Hematology and Hematopathology, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA. tefferi.ayalew@mayo.edu
R L Levine
K-H Lim
O Abdel-Wahab
T L Lasho
J Patel
C M Finke
A Mullally
C-Y Li
A Pardanani
D G Gilliland
Mayo Clinic in Arizona · USMemorial Sloan Kettering Cancer Center · USMayo Clinic · USBrigham and Women's Hospital · USDana-Farber Brigham Cancer Center · USMackay Memorial Hospital · TW

Funding

Molecular Pathogenesis and Therapy of ET and PMFR01CA151949 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LEVINE, ROSS L · 2010 to 2016
$2.3M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA151949
6 · The paper itself

Abstract

TET2 (TET oncogene family member 2) is a candidate tumor suppressor gene located at chromosome 4q24, and was recently reported to be mutated in approximately 14% of patients with JAK2V617F-positive myeloproliferative neoplasms. We used high-throughput DNA sequence analysis to screen for TET2 mutations in bone marrow-derived DNA from 48 patients with systemic mastocytosis (SM), including 42 who met the 2008 WHO (World Health Organization) diagnostic criteria for SM and 6 with FIP1L1-PDGFRA. Twelve (29%) SM, but no FIP1L1-PDGFRA patients, had TET2 mutations. A total of 17 mutations (13 frameshift, 2 nonsense and 2 missense) were documented in 2 (15%) of 13 indolent SM patients, 2 (40%) of 5 aggressive SM, and 8 (35%) of 23 SM associated with a clonal non-mast cell-lineage hematopoietic disease (P=0.52). KITD816V was detected by PCR sequencing in 50 or 20% of patients with or without TET2 mutation (P=0.05), respectively. Multivariable analysis showed a significant association between the presence of TET2 mutation and monocytosis (P=0.0003) or female sex (P=0.05). The association with monocytosis was also observed in non-indolent SM (n=29), in which the presence of mutant TET2 did not affect survival (P=0.98). We conclude that TET2 mutations are frequent in SM, segregate with KITD816V and influence phenotype without necessarily altering prognosis.

Indexed as

AgedAged, 80 and overDioxygenasesDNA-Binding ProteinsFemaleHumansMaleMastocytosis, SystemicMiddle AgedmRNA Cleavage and Polyadenylation FactorsMutationOncogene Proteins, FusionProto-Oncogene ProteinsProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor alphaSurvival RateDioxygenasesDNA-Binding ProteinsFIP1L1-PDGFRA fusion protein, humanmRNA Cleavage and Polyadenylation FactorsOncogene Proteins, FusionProto-Oncogene ProteinsProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor alphaTET2 protein, human

Identifiers

PMID19262599
PMCPMC4654631
OpenAlexW2043387647

What OpenQuestion holds

Textmetadata
LicenceTDM
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.