Evidence map›Paper›PMID 20068225›Full record

Trial reportBlood2010

Prevalence and prognostic impact of allelic imbalances associated with leukemic transformation of Philadelphia chromosome-negative myeloproliferative neoplasms.

Nils H Thoennissen, Utz O Krug, Dhong Hyun Tony Lee, Norihiko Kawamata, Gabriela B Iwanski, Terra Lasho, Tamara Weiss, Daniel Nowak, Maya Koren-Michowitz, Motohiro Kato and 11 more

Open access · bronzeAbstract readClinical TrialComparative StudyMulticenter Study
In one paragraph

Trial report in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Guideline
  2. Unraveling the role ofHemaSphere · 2026
    Review
  3. Article
  4. Article
  5. Myeloproliferative Neoplasms: Challenging Dogma.Journal of clinical medicine · 2024
    Review
  6. Circulating CD133+/–CD34– Have Increased c-Turkish journal of haematology : official journal of Turkish Society of Haematology · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. What are the molecular mechanisms driving the switch from MPNs to leukemia?Best practice & research. Clinical haematology · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 11 institutions in 7 countries.

Nils H ThoennissenDivision of Hematology and Oncology, Cedars-Sinai Medical Center, University of California Los Angeles School of Medicine, Los Angeles, CA 90048, USA. nils.thoennissen@cshs.org
Utz O Krug
Dhong Hyun Tony Lee
Norihiko Kawamata
Gabriela B Iwanski
Terra Lasho
Tamara Weiss
Daniel Nowak
Maya Koren-Michowitz
Motohiro Kato
Masashi Sanada
Lee-Yung Shih
Arnon Nagler
Sophie D Raynaud
Carsten Müller-Tidow
Ruben Mesa
Torsten Haferlach
D Gary Gilliland
Ayalew Tefferi
Seishi Ogawa
H Phillip Koeffler
Cedars-Sinai Medical Center · USMayo Clinic in Arizona · USUniversity of California, Los Angeles · USMunich Leukemia Laboratory (Germany) · DEThe University of Tokyo · JPUniversity of Münster · DEChang Gung Memorial Hospital · TWHarvard Stem Cell Institute · USHôpital l'Archet · FRJapan Science and Technology Agency · JPSheba Medical Center · IL

Funding

REGULATION OF HEMATOPOIETIC CYTOKINESR01CA026038 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOEFFLER, HAROLD PHILLIP · 1985 to 2013
$4.7M
NCI NIH HHS 5R01CA026038-31NCI NIH HHS R01 CA026038
6 · The paper itself

Abstract

Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) including polycythemia vera, essential thrombocythemia, and primary myelofibrosis show an inherent tendency for transformation into leukemia (MPN-blast phase), which is hypothesized to be accompanied by acquisition of additional genomic lesions. We, therefore, examined chromosomal abnormalities by high-resolution single nucleotide polymorphism (SNP) array in 88 MPN patients, as well as 71 cases with MPN-blast phase, and correlated these findings with their clinical parameters. Frequent genomic alterations were found in MPN after leukemic transformation with up to 3-fold more genomic changes per sample compared with samples in chronic phase (P < .001). We identified commonly altered regions involved in disease progression including not only established targets (ETV6, TP53, and RUNX1) but also new candidate genes on 7q, 16q, 19p, and 21q. Moreover, trisomy 8 or amplification of 8q24 (MYC) was almost exclusively detected in JAK2V617F(-) cases with MPN-blast phase. Remarkably, copy number-neutral loss of heterozygosity (CNN-LOH) on either 7q or 9p including homozygous JAK2V617F was related to decreased survival after leukemic transformation (P = .01 and P = .016, respectively). Our high-density SNP-array analysis of MPN genomes in the chronic compared with leukemic stage identified novel target genes and provided prognostic insights associated with the evolution to leukemia.

Indexed as

Loss of HeterozygosityPhiladelphia ChromosomeAgedBlast CrisisChromosomes, HumanDisease-Free SurvivalFemaleHematologic NeoplasmsHumansJanus Kinase 2MaleMiddle AgedNeoplasm ProteinsPrevalenceSurvival RateJAK2 protein, humanJanus Kinase 2Neoplasm Proteins

Identifiers

PMID20068225
PMCPMC2854432
OpenAlexW1984567268

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.