Evidence map›Paper›PMID 17938925›Full record

ReviewAnnals of hematology2008

The diagnosis of BCR/ABL-negative chronic myeloproliferative diseases (CMPD): a comprehensive approach based on morphology, cytogenetics, and molecular markers.

Torsten Haferlach, Ulrike Bacher, Wolfgang Kern, Susanne Schnittger, Claudia Haferlach

Open access · hybridAbstract readReview
In one paragraph

Review in Annals of hematology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Genetic alterations in myeloproliferative and myelodysplastic/myeloproliferative neoplasms - a practical guide to WHO-HAEM5.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2024
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. ICON: Eosinophil Disorders.The World Allergy Organization journal · 2012
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Therapeutic potential of Janus-activated kinase-2 inhibitors for the management of myelofibrosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    Review
  13. Review
  14. Review
  15. Article
  16. Article
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

5 authors at 2 institutions in 1 country.

Torsten HaferlachMLL Munich Leukemia Laboratory, Max-Lebsche-Platz 31, 81377, Munich, Germany. torsten.haferlach@mll-online.com
Ulrike Bacher
Wolfgang Kern
Susanne Schnittger
Claudia Haferlach
Munich Leukemia Laboratory (Germany) · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent years showed significant progress in the molecular characterization of the chronic myeloproliferative disorders (CMPD) which are classified according to the WHO classification of 2001 as polycythemia vera (PV), chronic idiopathic myelofibrosis (CIMF), essential thrombocythemia (ET), CMPD/unclassifiable (CMPD-U), chronic neutrophilic leukemia, and chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome, all to be delineated from BCR/ABL-positive chronic myeloid leukemia (CML). After 2001, the detection of the high frequency of the JAK2V617F mutation in PV, CIMF, and ET, and of the FIP1L1-PDGFRA fusion gene in CEL further added important information in the diagnosis of CMPD. These findings also enhanced the importance of tyrosine kinase mutations in CMPD and paved the way to a more detailed classification and to an improved definition of prognosis using also novel minimal residual disease (MRD) markers. Simultaneously, the broadening of therapeutic strategies in the CMPD, e.g., due to reduced intensity conditioning in allogeneic hematopoietic stem cell transplantation and the introduction of tyrosine kinase inhibitors in CML, in CEL, and in other ABL and PDGRFB rearrangements, increased the demands to diagnostics. Therefore, today, a multimodal diagnostic approach combining cytomorphology, cytogenetics, and individual molecular methods is needed in BCR/ABL-negative CMPD. A stringent diagnostic algorithm for characterization, choice of treatment, and monitoring of MRD will be proposed in this review.

Indexed as

CytogeneticsAlgorithmsBiomarkers, TumorChromosomes, HumanHumansLeukemia, Myeloid, Chronic, Atypical, BCR-ABL NegativeBiomarkers, Tumor

Identifiers

PMID17938925
PMCPMC2082654
OpenAlexW2000756161

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.