Evidence map›Paper›PMID 22388727›Full record

ArticleLeukemia2012

Frequent loss of RAF kinase inhibitor protein expression in acute myeloid leukemia.

A Zebisch, A Wölfler, I Fried, O Wolf, K Lind, C Bodner, M Haller, A Drasche, D Pirkebner, D Matallanas and 8 more

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In one paragraph

Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. RAF Kinase Inhibitor Protein in Myeloid Leukemogenesis.International journal of molecular sciences · 2019
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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  18. Expression of RKIP in chronic myelogenous leukemia K562 cell and inhibits cell proliferation by regulating the ERK/MAPK pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  19. Article
  20. 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

18 authors at 5 institutions in 4 countries.

A ZebischDivision of Hematology, Medical University of Graz, Graz, Austria.
A Wölfler
I Fried
O Wolf
K Lind
C Bodner
M Haller
A Drasche
D Pirkebner
D Matallanas
O Rath
K Blyth
R Delwel
E Taskesen
F Quehenberger
W Kolch
J Troppmair
H Sill
Medical University of Graz · ATInnsbruck Medical University · ATCancer Research UK Scotland Institute · GBErasmus MC · NLUniversity College Dublin · IE

Funding

Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

RAF kinase inhibitor protein (RKIP) is a negative regulator of the RAS-mitogen-activated protein kinase/extracellular signal-regulated kinase signaling cascade. We investigated its role in acute myeloid leukemia (AML), an aggressive malignancy arising from hematopoietic stem and progenitor cells (HSPCs). Western blot analysis revealed loss of RKIP expression in 19/103 (18%) primary AML samples and 4/17 (24%) AML cell lines but not in 10 CD34+ HSPC specimens. In in-vitro experiments with myeloid cell lines, RKIP overexpression inhibited cellular proliferation and colony formation in soft agar. Analysis of two cohorts with 103 and 285 AML patients, respectively, established a correlation of decreased RKIP expression with monocytic phenotypes. RKIP loss was associated with RAS mutations and in transformation assays, RKIP decreased the oncogenic potential of mutant RAS. Loss of RKIP further related to a significantly longer relapse-free survival and overall survival in uni- and multivariate analyses. Our data show that RKIP is frequently lost in AML and correlates with monocytic phenotypes and mutations in RAS. RKIP inhibits proliferation and transformation of myeloid cells and decreases transformation induced by mutant RAS. Finally, loss of RKIP seems to be a favorable prognostic parameter in patients with AML.

Indexed as

Gene Expression Regulation, LeukemicCell DifferentiationCell Line, TumorCell ProliferationCell Transformation, NeoplasticGenes, rasHumansLeukemia, Myeloid, AcuteMonocytesMutationMyeloid CellsPhosphatidylethanolamine Binding ProteinPrognosisPEBP1 protein, humanPhosphatidylethanolamine Binding Protein

Identifiers

PMID22388727
OpenAlexW1984926433

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.