Evidence map›Paper›PMID 28111465›Full record

ArticleLeukemia2017

Differential signaling networks of Bcr-Abl p210 and p190 kinases in leukemia cells defined by functional proteomics.

S Reckel, R Hamelin, S Georgeon, F Armand, Q Jolliet, D Chiappe, M Moniatte, O Hantschel

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Current and future of targeted therapies against BCR::ABL kinases.Journal of the Egyptian National Cancer Institute · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Importance of Rare Gene Alterations in the Prognosis of B-Cell Acute Lymphoblastic LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2024
    Article
  12. Review
  13. Review
  14. Journal of proteome research · 2023
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Ph+ ALL in 2022: is there an optimal approach?Hematology. American Society of Hematology. Education Program · 2022
    Article

5 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

8 authors at 1 institution in 1 country.

S ReckelISREC Foundation Chair in Translational Oncology, Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
R HamelinProteomics Core Facility, School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
S GeorgeonISREC Foundation Chair in Translational Oncology, Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
F ArmandProteomics Core Facility, School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
Q JollietProteomics Core Facility, School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
D ChiappeProteomics Core Facility, School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
M MoniatteProteomics Core Facility, School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
O HantschelISREC Foundation Chair in Translational Oncology, Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, École polytechnique fédérale de Lausanne (EPFL), Lausanne, Switzerland.
École Polytechnique Fédérale de Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The two major isoforms of the oncogenic Bcr-Abl tyrosine kinase, p210 and p190, are expressed upon the Philadelphia chromosome translocation. p210 is the hallmark of chronic myelogenous leukemia, whereas p190 occurs in the majority of B-cell acute lymphoblastic leukemia. Differences in protein interactions and activated signaling pathways that may be associated with the different diseases driven by p210 and p190 are unknown. We have performed a quantitative comparative proteomics study of p210 and p190. Strong differences in the interactome and tyrosine phosphoproteome were found and validated. Whereas the AP2 adaptor complex that regulates clathrin-mediated endocytosis interacts preferentially with p190, the phosphatase Sts1 is enriched with p210. Stronger activation of the Stat5 transcription factor and the Erk1/2 kinases is observed with p210, whereas Lyn kinase is activated by p190. Our findings provide a more coherent understanding of Bcr-Abl signaling, mechanisms of leukemic transformation, resulting disease pathobiology and responses to kinase inhibitors.

Indexed as

Fusion Proteins, bcr-ablHumansLeukemiaPhosphorylationProteomicsSignal TransductionSTAT5 Transcription FactorFusion Proteins, bcr-ablSTAT5 Transcription Factor

Identifiers

PMID28111465
PMCPMC5508078
OpenAlexW2580750923

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.