Evidence map›Paper›PMID 25294819›Full record

ArticleOncotarget2014

Ibrutinib inhibits SDF1/CXCR4 mediated migration in AML.

Lyubov Zaitseva, Megan Y Murray, Manar S Shafat, Matthew J Lawes, David J MacEwan, Kristian M Bowles, Stuart A Rushworth

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
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  6. Gene Expression Array Analyses Predict Proto-Oncogene Expression During Perineural Invasion in Pancreatic Ductal Adenocarcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
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  8. Article
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  13. Biomedicines · 2021
    Article
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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

7 authors at 4 institutions in 1 country.

Lyubov ZaitsevaDepartment of Molecular Haematology, Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
Megan Y MurrayDepartment of Molecular Haematology, Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
Manar S ShafatDepartment of Molecular Haematology, Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
Matthew J LawesDepartment of Haematology, Norfolk and Norwich University Hospitals NHS Trust, Colney Lane, Norwich United Kingdom.
David J MacEwanDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Kristian M BowlesDepartment of Molecular Haematology, Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, United Kingdom. Department of Haematology, Norfolk and Norwich University Hospitals NHS Trust, Colney Lane, Norwich United Kingdom.
Stuart A RushworthDepartment of Molecular Haematology, Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, United Kingdom.
University of East Anglia · GBNorwich Research Park · GBNorfolk and Norwich University Hospitals NHS Foundation Trust · GBUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological targeting of BTK using ibrutinib has recently shown encouraging clinical activity in a range of lymphoid malignancies. Recently we reported that ibrutinib inhibits human acute myeloid leukemia (AML) blast proliferation and leukemic cell adhesion to the surrounding bone marrow stroma cells. Here we report that in human AML ibrutinib, in addition, functions to inhibit SDF1/CXCR4-mediated AML migration at concentrations achievable in vivo. It has previously been shown that SDF1/CXCR4-induced migration is dependent on activation of downstream BTK in chronic lymphocytic leukaemia (CLL) and multiple myeloma. Here we show that SDF-1 induces BTK phosphorylation and downstream MAPK signalling in primary AML blast. Furthermore, we show that ibrutinib can inhibit SDF1-induced AKT and MAPK activation. These results reported here provide a molecular mechanistic rationale for clinically evaluating BTK inhibition in AML patients and suggests that in some AML patients the blasts count may initially rise in response to ibrutinib therapy, analgous to similar clinical observations in CLL.

Indexed as

AdenineAdultAgammaglobulinaemia Tyrosine KinaseAgedAged, 80 and overCell Line, TumorCell MovementCell ProliferationChemokine CXCL12FemaleGene Knockdown TechniquesHumansLeukemia, Myeloid, AcuteMaleMAP Kinase Signaling SystemMiddle AgedAdenineAgammaglobulinaemia Tyrosine KinaseBTK protein, humanChemokine CXCL12CXCL12 protein, humanibrutinibPiperidinesProtein-Tyrosine KinasesPyrazolesPyrimidines

Identifiers

PMID25294819
PMCPMC4259448
OpenAlexW2125392320

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.