Evidence map›Paper›PMID 24699303›Full record

ArticleLeukemia2014

Low expression of Abelson interactor-1 is linked to acquired drug resistance in Bcr-Abl-induced leukemia.

A Chorzalska, I Salloum, H Shafqat, S Khan, P Marjon, D Treaba, C Schorl, J Morgan, C R Bryke, V Falanga and 7 more

Open access · greenAbstract read
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  2. Article
  3. Article
  4. Article
  5. CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020
    Article
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  7. 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

17 authors at 6 institutions in 1 country.

A ChorzalskaSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
I SalloumSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
H ShafqatSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
S KhanSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
P MarjonSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
D TreabaHematopathology Laboratories at Rhode Island Hospital and Miriam Hospital, Providence, RI, USA.
C SchorlGenomics Core Facility, Brown University, Providence, RI, USA.
J MorganFlow Cytometry and Cell Sorting Core Facility, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Providence, RI, USA.
C R BrykeCytogenetics, Quest Diagnostics Nichols Institute, Chantilly, VA, USA.
V Falanga1] Department of Dermatology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA [2] Departments of Dermatology and Biochemistry, Boston University School of Medicine, Boston, MA, USA.
T C ZhaoCardiovascular Lab, Department of Surgery, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
J ReaganDivision of Hematology/Oncology, Rhode Island Hospital, Brown University Warren Alpert School of Medicine, Providence, RI, USA.
E WinerDivision of Hematology/Oncology, Rhode Island Hospital, Brown University Warren Alpert School of Medicine, Providence, RI, USA.
A J OlszewskiMemorial Hospital of Rhode Island, Brown University Warren Alpert School of Medicine, Pawtucket, RI, USA.
A S Al-HomsiAdult Blood and Marrow Transplantation, Spectrum Health, Michigan State University, Grand Rapids, MI, USA.
N KouttabDepartment of Pathology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
P M DubieleckaSignal Transduction Laboratory, NIH Center of Biomedical Excellence (COBRE) for Stem Cell Biology, Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
Roger Williams Medical Center · USBrown University · USRhode Island Hospital · USBoston University · USQuest Diagnostics (United States) · USSpectrum Health · US

Funding

WATER CHANNEL AQUAPORIN-3 IN BM-DERIVED EPIDERMAL CELLS PLAY ROLE WOUND HEALINGP20RR018757 · NCRR · ROGER WILLIAMS HOSPITAL · PI BOYD, ASHLEIGH · 2003 to 2011
$22.5M
New Approaches to Tissue RepairP20GM103414 · NIGMS · ROGER WILLIAMS HOSPITAL · PI FALANGA, VINCENT · 2012 to 2012
$2.3M
NCRR NIH HHS 5P20RR018757-10NCRR NIH HHS P20 RR018757NIGMS NIH HHS 8P20GM103414-10NIGMS NIH HHS P20 GM103414
6 · The paper itself

Abstract

The basis for persistence of leukemic stem cells in the bone marrow microenvironment remains poorly understood. We present evidence that signaling cross-talk between α4 integrin and Abelson interactor-1 (Abi-1) is involved in the acquisition of an anchorage-dependent phenotype and drug resistance in Bcr-Abl-positive leukemia cells. Comparison of Abi-1 (ABI-1) and α4 integrin (ITGA4) gene expression in relapsing Bcr-Abl-positive CD34+progenitor cells demonstrated a reduction in Abi-1 and an increase in α4 integrin mRNA in the absence of Bcr-Abl mutations. This inverse correlation between Abi-1 and α4 integrin expression, as well as linkage to elevated phospho-Akt and phospho-Erk signaling, was confirmed in imatinib mesylate -resistant leukemic cells. These results indicate that the α4-Abi-1 signaling pathway may mediate acquisition of the drug-resistant phenotype of leukemic cells.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, CD34Cell AdhesionCell Line, TransformedCell ProliferationCytoskeletal ProteinsDrug Resistance, NeoplasmFusion Proteins, bcr-ablGene Expression Regulation, LeukemicHumansIntegrin alpha4K562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMAP Kinase Signaling SystemMiceABI1 protein, humanAdaptor Proteins, Signal TransducingAntigens, CD34Cytoskeletal ProteinsFusion Proteins, bcr-ablIntegrin alpha4Proteasome Endopeptidase ComplexVascular Cell Adhesion Molecule-1

Identifiers

PMID24699303
PMCPMC4185277
OpenAlexW2050757349

What OpenQuestion holds

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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.