Evidence map›Paper›PMID 16254145›Full record

ArticleBlood2006

Regulation of survivin expression through Bcr-Abl/MAPK cascade: targeting survivin overcomes imatinib resistance and increases imatinib sensitivity in imatinib-responsive CML cells.

Bing Z Carter, Duncan H Mak, Wendy D Schober, Maria Cabreira-Hansen, Miloslav Beran, Teresa McQueen, Wenjing Chen, Michael Andreeff

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 102 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Bing Z CarterSection of Molecular Hematology and Therapy, Department of Blood and Marrow Transplantation, University of Texas, M. D. Anderson Cancer Center, 1400 Holcombe Blvd, Unit 448, Houston, TX 77030, USA.
Duncan H Mak
Wendy D Schober
Maria Cabreira-Hansen
Miloslav Beran
Teresa McQueen
Wenjing Chen
Michael Andreeff
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THALL, PETER F · 1990 to 2014
$41.8M
THE THERAPY OF AMLP01CA055164 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI THOMAS, MATTIE J · 1992 to 2011
$25.3M
NCI NIH HHS CA16672NCI NIH HHS P01-CA49639NCI NIH HHS P01 CA55164
6 · The paper itself

Abstract

KBM5 cells, derived from a patient with blast crisis Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML), and imatinib-resistant KBM5 (KBM5-STI571) cells were found to express high levels of survivin. Inhibition of Bcr-Abl by imatinib significantly decreased survivin expression and cell viability in KBM5, but much less so in KBM5-STI571 cells. Inhibition of MEK, downstream of the Bcr-Abl signaling cascade decreased survivin expression and cell viability in both KBM5 and KBM5-STI571 cells. In addition, down-regulation of survivin by a survivin antisense oligonucleotide (Sur-AS-ODN) inhibited cell growth and induced maximal G2M block at 48 hours, whereas cell death was observed only at 72 hours in both KBM5 and KBM5-STI571 cells as shown by annexin V staining. Further, the combination of Sur-AS-ODN and imatinib induced more cell death in KBM5 cells than did either treatment alone. Down-regulating survivin also decreased colony-forming units (CFUs) in blast crisis CML patient samples. Our data therefore suggest that survivin is regulated by the Bcr-Abl/MAPK cascade in Ph+ CML. The facts that down-regulating survivin expression induced cell-growth arrest and subsequent cell death regardless of the cell response to imatinib and enhanced the sensitivity to imatinib suggest the potential therapeutic utility of this strategy in patients with CML, both imatinib sensitive and resistant.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsBenzamidesCell Line, TumorDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansImatinib MesylateInhibitor of Apoptosis ProteinsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMAP Kinase Signaling SystemMicrotubule-Associated ProteinsNeoplasm ProteinsPiperazinesPyrimidinesSurvivinAntineoplastic AgentsBenzamidesBIRC5 protein, humanFusion Proteins, bcr-ablImatinib MesylateInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsNeoplasm ProteinsPiperazinesPyrimidinesSurvivin

Identifiers

PMID16254145
PMCPMC1895411
OpenAlexW2001590374

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.