Evidence map›Paper›PMID 20445577›Full record

ReviewLeukemia2010

BCR-ABL: a multi-faceted promoter of DNA mutation in chronic myelogeneous leukemia.

B A Burke, M Carroll

Abstract readReview
In one paragraph

Review in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  7. HighOncoTargets and therapy · 2023
    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

2 authors at 1 institution in 1 country.

B A BurkeDivision of Hematology and Oncology, University of Pennsylvania, Philadelphia, PA, USA.
M Carroll
University of Pennsylvania · US

Funding

The Role of BCR/ABL in Regulating DNA RepairR01CA100885 · NCI · UNIVERSITY OF PENNSYLVANIA · PI CARROLL, MARTIN · 2004 to 2008
$1.3M
NCI NIH HHS R01 CA100885
6 · The paper itself

Abstract

The role of the BCR-ABL oncogene in the progression of chronic myeloid leukemia (CML) to blast crisis (BC) is unknown. The appearance of chromosomal aberrations in patients with CML BC has led to many attempts to elucidate a mechanism whereby BCR-ABL affects DNA damage and repair. BCR-ABL-expressing cells have been found to accumulate genetic abnormalities, but the mechanism leading to this genomic instability is controversial. In this study, we review the effects of BCR-ABL on DNA repair mechanisms, centrosomes, checkpoint activation and apoptosis. BCR-ABL has diverse effects on these mechanisms, but which of these effects are necessary for the progression of CML to BC is still unresolved.

Indexed as

DNA DamageDNA, NeoplasmDNA RepairFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMutationPrognosisPromoter Regions, GeneticDNA, NeoplasmFusion Proteins, bcr-abl

Identifiers

PMID20445577
PMCPMC4425294
OpenAlexW2034814703

What OpenQuestion holds

Textmetadata
LicenceTDM
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.