Evidence map›Paper›PMID 19509239›Full record

ReviewMolecular cancer therapeutics2009

Mutation-associated fusion cancer genes in solid tumors.

Frederic J Kaye

Abstract readReview
In one paragraph

Review in Molecular cancer therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

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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

1 author.

Frederic J KayeNational Naval Medical Center, Bethesda, MD 20889, USA. kayef@mail.nih.gov

Funding

MECHANISMS OF ONCOGENE ACTION IN TUMORIGENESISZ01SC007256 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI KAYE, FREDERIC J. · 1996 to 2008
$1.6M
Mechanisms of Oncogene Action in TumorigenesisZIASC007256 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI KAYE, FREDERIC J. · 2009 to 2010
$1.1M
Intramural NIH HHS Z01 SC007256Wellcome Trust
6 · The paper itself

Abstract

Chromosomal translocations and fusion oncogenes serve as the ultimate biomarker for clinicians as they show specificity for distinct histopathologic malignancies while simultaneously encoding an etiologic mutation and a therapeutic target. Previously considered a minor mutational event in epithelial solid tumors, new methodologies that do not rely on the detection of macroscopic cytogenetic alterations, as well as access to large series of annotated clinical material, are expanding the inventory of recurrent fusion oncogenes in both common and rare solid epithelial tumors. Unexpectedly, related assays are also revealing a high number of tandem or chimeric transcripts in normal tissues including, in one provocative case, a template for a known fusion oncogene. These observations may force us to reassess long-held views on the definition of a gene. They also raise the possibility that some rearrangements might represent constitutive forms of a physiological chimeric transcript. Defining the chimeric transcriptome in both health (transcription-induced chimerism and intergenic splicing) and disease (mutation-associated fusion oncogenes) will play an increasingly important role in the diagnosis, prognosis, and therapy of patients with cancer.

Indexed as

MutationAlternative SplicingAnimalsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansNeoplasmsOncogene Proteins, FusionPrognosisTranslocation, GeneticOncogene Proteins, Fusion

Identifiers

PMID19509239
PMCPMC6948837

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Registered trials

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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.