Evidence map›Paper›PMID 26913079›Full record

ArticleMolecular cytogenetics2016

Genomic imbalances pinpoint potential oncogenes and tumor suppressors in Wilms tumors.

A C V Krepischi, M Maschietto, E N Ferreira, A G Silva, S S Costa, I W da Cunha, B D F Barros, P E Grundy, C Rosenberg, D M Carraro

Open access · goldAbstract read
In one paragraph

Article in Molecular cytogenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 56 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

10 authors at 4 institutions in 2 countries.

A C V Krepischi *International Research Center, AC Camargo Cancer Center, São Paulo, Brazil.
M Maschietto *International Research Center, AC Camargo Cancer Center, São Paulo, Brazil.
E N FerreiraInternational Research Center, AC Camargo Cancer Center, São Paulo, Brazil.
A G SilvaInstitute of Biosciences, University of São Paulo, São Paulo, Brazil.
S S CostaInstitute of Biosciences, University of São Paulo, São Paulo, Brazil.
I W da CunhaDepartment of Surgical and Investigative Pathology, AC Camargo Cancer Center, São Paulo, Brazil.
B D F BarrosInternational Research Center, AC Camargo Cancer Center, São Paulo, Brazil.
P E GrundyAlberta Health Services, Cancer Control Alberta, Alberta, Canada.
C RosenbergInstitute of Biosciences, University of São Paulo, São Paulo, Brazil.
D M CarraroInternational Research Center, AC Camargo Cancer Center, São Paulo, Brazil.
AC Camargo Hospital · BRUniversidade de São Paulo · BRAlberta Health Services · CABrazilian Biosciences National Laboratory · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWilms tumor (WT) has a not completely elucidated pathogenesis. DNA copy number alterations (CNAs) are common in cancer, and often define key pathogenic events. The aim of this work was to investigate CNAs in order to disclose new candidate genes for Wilms tumorigenesis.

resultsArray-CGH of 50 primary WTs without pre-chemotherapy revealed a few recurrent CNAs not previously reported, such as 7q and 20q gains, and 7p loss. Genomic amplifications were exclusively detected in 3 cases of WTs that later relapsed, which also exhibited an increased frequency of gains affecting a 16.2 Mb 1q21.1-q23.2 region, losses at 11p, 11q distal, and 16q, and WT1 deletions. Conversely, aneuploidies of chromosomes 13 and 19 were found only in WTs without further relapse. The 1q21.1-q23.2 gain associated with WT relapse harbours genes such as CHD1L, CRABP2, GJA8, MEX3A and MLLT11 that were found to be over-expressed in WTs. In addition, down-regulation of genes encompassed by focal deletions highlighted new potential tumor suppressors such as CNKSR1, MAN1C1, PAQR7 (1p36), TWIST1, SOSTDC1 (7p14.1-p12.2), BBOX and FIBIN (11p13), and PLCG2 (16q).

conclusionThis study confirmed the presence of CNAs previously related to WT and characterized new CNAs found only in few cases. The later were found in higher frequency in relapsed cases, suggesting that they could be associated with WT progression.

Indexed as

1q21.1-q23.2 gainArray-CGHCNACopy number alterationRelapseWilms tumor

Identifiers

PMID26913079
PMCPMC4765068
OpenAlexW2275758287

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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.