Evidence map›Paper›PMID 26909863›Full record

ArticleOncotarget2016

Mapping of deletion breakpoints at the CDKN2A locus in melanoma: detection of MTAP-ANRIL fusion transcripts.

Huaping Xie, P Sivaramakrishna Rachakonda, Barbara Heidenreich, Eduardo Nagore, Antje Sucker, Kari Hemminki, Dirk Schadendorf, Rajiv Kumar

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  18. Frontiers in endocrinology · 2018
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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 6 institutions in 4 countries.

Huaping XieDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
P Sivaramakrishna RachakondaDivision of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany.
Barbara HeidenreichDivision of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany.
Eduardo NagoreDepartment of Dermatology, Instituto Valenciano de Oncologia, Valencia, Spain.
Antje SuckerDepartment of Dermatology, University Hospital Essen, Essen, Germany.
Kari HemminkiDivision of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany.
Dirk SchadendorfDepartment of Dermatology, University Hospital Essen, Essen, Germany.
Rajiv KumarDivision of Molecular Genetic Epidemiology, German Cancer Research Center, Heidelberg, Germany.
German Cancer Research Center · DEHeidelberg University · DEDeutschen Konsortium für Translationale Krebsforschung · DEEssen University Hospital · DEFundación Instituto Valenciano de Oncología · ESLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic locus at chromosome 9p21 that contains the CDKN2A and CDKN2B tumor suppressor genes is inactivated through mutations, deletions and promoter methylation in multiple human cancers. Additionally, the locus encodes an anti-sense RNA (ANRIL). Both hemizygous and homozygous deletions at the locus targeting multiple genes are fairly common in different cancers. We in this study investigated breakpoints in five melanoma cell lines, derived from metastasized tumors, with previously identified homozygous deletions using array comparative genomic hybridization (aCGH). For breakpoint mapping, we used primer approximation multiplex PCR (PAMP) and inverse PCR techniques. Our results showed that three cell lines carried complex rearrangements. In two other cell lines, with focal deletions of 141 kb and 181 kb, we identified fusion gene products, involving MTAP and ANRIL. We also confirmed the complex rearrangements and focal deletions in DNA from tumor tissues corresponding to three cell lines. The rapid amplification of 3'cDNA ends (3'RACE) carried out on transcripts resulted in identification of three isoforms of MTAP-ANRIL fusion gene. Screening of cDNA from 64 melanoma cell lines resulted in detection of fusion transcripts in 13 (20%) cell lines that involved exons 4-7 of the MTAP and exon 2 or 5 of the ANRIL genes. We also detected fusion transcripts involving MTAP and ANRIL in two of the seven primary melanoma tumors with focal deletion at the locus. The results from the study, besides identifying complex rearrangements involving CDKN2A locus, show frequent occurrence of fusion transcripts involving MTAP and ANRIL genes.

Indexed as

Chromosome BreakpointsGene DeletionChromosome MappingComparative Genomic HybridizationCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Gene FusionHumansMelanomaPurine-Nucleoside PhosphorylaseRNA, Long NoncodingTranscription, Genetic5'-methylthioadenosine phosphorylaseCDKN2A protein, humanCDKN2B antisense RNA, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18Purine-Nucleoside PhosphorylaseRNA, Long Noncodingbreak pointsCDKN2Adeletionsmelanoma

Identifiers

PMID26909863
PMCPMC4941330
OpenAlexW2292769011

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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.