Evidence map›Paper›PMID 9520460›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Transcriptional map of 170-kb region at chromosome 11p15.5: identification and mutational analysis of the BWR1A gene reveals the presence of mutations in tumor samples.

C Schwienbacher, S Sabbioni, M Campi, A Veronese, G Bernardi, A Menegatti, I Hatada, T Mukai, H Ohashi, G Barbanti-Brodano and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-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

21 citing papers in PubMed, 56 citations in OpenAlex.

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  10. Rhabdomyosarcomas: an overview on the experimental animal models.Journal of cellular and molecular medicine · 2012
    Review
  11. Caveolins in rhabdomyosarcoma.Journal of cellular and molecular medicine · 2011
    Review
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  19. Gain of imprinting at chromosome 11p15: A pathogenetic mechanism identified in human hepatocarcinomas.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  20. Genomic imprinting: implications for human disease.The American journal of pathology · 1999
    Review
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

12 authors at 3 institutions in 3 countries.

C SchwienbacherDepartment of Experimental and Diagnostic Medicine, Section of Microbiology, and Interdepartment Center for Biotechnology, University of Ferrara, 44100, Ferrara, Italy.
S Sabbioni
M Campi
A Veronese
G Bernardi
A Menegatti
I Hatada
T Mukai
H Ohashi
G Barbanti-Brodano
C M Croce
M Negrini
Sidney Kimmel Cancer Center · USUniversity of Ferrara · ITThomas Jefferson University · US

Funding

Telethon E.0366
6 · The paper itself

Abstract

Chromosome region 11p15.5 harbors unidentified genes involved in neoplasms and in the genetic disease Beckwith-Wiedemann syndrome. The genetic analysis of a 170-kb region at 11p15.5 between loci D11S601 and D11S679 resulted in the identification of six transcriptional units. Three genes, hNAP2, CDKN1C, and KVLQT1, are well characterized, whereas three genes are novel. The three additional genes were designated BWR1A, BWR1B, and BWR1C. Full-length cDNAs for these three genes were cloned and nucleotide sequences were determined. While our work was in progress, BWR1C cDNA was described as IPL [Qian, N., Franck, D., O'Keefe, D., Dao, D. , Zhao, L., Yuan, L., Wang, Q., Keating, M., Walsh, C. & Tycko, B. (1997) Hum. Mol. Genet. 6, 2021-2029]. The cloning and mapping of these genes together with the fine mapping of the three known genes indicates that the transcriptional map of this region is likely to be complete. Because this region frequently is altered in neoplasms and in the genetic disease Beckwith-Wiedemann syndrome, we carried out a mutational analysis in tumor cell lines and Beckwith-Wiedemann syndrome samples that resulted in the identification of genetic alterations in the BWR1A gene: an insertion that introduced a stop codon in the breast cancer cell line BT549 and a point mutation in the rhabdomyosarcoma cell line TE125-T. These results indicate that BWR1A may play a role in tumorigenesis.

Indexed as

Chromosome MappingChromosomes, Human, Pair 11MutationOrganic Cation Transport ProteinsBeckwith-Wiedemann SyndromeDNA Mutational AnalysisFemaleHumansMolecular Sequence DataNeoplasmsProteinsTranscription, GeneticTumor Cells, CulturedOrganic Cation Transport ProteinsProteinsSLC22A18 protein, human

Identifiers

PMID9520460
PMCPMC19930
OpenAlexW2112779230

What OpenQuestion holds

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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.