Evidence map›Paper›PMID 16280054›Full record

ArticleBreast cancer research : BCR2005

Expression analysis of candidate breast tumour suppressor genes on chromosome 16q.

Tom van Wezel, Marcel Lombaerts, Eddy H van Roon, Katja Philippo, Hans J Baelde, Karoly Szuhai, Cees J Cornelisse, Anne-Marie Cleton-Jansen

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Role of columnar cell lesions in breast carcinogenesis: analysis of chromosome 16 copy number changes by multiplex ligation-dependent probe amplification.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
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  5. Article
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  8. Genetic alterations of the WWOX gene in breast cancer.Medical oncology (Northwood, London, England) · 2012
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Non-operative breast pathology: lobular neoplasia.Journal of clinical pathology · 2007
    Review
  15. Infrequent mutation of ATBF1 in human breast cancer.Journal of cancer research and clinical oncology · 2007
    Article
  16. Article
  17. Article
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 1 institution in 1 country.

Tom van WezelDepartment of Pathology, Leiden University Medical Center, Albiniusdreef 2, 2333ZA Leiden, The Netherlands. t.van_wezel@lumc.nl
Marcel Lombaerts
Eddy H van Roon
Katja Philippo
Hans J Baelde
Karoly Szuhai
Cees J Cornelisse
Anne-Marie Cleton-Jansen
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChromosome arm 16q is the second most frequent target of loss of heterozygosity in breast cancer and is, therefore, a candidate to contain one or more classic tumour suppressor genes (TSGs). E-cadherin at 16q22 was identified as a TSG in lobular breast cancer, but TSGs in ductal breast cancer remain elusive. Several genes have been suggested as potential candidates (e.g. CBFA2T3, CTCF and WWOX) but no inactivating mutations could be identified in these genes and they thus fail to fit the classic two-hit model for a TSG. With the completion of the human transcriptome, new candidate genes can be distinguished. Besides mutational inactivation, a TSG could, at least in a subset of the tumours, be transcriptionally suppressed or even inactivated. Studying candidate genes for expression and somatic mutations could thus identify the TSGs.

methodsPossible candidates CBFA2T3, TERF2 and TERF2IP, FBXL8 and LRRC29 and FANCA were studied for insertion and deletion mutations and for expression differences using quantitative RT-PCR in a panel of tumour cell lines and primary tumours with and without loss of 16q.

resultsNone of the genes showed mutations or obvious expression differences. FANCA expression increased with tumour grade.

conclusionApparently, the underlying genetics at chromosome 16q are complex or the TSGs remain to be identified. Multiple mechanisms, such as mutations, promoter hypermethylation or haploinsufficiency, might lead to the inactivation of a TSG.

Indexed as

Chromosomes, Human, Pair 16Gene Expression ProfilingGenes, Tumor SuppressorBreast NeoplasmsCell Line, TumorDNA Mutational AnalysisFemaleFrameshift MutationHumansLoss of HeterozygosityReverse Transcriptase Polymerase Chain Reaction

Identifiers

PMID16280054
PMCPMC1410740
OpenAlexW2145374468

What OpenQuestion holds

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LicenceCC BY
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.