Evidence map›Paper›PMID 14583777›Full record

ArticleBritish journal of cancer2003

Characterisation of p53 status at the gene, chromosomal and protein levels in oesophageal adenocarcinoma.

S H Doak, G J S Jenkins, E M Parry, A P Griffiths, V Shah, J N Baxter, J M Parry

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In one paragraph

Article in British journal of cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 36 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

7 authors at 4 institutions in 1 country.

S H DoakHuman Molecular Pathology Group, School of Biological Sciences, University of Wales, Swansea SA2 8PP, UK. 145263@swansea.ac.uk
G J S Jenkins
E M Parry
A P Griffiths
V Shah
J N Baxter
J M Parry
Morriston Hospital · GBSwansea University · GBUniversity of Wales · GBSingleton Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 mutations and loss of heterozygosity have been commonly associated with oesophageal adenocarcinoma. In this investigation, the p53 status of a Welsh population of Barrett's-associated oesophageal adenocarcinomas were fully characterised at the gene sequence, chromosomal, mRNA and protein levels. In total, 31 tumours were examined for p53 gene sequence mutations using RFLP with sequencing, allelic loss of the gene was characterised by FISH, mRNA expression by p53 pathway signalling arrays and protein levels by p53 immunohistochemistry. In all, 9.6% of adenocarcinomas harboured p53 mutations, 24% displayed p53 allelic loss and 83% exhibited p53 protein accumulation. Point mutations and deletions of the gene did not coexist within the same samples. All samples containing p53 mutations also displayed positive immunostaining; however; in the majority of cases, p53 protein accumulation developed in the absence of mutations. The gene expression analysis demonstrated no differences in p53 and mdm-2 transcription levels between the p53 immunonegative and immunopositive samples, indicating other mechanisms underlie the proteins' overexpression. In conclusion, p53 mutations and deletions do not appear to be frequent events in oesophageal adenocarcinomas; however, abnormal accumulation of the protein is present in a vast majority of cases. P53 gene mutations are not the primary cause of protein overexpression--an alternative mechanism is responsible for the positive p53 immunohistochemistry detected.

Indexed as

Gene Expression ProfilingAdenocarcinomaAdultAgedAged, 80 and overBarrett EsophagusDNA Mutational AnalysisEsophageal NeoplasmsFemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMaleMiddle AgedMutationOligonucleotide Array Sequence AnalysisTumor Suppressor Protein p53

Identifiers

PMID14583777
PMCPMC2394414
OpenAlexW2060639749

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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.