Evidence map›Paper›PMID 24742107›Full record

ArticleBMC gastroenterology2014

Cyclin E involved in early stage carcinogenesis of esophageal adenocarcinoma by SNP DNA microarray and immunohistochemical studies.

Zhongren Zhou, Santhoshi Bandla, Jiqing Ye, Yinglin Xia, Jianwen Que, James D Luketich, Arjun Pennathur, Jeffrey H Peters, Dongfeng Tan, Tony E Godfrey

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Multicenter Phase II Trial of the WEE1 Inhibitor Adavosertib in Refractory Solid Tumors HarboringJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
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  9. Prognostic Values ofJournal of Cancer · 2018
    Article
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  12. Novel Molecular Markers for Breast Cancer.Biomarkers in cancer · 2016
    Review
  13. Article
  14. 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

10 authors at 5 institutions in 1 country.

Zhongren ZhouDepartments of Pathology and Laboratory Medicine, University of Rochester, Rochester, 601 Elmwood Ave, Box 626, Rochester, NY 14642, USA. David_zhou@urmc.rochester.edu.
Santhoshi Bandla
Jiqing Ye
Yinglin Xia
Jianwen Que
James D Luketich
Arjun Pennathur
Jeffrey H Peters
Dongfeng Tan
Tony E Godfrey
University of Rochester · USUniversity of Pittsburgh Medical Center · USBoston University · USThe University of Texas MD Anderson Cancer Center · USUniversity of Rochester Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCyclin E is a cell cycle regulator which is critical for driving G1/S transition. Abnormal levels of cyclin E have been found in many cancers. However, the level changes of cyclin E in esophageal adenocarcinoma and its precancerous lesion have not been well studied. Here, we focus on the gene amplification and expression of cyclin E in these lesions, and aim to ascertain the relationship with clinicopathological characteristics.

methodsGenomic DNA was analyzed from 116 esophageal adenocarcinoma and 26 precancerous lesion patients using Affymetrix SNP 6.0 arrays. The protein overexpression of cyclin E was also detected using immunohistochemistry from tissue microarrays containing esophageal adenocarcinoma and precancerous lesions. Patient survival and other clinical data were collected and analyzed. The intensity and percentage of the cyclin E expressing cells in tissue microarrays were scored by two pathologists. Fisher exact tests and Kaplan-Meier methods were used to analyze data.

resultsBy genomic analysis, cyclin E was amplified in 19.0% of the EAC samples. By immunohistochemistry, high expression of cyclin E was observed in 2.3% of squamous mucosa tissues, 3.7% in columnar cell metaplasia, 5.8% in Barrett's esophagus, 19.0% in low grade dysplasia, 35.7% in high grade dysplasia, and 16.7% in esophageal adenocarcinoma. The differences in cyclin E high expression between neoplastic groups and non-dysplasia groups are statistically significant (p < 0.05). The prognosis for patients with high cyclin E expression appeared slightly better than for those with low cyclin E expression although this was not statistically significant (p = 0.13).

conclusionsThe expression of cyclin E significantly increases from non-dysplasia esophageal lesion to low and high grade dysplasia, suggesting that cyclin E plays an important role in the early stage of carcinogenesis. Importantly, cyclin E is also amplified and highly expressed in a subset of esophageal adenocarcinoma patients, but this increase is not associated with worse prognosis.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAdultAgedAged, 80 and overBarrett EsophagusCarcinogenesisCyclin EEsophageal NeoplasmsFemaleHumansImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisOncogene ProteinsCCNE1 protein, humanCyclin EOncogene Proteins

Identifiers

PMID24742107
PMCPMC3998234
OpenAlexW2112473227

What OpenQuestion holds

Textmetadata
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.