Evidence map›Paper›PMID 27421772›Full record

ArticleBMC cancer2016

Subcellular differential expression of Ep-ICD in oral dysplasia and cancer is associated with disease progression and prognosis.

Raj Thani Somasundaram, Jatinder Kaur, Iona Leong, Christina MacMillan, Ian J Witterick, Paul G Walfish, Ranju Ralhan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
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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 1 institution in 1 country.

Raj Thani SomasundaramAlex and Simona Shnaider Laboratory, Laboratory Medicine in Molecular Onocolgy, Mount Sinia Hospital, Room 6-318, 600 University Avenue, Toronto, ON, M5G 1X5, Canada.
Jatinder KaurAlex and Simona Shnaider Laboratory, Laboratory Medicine in Molecular Onocolgy, Mount Sinia Hospital, Room 6-318, 600 University Avenue, Toronto, ON, M5G 1X5, Canada.
Iona LeongDepartment of Otolaryngology, Head and Neck Surgery, Mount Sinai Hospital, Joseph and Wolf Lebovic Health Complex, 600 University Avenue, 6-500, Toronto, ON, M5G 1X5, Canada.
Christina MacMillanDepartment of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, ON, M5G 1X5, Canada.
Ian J WitterickJoseph and Mildred Sonshine Family Centre for Head and Neck Diseases, Mount Sinai Hospital, Toronto, ON, M5G 1X5, Canada.
Paul G WalfishAlex and Simona Shnaider Laboratory, Laboratory Medicine in Molecular Onocolgy, Mount Sinia Hospital, Room 6-318, 600 University Avenue, Toronto, ON, M5G 1X5, Canada. pwalfish@mtsinai.on.ca.
Ranju RalhanAlex and Simona Shnaider Laboratory, Laboratory Medicine in Molecular Onocolgy, Mount Sinia Hospital, Room 6-318, 600 University Avenue, Toronto, ON, M5G 1X5, Canada. rralhan@mtsinai.on.ca.
Mount Sinai Hospital · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundIdentification of patients with oral dysplasia at high risk of cancer development and oral squamous cell carcinoma (OSCC) at increased risk of disease recurrence will enable rigorous personalized treatment. Regulated intramembranous proteolysis of Epithelial cell adhesion molecule (EpCAM) resulting in release of its intracellular domain Ep-ICD into cytoplasm and nucleus triggers oncogenic signaling. We analyzed the expression of Ep-ICD in oral dysplasia and cancer and determined its clinical significance in disease progression and prognosis.

methodsIn a retrospective study, immunohistochemical analysis of nuclear and cytoplasmic Ep-ICD and EpEx (extracellular domain of EpCAM), was carried out in 115 OSCC, 97 oral dysplasia and 105 normal oral tissues, correlated with clinicopathological parameters and disease outcome over 60 months for oral dysplasia and OSCC patients. Disease-free survival (DFS) was determined by Kaplan-Meier method and multivariate Cox regression analysis.

resultsIn comparison with normal oral tissues, significant increase in nuclear Ep-ICD and membrane EpEx was observed in dysplasia, and OSCC (p = 0.013 and < 0.001 respectively). Oral dysplasia patients with increased overall Ep-ICD developed cancer in short time period (mean = 47 months; p = 0.044). OSCC patients with increased nuclear Ep-ICD and membrane EpEx had significantly reduced mean DFS of 33.7 months (p = 0.018).

conclusionsOur study provided clinical evidence for Ep-ICD as a predictor of cancer development in patients with oral dysplasia and recurrence in OSCC patients, suggesting its potential utility in enhanced management of those patients detected to have increased risk of progression to cancer and recurrence in OSCC patients.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Squamous CellDisease-Free SurvivalDisease ProgressionEpithelial Cell Adhesion MoleculeFemaleHumansImmunohistochemistryKaplan-Meier EstimateMaleMiddle AgedMouth NeoplasmsNeoplasm Recurrence, LocalBiomarkers, TumorEPCAM protein, humanEpithelial Cell Adhesion MoleculeDysplasiaEpCAMEp-ICDOral cancerOral lesionPrognosisSquamous cell carcinoma

Identifiers

PMID27421772
PMCPMC4947324
OpenAlexW2462535653

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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.