Evidence map›Paper›PMID 28574829›Full record

ArticleOncotarget2017

The impact of EpCAM expression on response to chemotherapy and clinical outcomes in patients with epithelial ovarian cancer.

Shingo Tayama, Takeshi Motohara, Dashdemberel Narantuya, Chenyan Li, Koichi Fujimoto, Isao Sakaguchi, Hironori Tashiro, Hideyuki Saya, Osamu Nagano, Hidetaka Katabuchi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 101 citations in OpenAlex.

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  3. The Binding Affinities of Serum Proteins to Nanoparticles.Journal of the American Chemical Society · 2025
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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

10 authors at 2 institutions in 1 country.

Shingo TayamaDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Takeshi MotoharaDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Dashdemberel NarantuyaDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Chenyan LiDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Koichi FujimotoDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Isao SakaguchiDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Hironori TashiroDepartment of Maternal-Newborn Nursing, Kumamoto University, Chuo-Ku, Kumamoto 860-0976, Japan.
Hideyuki SayaDivision of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Shinjuku-Ku, Tokyo 160-8582, Japan.
Osamu NaganoDivision of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Shinjuku-Ku, Tokyo 160-8582, Japan.
Hidetaka KatabuchiDepartment of Obstetrics and Gynecology, Faculty of Life Sciences, Kumamoto University, Chuo-Ku, Kumamoto 860-8556, Japan.
Kumamoto University · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial ovarian cancer is a highly lethal malignancy; moreover, overcoming chemoresistance is the major challenging in treating ovarian cancer patients. The cancer stem cell (CSC) hypothesis considers CSCs to be the main culprits in driving tumor initiation, metastasis, and resistance to conventional therapy. Although growing evidence suggest that CSCs are responsible for chemoresistance, the contribution of CSC marker EpCAM to resistance to chemotherapy remains unresolved.Here we have demonstrated that ovarian cancers containing high levels of EpCAM have a significantly much lower probability of achieving overall responsive rates after first-line chemotherapy. In addition, multivariate analysis revealed that EpCAM expression is an independent risk factor for chemoresistance, indicating that EpCAM expression is a predictive biomarker of chemotherapeutic response. Consistent with these clinical observations, in vitro assays, we found that the subpopulation of EpCAM-positive ovarian cancer cells shows a significantly higher viability compared with EpCAM-negative cells in response to cisplatin treatment by preventing chemotherapy-induced apoptosis, which is regulated by EpCAM-Bcl-2 axis. Furthermore, in an in vivo mouse model, platinum agents preferentially eliminated EpCAM-negative cells in comparison with EpCAM-positive cells, suggesting that the remaining subpopulation of EpCAM-positive cells contributes to tumor recurrence after chemotherapy. Finally, we also found that an increased expression of EpCAM is associated with poor prognosis in ovarian cancer patients.Our findings highlight the clinical significance of EpCAM in the resistance to chemotherapy and provide a rationale for EpCAM-targeted therapy to improve chemoresistance. Targeting EpCAM should be a promising approach to effectively extirpate the CSCs as the putative root of ovarian cancer.

Indexed as

Gene ExpressionAdultAgedAged, 80 and overAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBiomarkers, TumorCarcinoma, Ovarian EpithelialDisease Models, AnimalDrug Resistance, NeoplasmEpithelial Cell Adhesion MoleculeFemaleHumansMiceMiddle AgedBiomarkers, TumorEPCAM protein, humanEpithelial Cell Adhesion Moleculecancer stem cellchemoresistanceEpCAMovarian cancerprognosis

Identifiers

PMID28574829
PMCPMC5546482
OpenAlexW2617696599

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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.