Evidence map›Paper›PMID 41454190›Full record

Trial reportAnnals of surgical oncology2026

High E2F7 Expression Indicates Pancreatic Cancer Aggressiveness and Downregulation of E2F7 Enhances Sensitivity to S-1.

Keizo Fujita, Yukiyasu Okamura, Masamichi Hayashi, Ryo Ashida, Tomohisa Otsu, Akihiro Sakai, Shinji Mii, Motokazu Sugimoto, Naoto Yamamoto, Hirochika Toyama and 11 more

Abstract readRandomized Controlled Trial
In one paragraph

Trial report in Annals of surgical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

21 authors.

Keizo FujitaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yukiyasu OkamuraDivision of Digestive Surgery, Department of Surgery, Nihon University School of Medicine, Tokyo, Japan.
Masamichi HayashiDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan. hayashi.masamichi.b9@f.mail.nagoya-u.ac.jp.
Ryo AshidaDivision of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.
Tomohisa OtsuDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akihiro SakaiDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shinji MiiDepartment of Molecular Pathology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Motokazu SugimotoDepartment of Hepatobiliary-Pancreatic Surgery, National Cancer Center Hospital East, Kashiwa, Japan.
Naoto YamamotoDepartment of Gastrointestinal Surgery, Kanagawa Cancer Center, Yokohama, Japan.
Hirochika ToyamaDepartment of Surgery, Division of Hepato-Biliary-Pancreatic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Atsuyuki MaedaDepartment of Surgery, Ogaki Municipal Hospital, Ogaki, Japan.
Nobumasa MizunoDepartment of Gastroenterology, Aichi Cancer Center Hospital, Nagoya, Japan.
Yukihiro YokoyamaDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Junpei YamaguchiDivision of Surgical Oncology, Department of Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nobuhiko NakagawaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keisuke KurimotoDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Haruyoshi TanakaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hideki TakamiDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Katsuhiko UesakaDivision of Hepato-Biliary-Pancreatic Surgery, Shizuoka Cancer Center, Shizuoka, Japan.
Mitsuro KandaDepartment of Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer (PC) remains a highly lethal disease with few reliable biomarkers to guide chemotherapy choices. New biomarkers for selecting anticancer drugs are needed to enhance the effectiveness of current multimodal treatment approaches. This study aimed to find a new biomarker by using clinical data and specimens collected for a Japanese randomized controlled trial (RCT).

methodsGene expression array analysis was performed using PC tissues collected for the ancillary research of JASPAC01, a nationwide phase 3 RCT of adjuvant chemotherapy for patients with PC in Japan. A candidate gene was validated using tissue and blood samples from a second PC patient cohort undergoing radical surgery at the authors' institution. Additionally, experiments were performed with cancer cell lines to investigate the functions of the candidate gene.

resultsExpression of E2F7 mRNA was the most influential prognostic factor of postoperative overall survival outcomes in the primary tissue-available cases in the JASPAC01 cohort (hazard ratio [HR], 1.386; 95% confidence interval [CI], 1.005-1.912; p = 0.045). High E2F7 expression itself correlates with poor survival outcomes (p = 0.045 for OS). Moreover, the benefits of adjuvant S-1 treatment were reduced in high E2F7 cases (p = 0.042 for OS; p = 0.007 for RFS). In vitro experiments demonstrated that E2F7 inhibition suppressed cancer cell proliferation and minimized the 50% inhibitory concentration of S-1.

conclusionsTissue mRNA expression levels of E2F7 correlated with patient prognosis in PC. In the low E2F7 mRNA expression group, patients who received S-1 as adjuvant chemotherapy had a better prognosis than those who received gemcitabine (GEM).

Indexed as

Antimetabolites, AntineoplasticBiomarkers, TumorE2F7 Transcription FactorOxonic AcidPancreatic NeoplasmsTegafurAgedCell ProliferationChemotherapy, AdjuvantDown-RegulationDrug CombinationsFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMaleAntimetabolites, AntineoplasticBiomarkers, TumorDrug CombinationsE2F7 protein, humanE2F7 Transcription FactorOxonic AcidRNA, MessengerS 1 (combination)TegafurE2F7GemcitabinePancreatic cancerS-1

Identifiers

PMID41454190
PMCPMC13179229

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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.