Evidence map›Paper›PMID 29348852›Full record

ArticleOncotarget2017

Reduced FBXW7 expression in pancreatic cancer correlates with poor prognosis and chemotherapeutic resistance via accumulation of MCL1.

Norihiro Ishii, Kenichiro Araki, Takehiko Yokobori, Dorgormaa Gantumur, Takahiro Yamanaka, Bolag Altan, Mariko Tsukagoshi, Takamichi Igarashi, Akira Watanabe, Norio Kubo and 3 more

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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  6. Translational cancer research · 2022
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  16. Article
  17. The prognostic significance of FBXO2 expression in colorectal cancer.International journal of clinical and experimental pathology · 2018
    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

13 authors at 2 institutions in 1 country.

Norihiro IshiiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Kenichiro ArakiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Takehiko YokoboriResearch Program for Omics-Based Medical Science, Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research, Maebashi, Japan.
Dorgormaa GantumurDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Takahiro YamanakaDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Bolag AltanDepartment of Oncology Clinical Development, Gunma University, Graduate School of Medicine, Maebashi, Japan.
Mariko TsukagoshiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Takamichi IgarashiDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Akira WatanabeDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Norio KuboDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Yasuo HosouchiDepartment of Surgery and Laparoscopic Surgery, Gunma Prefecture Saiseikai-Maebashi Hospital, Maebashi, Japan.
Hiroyuki KuwanoDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Ken ShirabeDepartment of Hepatobiliary and Pancreatic Surgery, Gunma University, Graduate School of Medicine, Showamachi, Maebashi, Japan.
Gunma University · JPGunma Saiseikai Maebashi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is a highly malignant tumor type with poor outcomes, and elucidation of the mechanisms involved in cancer progression and therapeutic resistance is critical. FBXW7 is a key regulator of tumor malignant potential, and its substrate MCL1 regulates therapeutic resistance in human malignancies. Therefore, determination of the relevance of FBXW7 expression is critical for improving patient outcomes. In this study, we investigated the function and clinical significance of FBXW7 in pancreatic cancer. FBXW7 expression was evaluated by immunohistochemistry in 122 pancreatic cancer tissues. Reduced FBXW7 expression was significantly associated with advanced venous invasion, high MCL1 expression, enhanced Ki-67 expression, and poor prognosis and was an independent poor prognostic factor. Among patients who underwent gemcitabine treatment after surgery, reduced FBXW7 expression was also significantly associated with poor prognosis. Knockdown of FBXW7

Indexed as

chemosensitivityMCL1nab-paclitaxeltumor suppressorubiquitin ligase

Identifiers

PMID29348852
PMCPMC5762537
OpenAlexW2769232919

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.