Evidence map›Paper›PMID 20726858›Full record

ArticleCancer science2010

Amphiregulin regulates the activation of ERK and Akt through epidermal growth factor receptor and HER3 signals involved in the progression of pancreatic cancer.

Fusanori Yotsumoto, Tatsuya Fukami, Hiroshi Yagi, Akihiro Funakoshi, Toshiyuki Yoshizato, Masahide Kuroki, Shingo Miyamoto

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  3. [Therapeutic mechanism of aqueous extract ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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  13. Dickkopf-1 and Amphiregulin as Novel Biomarkers and Potential Therapeutic Targets in Hepatocellular Carcinoma.International journal of hematology-oncology and stem cell research · 2019
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  20. Novel therapeutic targets for pancreatic cancer.World journal of gastroenterology · 2014
    Review
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 3 institutions in 2 countries.

Fusanori YotsumotoDepartment of Biochemistry, School of Medicine Center for Advanced Molecular Medicine Department of Obstetrics & Gynecology, School of Medicine, Fukuoka University, Fukuoka, Japan.
Tatsuya Fukami
Hiroshi Yagi
Akihiro Funakoshi
Toshiyuki Yoshizato
Masahide Kuroki
Shingo Miyamoto
Fukuoka University · JPNational Hospital Organization Kyushu Cancer Center · JPNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is one of the most lethal malignancies. Epidermal growth factor receptor (EGFR), HER3, Akt, and amphiregulin have been recognized as targets for pancreatic cancer therapy. Although gemcitabine + erlotinib has been the recommended chemotherapy for pancreatic cancer, the prognosis is extremely poor. The development of molecularly targeted therapies has been required for patients with pancreatic cancer. To assess the validation of amphiregulin as a target for pancreatic cancer therapy, we examined its expression in pancreatic cancer using real-time PCR analyses and ELISA. We also measured the apoptotic cell rate using TUNEL assays. In addition, alterations in signaling pathways were detected by immunoblotting analyses. Treatment with gemcitabine, which reduced the cell viability and augmented the cell apoptotic rate, activated and subsequently attenuated ERK and EGFR signals. However, gemcitabine, paclitaxel, or cisplatin treatment enhanced the Akt activation, heterodimer formation of EGFR with HER3, and secretion of amphiregulin, indicating that the presence of gemcitabine promoted the activity of targeted molecules including amphiregulin, Akt, and HER3 for pancreatic cancer therapy. Combined treatment with an inhibitor for amphiregulin and gemcitabine, paclitaxel, or cisplatin induced synergistic antitumor effects, accompanied by the suppression of Akt and ERK activation. Blockade of amphiregulin suppressed the activities of EGFR, HER3, and Akt and the expression of amphiregulin itself. According to this evidence, combination chemotherapy of conventional anticancer drugs plus an inhibitor for amphiregulin would allow us to provide more favorable clinical outcomes for patients with pancreatic cancer.

Indexed as

AmphiregulinAntibodiesApoptosisCell Line, TumorCell SurvivalCisplatinDeoxycytidineDose-Response Relationship, DrugDrug SynergismEGF Family of ProteinsEnzyme ActivationEnzyme-Linked Immunosorbent AssayErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGemcitabineGlycoproteinsAmphiregulinAntibodiesAREG protein, humanCisplatinDeoxycytidineEGF Family of ProteinsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGemcitabineGlycoproteinsIntercellular Signaling Peptides and ProteinsPaclitaxelProto-Oncogene Proteins c-aktReceptor, ErbB-3

Identifiers

PMID20726858
PMCPMC11158290
OpenAlexW2026130715

What OpenQuestion holds

Textmetadata
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.