Evidence map›Paper›PMID 25915843›Full record

ArticleOncogene2016

An antibody to amphiregulin, an abundant growth factor in patients' fluids, inhibits ovarian tumors.

S Carvalho, M Lindzen, M Lauriola, N Shirazi, S Sinha, A Abdul-Hai, K Levanon, J Korach, I Barshack, Y Cohen and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
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  11. The role of amphiregulin in ovarian function and disease.Cellular and molecular life sciences : CMLS · 2023
    Review
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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

13 authors at 4 institutions in 3 countries.

S CarvalhoDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
M LindzenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
M LauriolaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
N ShiraziDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
S SinhaDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
A Abdul-HaiKaplan Medical Center, Rehovot, Israel.
K LevanonThe Dr. Pinchas Borenstein Talpiot Medical Leadership Program and Institute of Oncology, The Institute of Oncology, Chaim Sheba Medical Center, Ramat Gan, Israel.
J KorachDepartment of Gynecologic Oncology, Chaim Sheba Medical Center, Ramat Gan, Israel.
I BarshackDepartment of Pathology, Sheba Medical Center, Ramat Gan, Israel.
Y CohenInstitutional Tissue Banks, Sheba Medical Center, Ramat Gan, Israel.
A OnnInstitute of Pulmonary Oncology, Chaim Sheba Medical Center Ramat Gan, Israel.
G MillsDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Y YardenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · ILSheba Medical Center · ILKaplan Medical Center · ILThe University of Texas MD Anderson Cancer Center · US

Funding

Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
6 · The paper itself

Abstract

Growth factors of the epidermal growth factor (EGF)/neuregulin family are involved in tumor progression and, accordingly, antibodies that intercept a cognate receptor, epidermal growth factor receptor (EGFR)/ERBB1, or a co-receptor, HER2, have been approved for cancer therapy. Although they might improve safety and delay onset of chemoresistance, no anti-ligand antibodies have been clinically approved. To identify suitable ligands, we surveyed fluids from ovarian and lung cancer patients and found that amphiregulin (AREG) is the most abundant and generalized ligand secreted by advanced tumors. AREG is a low affinity EGFR ligand, which is upregulated following treatment with chemotherapeutic drugs. Because AREG depletion retarded growth of xenografted ovarian tumors in mice, we generated a neutralizing monoclonal anti-AREG antibody. The antibody inhibited growth of ovarian cancer xenografts and strongly enhanced chemotherapy efficacy. Taken together, these results raise the possibility that AREG and other low- or high-affinity binders of EGFR might serve as potential targets for cancer therapy.

Indexed as

AmphiregulinAnimalsAntibodies, MonoclonalAntineoplastic AgentsCulture Media, ConditionedEGF Family of ProteinsErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMice, NudeMolecular Targeted TherapyOvarian NeoplasmsTransforming Growth Factor alphaTumor Cells, CulturedUbiquitinationAmphiregulinAntibodies, MonoclonalAntineoplastic AgentsAREG protein, humanCulture Media, ConditionedEGF Family of ProteinsEGFR protein, humanErbB ReceptorsTransforming Growth Factor alpha

Identifiers

PMID25915843
OpenAlexW2018221147

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.