Evidence map›Paper›PMID 26708506›Full record

ReviewCancer letters2016

Estrogen receptor beta as target for colorectal cancer prevention.

Cecilia Williams, Alfredo DiLeo, Yaron Niv, Jan-Åke Gustafsson

Abstract readReview
In one paragraph

Review in Cancer letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 3 pooled it
8.6field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 3 syntheses or guidelines pooled it, 174 citations in OpenAlex.

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  4. Uncovering hypothesis-generating associations between prescription drugs and digestive cancer risk: a case-control drug-wide association study (DWAS).Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
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45 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 4 countries.

Cecilia WilliamsCenter for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5056, USA; SciLifeLab, School of Biotechnology, KTH Royal Institute of Technology, 171 21 Solna, Sweden; Department of Biosciences and Nutrition, Novum, Karolinska Institutet, 141 83 Stockholm, Sweden. Electronic address: Cecilia.Williams@scilifelab.se.
Alfredo DiLeoDepartment of Emergency and Organ Transplantation, University of Bari, Bari, Italy.
Yaron NivDepartment of Gastroenterology, Rabin Medical Center, Tel Aviv University, Petach Tikva 49100, Israel.
Jan-Åke GustafssonCenter for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204-5056, USA; Department of Biosciences and Nutrition, Novum, Karolinska Institutet, 141 83 Stockholm, Sweden.
Science for Life Laboratory · SETel Aviv University · ILUniversity of Bari Aldo Moro · IT

Funding

Elucidating the mechanism of ERbeta in colon carcinogenesisR01CA172437 · NCI · UNIVERSITY OF HOUSTON · PI WILLIAMS, CECILIA MARIE · 2013 to 2018
$1.4M
NCI NIH HHS R01 CA172437NCI NIH HHS R01CA172437
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of death in the United States. Despite its slow development and the capacity for early diagnosis, current preventive approaches are not sufficient. However, a role for estrogen has been demonstrated in multiple epidemiologic studies, which may benefit CRC prevention. A large body of evidence from preclinical studies indicates that expression of the estrogen receptor beta (ERβ/ESR2) demonstrates an inverse relationship with the presence of colorectal polyps and stage of tumors, and can mediate a protective response. Natural compounds, including phytoestrogens, or synthetic ERβ selective agonists, can activate or upregulate ERβ in the colon and promote apoptosis in preclinical models and in clinical experience. Importantly, this activity has been associated with a reduction in polyp formation and, in rodent models of CRC, has been shown to lower incidence of colon adenocarcinoma. Collectively, these findings indicate that targeted activation of ERβ may represent a novel clinical approach for management of colorectal adenomatous polyps and prevention of colorectal carcinoma in patients at risk for this condition. In this review, we discuss the potential of new chemopreventive or dietary approaches based on estrogen signaling.

Indexed as

AdenocarcinomaAdenomatous PolypsAnimalsAnticarcinogenic AgentsCell Transformation, NeoplasticColonColonic PolypsColorectal NeoplasmsEstrogen Receptor AntagonistsEstrogen Receptor betaGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyRisk FactorsSignal TransductionAnticarcinogenic AgentsEstrogen Receptor AntagonistsEstrogen Receptor betaColorectal cancerEstrogenEstrogen receptor betaGene expressionPhytoestrogensPrevention

Identifiers

PMID26708506
PMCPMC4744541
OpenAlexW2210107480

What OpenQuestion holds

Textmetadata
LicenceTDM
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.