Evidence map›Paper›PMID 22389237›Full record

ArticleMolecular carcinogenesis2013

Dietary tocopherols inhibit cell proliferation, regulate expression of ERα, PPARγ, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia.

Amanda K Smolarek, Jae Young So, Paul E Thomas, Hong Jin Lee, Shiby Paul, Anne Dombrowski, Chung-Xiou Wang, Constance Lay-Lay Saw, Tin Oo Khor, Ah-Ng Tony Kong and 4 more

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

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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

14 authors at 4 institutions in 2 countries.

Amanda K SmolarekDepartment of Pharmacology and Toxicology, Rutgers, The State University of New Jersey, Piscataway, New Jersey
Jae Young So
Paul E Thomas
Hong Jin Lee
Shiby Paul
Anne Dombrowski
Chung-Xiou Wang
Constance Lay-Lay Saw
Tin Oo Khor
Ah-Ng Tony Kong
Kenneth Reuhl
Mao-Jung Lee
Chung S Yang
Nanjoo Suh
Rutgers, The State University of New Jersey · USCancer Institute of Florida · USChung-Ang University · KRRutgers Cancer Institute of New Jersey

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
Tocopherol-mediated inhibition of breast carcinogenesisR03CA141756 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI SUH, NANJOO · 2009 to 2010
$155k
NCI NIH HHS P30 CA072720NCI NIH HHS R03 CA141756NIEHS NIH HHS P30 ES005022
6 · The paper itself

Abstract

Previous clinical and epidemiological studies of vitamin E have used primarily α-tocopherol for the prevention of cancer. However, γ-tocopherol has demonstrated greater anti-inflammatory and anti-tumor activity than α-tocopherol in several animal models of cancer. This study assessed the potential chemopreventive activities of a tocopherol mixture containing 58% γ-tocopherol (γ-TmT) in an established rodent model of mammary carcinogenesis. Female ACI rats were utilized due to their sensitivity to 17β-estradiol (E2 ) to induce mammary hyperplasia and neoplasia. The rats were implanted subcutaneously with sustained release E2 pellets and given dietary 0.3% or 0.5% γ-TmT for 2 or 10 wk. Serum E2 levels were significantly reduced by the treatment with 0.5% γ-TmT. Serum levels of inflammatory markers, prostaglandin E2 and 8-isoprostane, were suppressed by γ-TmT treatment. Histology of mammary glands showed evidence of epithelial hyperplasia in E2 -treated rats. Immunohistochemical analysis of the mammary glands revealed a decrease in proliferating cell nuclear antigen (PCNA), cyclooxygenase-2 (COX-2), and estrogen receptor α (ERα), while there was an increase in cleaved-caspase 3, peroxisome proliferator-activated receptor γ (PPARγ), and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in γ-TmT-treated rats. In addition, treatment with γ-TmT resulted in a decrease in the expression of ERα mRNA, whereas mRNA levels of ERβ and PPARγ were increased. In conclusion, γ-TmT was shown to suppress inflammatory markers, inhibit E2 -induced cell proliferation, and upregulate PPARγ and Nrf2 expression in mammary hyperplasia, suggesting that γ-TmT may be a promising agent for human breast cancer prevention.

Indexed as

Cell ProliferationDietAnimalsAntioxidantsBiomarkers, TumorBlotting, WesternCell Transformation, NeoplasticEstradiolEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHyperplasiaImmunoenzyme TechniquesInflammation MediatorsMammary Neoplasms, ExperimentalMicrosomes, LiverAntioxidantsBiomarkers, TumorEstradiolEstrogen Receptor alphaInflammation MediatorsNfe2l2 protein, ratNF-E2-Related Factor 2PPAR gammaRNA, MessengerTocopherols

Identifiers

PMID22389237
PMCPMC3374909
OpenAlexW2069579177

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.