Evidence map›Paper›PMID 26130252›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2015

Dietary γ-Tocopherol-Rich Mixture Inhibits Estrogen-Induced Mammary Tumorigenesis by Modulating Estrogen Metabolism, Antioxidant Response, and PPARγ.

Soumyasri Das Gupta, Sudathip Sae-tan, Joseph Wahler, Jae Young So, Min Ji Bak, Larry C Cheng, Mao-Jung Lee, Yong Lin, Weichung Joe Shih, James D Shull and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Rat Models of Hormone Receptor-Positive Breast Cancer.Journal of mammary gland biology and neoplasia · 2024
    Review
  3. Article
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  15. Review
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  17. Article
  18. Inhibitory Effects of γ- and δ-Tocopherols on Estrogen-Stimulated Breast CancerCancer prevention research (Philadelphia, Pa.) · 2017
    Article
  19. Review
  20. 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

13 authors at 3 institutions in 2 countries.

Soumyasri Das GuptaDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Sudathip Sae-tanDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Joseph WahlerDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Jae Young SoDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Min Ji BakDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Larry C ChengDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Mao-Jung LeeDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey.
Yong LinDepartment of Biostatistics, School of Public Health, Rutgers University. Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey.
Weichung Joe ShihDepartment of Biostatistics, School of Public Health, Rutgers University. Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey.
James D ShullMcArdle Laboratory for Cancer Research, Department of Oncology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin.
Stephen SafeDepartment of Veterinary Physiology and Pharmacology, Texas A & M University, College Station, Texas.
Chung S YangDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey. Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey.
Nanjoo SuhDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey. Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey. nsuh@pharmacy.rutgers.edu.
Rutgers, The State University of New Jersey · USTexas A&M University · USUniversity of Wisconsin–Madison · US

Funding

Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
GENETIC SUSCEPTIBILITY TO ESTROGEN INDUCED MAMMARY CAR01CA077876 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SHULL, JAMES D · 1998 to 2012
$4.4M
TARGETED GENOMICS FACILITY COREP30ES023512 · NIEHS · TEXAS A&M AGRILIFE RESEARCH · PI DEUTZ, NICOLAAS E · 2014 to 2017
$3.3M
Prevention of estrogen-mediated mammary carcinogenesis by mixtures of tocopherolsR01AT007036 · NCCIH · RUTGERS, THE STATE UNIV OF N.J. · PI SUH, NANJOO · 2012 to 2016
$1.9M
NCCIH NIH HHS R01 AT007036NCI NIH HHS R01 CA077876NIEHS NIH HHS ES005022NIEHS NIH HHS P30 ES005022NIEHS NIH HHS P30 ES023512
6 · The paper itself

Abstract

This study evaluated the anticancer activity and mechanism of action of a γ-tocopherol-rich tocopherol mixture, γ-TmT, in two different animal models of estrogen-induced breast cancer. The chemopreventive effect of γ-TmT at early (6 weeks), intermediate (18 weeks), and late (31 weeks) stages of mammary tumorigenesis was determined using the August-Copenhagen Irish rat model. Female rats receiving 17β-estradiol (E2) implants were administered with different doses (0%, 0.05%, 0.1%, 0.3%, and 0.5%) of γ-TmT diet. Treatment with 0.3% and 0.5% γ-TmT decreased tumor volume and multiplicity. At 31 weeks, serum concentrations of E2 were significantly decreased by γ-TmT. γ-TmT preferentially induced expression of the E2-metabolizing enzyme CYP1A1, over CYP1B1 in the rat mammary tissues. Nrf2-dependent antioxidant response was stimulated by γ-TmT, as evident from enhanced expression of its downstream targets, NQO1, GCLM, and HMOX1. Serum concentrations of the oxidative stress marker, 8-isoprostane, were also decreased in the γ-TmT-treated groups. Treatment with γ-TmT increased expression of PPARγ and its downstream genes, PTEN and p27, whereas the cell proliferation marker, PCNA, was significantly reduced in γ-TmT-treated mammary tumors. In an orthotopic model in which human MCF-7 breast cancer cells were injected into the mammary fat pad of immunodeficient mice, γ-TmT inhibited E2-dependent tumor growth at all the doses tested. In conclusion, γ-TmT reduced mammary tumor development, in part through decreased E2 availability and reduced oxidative stress in mammary tissues; γ-TmT could thus be an effective agent for the prevention and treatment of E2-induced breast cancer.

Indexed as

AnimalsAntioxidantsCell Line, TumorCyclin-Dependent Kinase Inhibitor p27DinoprostEstradiolEstrogensFemalegamma-TocopherolGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesImmunohistochemistryMammary Glands, AnimalMammary Neoplasms, AnimalMammary Neoplasms, Experimental8-epi-prostaglandin F2alphaAntioxidantsCdkn1b protein, ratCyclin-Dependent Kinase Inhibitor p27DinoprostEstradiolEstrogensgamma-TocopherolPPAR gammaProliferating Cell Nuclear AntigenPTEN PhosphohydrolasePten protein, ratRNA, Messenger

Identifiers

PMID26130252
PMCPMC4560648
OpenAlexW2332203406

What OpenQuestion holds

Textmetadata
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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.