Evidence map›Paper›PMID 21948867›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2011

Activation of the aryl hydrocarbon receptor by TCDD inhibits mammary tumor metastasis in a syngeneic mouse model of breast cancer.

Tao Wang, Katie L Wyrick, Gary G Meadows, Tamara B Wills, Beth A Vorderstrasse

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Environmental chemicals, breast cancer progression and drug resistance.Environmental health : a global access science source · 2020
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Role of the aryl hydrocarbon receptor in carcinogenesis and potential as a drug target.Toxicological sciences : an official journal of the Society of Toxicology · 2013
    Review
  18. Review
  19. Article
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

5 authors at 2 institutions in 2 countries.

Tao WangDepartment of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, Washington 99164, USA.
Katie L Wyrick
Gary G Meadows
Tamara B Wills
Beth A Vorderstrasse
Washington State University · USInstitut de Médecine de la Reproduction · FR

Funding

Mechanisms on metastasis and survival in alcoholic miceR01AA007293 · NIAAA · WASHINGTON STATE UNIVERSITY · PI MEADOWS, GARY G · 1987 to 2010
$2.5M
Mechanistic efforts of chronic alcohol on tumor metastasis and survivalK05AA017149 · NIAAA · WASHINGTON STATE UNIVERSITY · PI MEADOWS, GARY G · 2008 to 2012
$1.1M
NIAAA NIH HHS K05 AA017149NIAAA NIH HHS K05AA017149NIAAA NIH HHS R01 AA007293NIAAA NIH HHS R01AA07293
6 · The paper itself

Abstract

Treatment with aryl hydrocarbon receptor (AhR) agonists can slow or reverse the growth of primary mammary tumors in rodents, which has fostered interest in developing selective AhR modulators for treatment of breast cancer. However, the major goal of breast cancer therapy is to inhibit metastasis, the primary cause of mortality in women with this disease. Studies conducted using breast cancer cell lines have demonstrated that AhR agonists suppress proliferation, invasiveness, and colony formation in vitro; however, further exploration using in vivo models of metastasis is warranted. To test the effect of AhR activation on metastasis, 4T1.2 mammary tumor cells were injected into the mammary gland fat pad of syngeneic Balb/c mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Primary tumor growth was monitored for 4 weeks, at which time metastasis was determined. TCDD treatment suppressed metastasis by approximately 50%, as measured both in the lung and in mammary glands at sites distant from the primary tumor. Primary tumor growth was not suppressed by TCDD exposure nor was proliferation of 4T1.2 cells affected by TCDD treatment in vitro. Taken together, these results suggest that the protective effect of AhR activation was selective for the metastatic process and not simply the result of a direct decrease in tumor cell proliferation or survival at the primary site. These observations in immunologically intact animals warrant further investigation into the mechanism of the protective effects of AhR activation and support the promise for use of AhR modulators to treat breast cancer.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationFemaleMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm MetastasisNeoplasm TransplantationPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID21948867
PMCPMC3216416
OpenAlexW1984678083

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.