Evidence map›Paper›PMID 22161831›Full record

ArticleThe International journal of developmental biology2011

Non-steroidal anti-inflammatory drugs target the pro-tumorigenic extracellular matrix of the postpartum mammary gland.

Jenean O'Brien, Kirk Hansen, Dalit Barkan, Jeffrey Green, Pepper Schedin, Jenean O'Brien, Kirk Hansen, Dalit Barkan, Jeffrey Green, Pepper Schedin

Abstract read
In one paragraph

Article in The International journal of developmental biology, 2011. 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 12% 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, 52 citations in OpenAlex.

  1. Review
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  9. Postpartum breast cancer: mechanisms underlying its worse prognosis, treatment implications, and fertility preservation.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2021
    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

10 authors at 3 institutions in 2 countries.

Jenean O'BrienSchool of Medicine, Division of Medical Oncology, University of Colorado Anschutz Medical Campus, 12801 E 17th Ave, Aurora, CO, USA.
Kirk Hansen
Dalit Barkan
Jeffrey Green
Pepper Schedin
Jenean O'Brien
Kirk Hansen
Dalit Barkan
Jeffrey Green
Pepper Schedin
University of Colorado Anschutz Medical Campus · USNational Institutes of Health · USUniversity of Haifa · IL

Funding

LTQ FT-ICR Hybrid Mass Spectrometer PurchaseS10RR023015 · NCRR · UNIVERSITY OF COLORADO DENVER · PI HANSEN, KIRK C · 2007 to 2007
$1.1M
Endocrine Status of MG Stroma Alters Breast CA InvasionR01CA085944 · NCI · UNIVERSITY OF COLORADO DENVER · PI SCHEDIN, PEPPER J · 2001 to 2004
$1.1M
Methods for the Analysis of Tumor Extracellular MatrixR21CA132741 · NCI · UNIVERSITY OF COLORADO DENVER · PI HANSEN, KIRK C · 2010 to 2011
$361k
Intramural NIH HHSNCI NIH HHS R01 CA085944NCI NIH HHS R21 CA132741NCRR NIH HHS S10 RR023015
6 · The paper itself

Abstract

Breast cancer patients diagnosed postpartum have poor prognosis. The postpartum mammary gland undergoes tissue regression to return to the pre-pregnant state. This involution is characterized by wound healing programs known to be tumor promotional in other contexts. Previous studies have shown that mammary extracellular matrix (ECM) from nulliparous rats has tumor suppressive attributes, while mammary ECM from involuting mammary glands is promotional. In models of pregnancy-associated breast cancer, non-steroidal anti-inflammatory drug (NSAID) treatment targeted to postpartum involution inhibits tumor progression, in part by suppressing COX-2 dependent collagen deposition. Because mammary ECM proteins are coordinately regulated, NSAID treatment is anticipated to result in additional protective changes in the mammary extracellular matrix. Here, systemic NSAID treatment was utilized during postpartum involution to reduce mammary COX-2 activity. ECM was isolated from actively involuting glands of rats treated with NSAIDs and compared to ECM isolated from control-involution and nulliparous rats in 3D cell culture and xenograft assays. Compositional changes in ECM between groups were identified by proteomics. In four distinct 3D culture assays, normal and transformed mammary epithelial cells plated in NSAID-involution ECM, phenocopied cells plated in ECM from nulliparous rats rather than ECM from control-involution rats. Tumor cells mixed with NSAID-involution ECM and injected orthotopically in mice formed smaller tumors than cells mixed with control-involution ECM. Proteomic analyses identified and 3D culture assays implicated the ECM protein tenascin-C as a potential mediator of tumor progression during involution that is decreased by NSAID treatment. In summary, NSAID treatment decreases tumor-promotional attributes of postpartum involution mammary ECM.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCarcinogensCell Line, TumorCyclooxygenase 2Extracellular MatrixFemaleHumansMammary Glands, AnimalMammary Neoplasms, ExperimentalMicePostpartum PeriodPregnancyRatsRats, Sprague-DawleyTenascinAnti-Inflammatory Agents, Non-SteroidalCarcinogensCyclooxygenase 2Ptgs2 protein, ratTenascin

Identifiers

PMID22161831
PMCPMC13590027
OpenAlexW1992444004

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.