Evidence map›Paper›PMID 24010522›Full record

ArticleBMC cancer2013

Stromal matrix metalloprotease-13 knockout alters Collagen I structure at the tumor-host interface and increases lung metastasis of C57BL/6 syngeneic E0771 mammary tumor cells.

Seth W Perry, Jill M Schueckler, Kathleen Burke, Giuseppe L Arcuri, Edward B Brown

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

5 authors at 1 institution in 1 country.

Seth W PerryDepartment of Biomedical Engineering, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA. Seth_Perry@urmc.rochester.edu.
Jill M Schueckler
Kathleen Burke
Giuseppe L Arcuri
Edward B Brown
University of Rochester · US

Funding

The T32 Predoctoral Training Program in Immunology (PTPI)T32AI007285 · NIAID · UNIVERSITY OF ROCHESTER · PI Scott Andrew Gerber, JACQUES Robert · 1986 to 2026
$7.6M
Exploiting collagen organization to predict and prevent tumor metastasisDP2OD006501 · OD · UNIVERSITY OF ROCHESTER · PI BROWN, EDWARD BERNARD · 2009 to 2009
$2.3M
GSK3, endocytosis, and enhanced HIV infection: abused drugs and novel therapiesR21DA030256 · NIDA · UNIVERSITY OF ROCHESTER · PI PERRY, SETH · 2010 to 2011
$417k
NIAID NIH HHS T32 AI007285NIDA NIH HHS R21 DA030256NIH HHS 1DP2 OD006501-01
6 · The paper itself

Abstract

backgroundMatrix metalloproteases and collagen are key participants in breast cancer, but their precise roles in cancer etiology and progression remain unclear. MMP13 helps regulate collagen structure and has been ascribed largely harmful roles in cancer, but some studies demonstrate that MMP13 may also protect against tumor pathology. Other studies indicate that collagen's organizational patterns at the breast tumor-host interface influence metastatic potential. Therefore we investigated how MMP13 modulates collagen I, a principal collagen subtype in breast tissue, and affects tumor pathology and metastasis in a mouse model of breast cancer.

methodsTumors were implanted into murine mammary tissues, and their growth analyzed in Wildtype and MMP13 KO mice. Following extraction, tumors were analyzed for collagen I levels and collagen I macro- and micro-structural properties at the tumor-host boundary using immunocytochemistry and two-photon and second harmonic generation microscopy. Lungs were analyzed for metastases counts, to correlate collagen I changes with a clinically significant functional parameter. Statistical analyses were performed by t-test, analysis of variance, or Wilcoxon-Mann-Whitney tests as appropriate.

resultsWe found that genetic ablation of host stromal MMP13 led to: 1. Increased mammary tumor collagen I content, 2. Marked changes in collagen I spatial organization, and 3. Altered collagen I microstructure at the tumor-host boundary, as well as 4. Increased metastasis from the primary mammary tumor to lungs.

conclusionsThese results implicate host MMP13 as a key regulator of collagen I structure and metastasis in mammary tumors, thus making it an attractive potential therapeutic target by which we might alter metastatic potential, one of the chief determinants of clinical outcome in breast cancer. In addition to identifying stromal MMP13 is an important regulator of the tumor microenvironment and metastasis, these results also suggest that stromal MMP13 may protect against breast cancer pathology under some conditions, a finding with important implications for development of chemotherapies directed against matrix metalloproteases.

Indexed as

AnimalsCell Line, TumorCollagen Type IFemaleHumansLung NeoplasmsMammary Neoplasms, ExperimentalMatrix Metalloproteinase 13MiceMice, Inbred C57BLMice, KnockoutTransplantation, IsogeneicTumor BurdenCollagen Type IMatrix Metalloproteinase 13

Identifiers

PMID24010522
PMCPMC3766650
OpenAlexW2169064382

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.