Evidence map›Paper›PMID 21105047›Full record

ArticleInternational journal of cancer2011

Markers of fibrosis and epithelial to mesenchymal transition demonstrate field cancerization in histologically normal tissue adjacent to breast tumors.

Kristina A Trujillo, Christopher M Heaphy, Minh Mai, Keith M Vargas, Anna C Jones, Phung Vo, Kimberly S Butler, Nancy E Joste, Marco Bisoffi, Jeffrey K Griffith

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

57 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Opioid System and Epithelial-Mesenchymal Transition.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Field cancerization in breast cancer.The Journal of pathology · 2022
    Review
  17. Histamine H4 Receptor Expression in Triple-negative Breast Cancer: An Exploratory Study.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022
    Article
  18. Review
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Kristina A TrujilloDepartment of Biochemistry and Molecular Biology, MSC08 4670 University of New Mexico, Albuquerque, NM 87173, USA.
Christopher M Heaphy
Minh Mai
Keith M Vargas
Anna C Jones
Phung Vo
Kimberly S Butler
Nancy E Joste
Marco Bisoffi
Jeffrey K Griffith
University of New Mexico · USJohns Hopkins University · US

Funding

ZUNI HEALTH INITIATIVE-PILOT STUDYP20RR016480 · NCRR · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI ZHANG, PENG F · 2001 to 2011
$33.7M
NCI NIH HHS P30CA118110NCRR NIH HHS P20 RR016480NCRR NIH HHS RR0164880
6 · The paper itself

Abstract

Previous studies have shown that a field of genetically altered but histologically normal tissue extends 1 cm or more from the margins of human breast tumors. The extent, composition and biological significance of this field are only partially understood, but the molecular alterations in affected cells could provide mechanisms for limitless replicative capacity, genomic instability and a microenvironment that supports tumor initiation and progression. We demonstrate by microarray, qRT-PCR and immunohistochemistry a signature of differential gene expression that discriminates between patient-matched, tumor-adjacent histologically normal breast tissues located 1 cm and 5 cm from the margins of breast adenocarcinomas (TAHN-1 and TAHN-5, respectively). The signature includes genes involved in extracellular matrix remodeling, wound healing, fibrosis and epithelial to mesenchymal transition (EMT). Myofibroblasts, which are mediators of wound healing and fibrosis, and intra-lobular fibroblasts expressing MMP2, SPARC, TGF-β3, which are inducers of EMT, were both prevalent in TAHN-1 tissues, sparse in TAHN-5 tissues, and absent in normal tissues from reduction mammoplasty. Accordingly, EMT markers S100A4 and vimentin were elevated in both luminal and myoepithelial cells, and EMT markers α-smooth muscle actin and SNAIL were elevated in luminal epithelial cells of TAHN-1 tissues. These results identify cellular processes that are differentially activated between TAHN-1 and TAHN-5 breast tissues, implicate myofibroblasts as likely mediators of these processes, provide evidence that EMT is occurring in histologically normal tissues within the affected field and identify candidate biomarkers to investigate whether or how field cancerization contributes to the development of primary or recurrent breast tumors.

Indexed as

BiomarkersBreastBreast NeoplasmsCell Transformation, NeoplasticEpithelial CellsEpithelial-Mesenchymal TransitionFemaleFibrosisGene ExpressionHumansMyofibroblastsBiomarkers

Identifiers

PMID21105047
PMCPMC3249233
OpenAlexW2076061584

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.