Evidence map›Paper›PMID 21875931›Full record

ArticleMolecular cancer research : MCR2011

ADAM12 produced by tumor cells rather than stromal cells accelerates breast tumor progression.

Camilla Fröhlich, Camilla Nehammer, Reidar Albrechtsen, Pauliina Kronqvist, Marie Kveiborg, Atsuko Sehara-Fujisawa, Arthur M Mercurio, Ulla M Wewer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. ADAM12 promotes gemcitabine resistance by activating EGFR signaling pathway and induces EMT in bladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  5. Review
  6. Article
  7. Cancers · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Identification of ADAM12 as a Novel Basigin Sheddase.International journal of molecular sciences · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  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

8 authors at 3 institutions in 4 countries.

Camilla FröhlichDepartment of Biomedical Sciences and Biotech Research & Innovation Centre, University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark. ullaw@sund.ku.dk
Camilla Nehammer
Reidar Albrechtsen
Pauliina Kronqvist
Marie Kveiborg
Atsuko Sehara-Fujisawa
Arthur M Mercurio
Ulla M Wewer
University of Copenhagen · DKUniversity of Massachusetts Chan Medical School · USKyoto University · JP

Funding

INTEGRIN FUNCTION AND SIGNALING IN CARCINOMA PROGRESSIONR01CA080789 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MERCURIO, ARTHUR M · 1999 to 2012
$4.7M
MECHANISMS OF BREAST CARCINOMA SURVIVALR01CA089209 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MERCURIO, ARTHUR M · 2001 to 2010
$3.3M
NCI NIH HHS CA80789NCI NIH HHS R01 CA080789NCI NIH HHS R01 CA089209
6 · The paper itself

Abstract

Expression of ADAM12 is low in most normal tissues but is markedly increased in numerous human cancers, including breast carcinomas. We have previously shown that overexpression of ADAM12 accelerates tumor progression in a mouse model of breast cancer (PyMT). In this study, we found that ADAM12 deficiency reduces breast tumor progression in the PyMT model. However, the catalytic activity of ADAM12 seems to be dispensable for its tumor-promoting effect. Interestingly, we show that ADAM12 endogenously expressed in tumor-associated stroma in the PyMT model does not influence tumor progression, but that ADAM12 expression by tumor cells is necessary for tumor progression in these mice. This finding is consistent with our observation that in human breast carcinoma, ADAM12 is almost exclusively located in tumor cells and, only rarely, seen in the tumor-associated stroma. We hypothesized, however, that the tumor-associated stroma may stimulate ADAM12 expression in tumor cells, on the basis of the fact that TGF-β1 stimulates ADAM12 expression and is a well-known growth factor released from tumor-associated stroma. TGF-β1 stimulation of ADAM12-negative Lewis lung tumor cells induced ADAM12 synthesis, and growth of these cells in vivo induced more than 200-fold increase in ADAM12 expression. Our observation that ADAM12 expression is significantly higher in the terminal duct lobular units (TDLU) adjacent to human breast carcinoma compared with TDLUs found in normal breast tissue supports our hypothesis that tumor-associated stroma triggers ADAM12 expression.

Indexed as

ADAM12 ProteinADAM ProteinsAnimalsBreast NeoplasmsCell Growth ProcessesCell Line, TumorDisease ProgressionFemaleHumansImmunohistochemistryMaleMammary Neoplasms, ExperimentalMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutADAM12 ProteinADAM12 protein, humanAdam12 protein, mouseADAM ProteinsMembrane Proteins

Identifiers

PMID21875931
PMCPMC3219818
OpenAlexW2170699309

What OpenQuestion holds

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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.