Evidence map›Paper›PMID 19665836›Full record

ArticleCancer letters2010

Wnt signaling can substitute for estrogen to induce division of ERalpha-positive cells in a mouse mammary tumor model.

Melissa Mastroianni, Soyoung Kim, Young Chul Kim, Amanda Esch, Caroline Wagner, Caroline M Alexander

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. miR-190 enhances endocrine therapy sensitivity by regulating SOX9 expression in breast cancer.Journal of experimental & clinical cancer research : CR · 2019
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

6 authors at 1 institution in 1 country.

Melissa MastroianniMcArdle Lab for Cancer Research, University of Wisconsin, 1400 University Avenue, Madison 53706, United States.
Soyoung Kim
Young Chul Kim
Amanda Esch
Caroline Wagner
Caroline M Alexander
University of Wisconsin–Madison · US

Funding

The Role of Syndecan-1 in Mouse Mammary NeoplasiaR01CA090877 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI ALEXANDER, CAROLINE M · 2002 to 2012
$3.0M
MOLECULAR MECHS REGULATING CANCER CELL PROLIFERATIONT32CA009681 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI HOFFMANN, F. MICHAEL · 1993 to 2007
$1.9M
NCI NIH HHS R01 CA090877NCI NIH HHS T32 CA009681NCI NIH HHS T32 CA09681
6 · The paper itself

Abstract

The interaction of estrogen with the estrogen receptor (ER, principally ERalpha) induces growth of human breast tumor cells. In contrast, ERalpha-positive cells have been described as non-dividing cells in normal breast (though estrogen stimulation of ERalpha cells directs the division of neighboring cells). However, there is a small sub-population of cells in normal mammary tissue that are ERalpha-positive, that can divide, and therefore share this property with human breast tumor cells. In order to investigate their pattern of growth regulation, we measured the fraction of dividing ERalpha(+) cells during normal growth and compared that to glands stimulated by oncogenic Wnt effectors. First, we found there was no difference between the rate of division of ERalpha(+) cells and ERalpha(-) cells, whether the population was responding to estrogen or Wnt mitogens. The proportion of dividing ERalpha(+) mammary epithelial cells was increased (10x) in response to pregnancy, and similar increases were observed in response to ectopic Wnt signaling. We propose that Wnt signaling can substitute for estrogen to drive total population growth (that includes ERalpha(+) cells). Although the E-ERalpha-derived mitogenic response is situated in a minority of the luminal cells, and the Wnt-LRP5/6-derived mitogenic response is situated in a minority of basal cells, overall, the growth response of the mammary epithelial population is remarkably similar.

Indexed as

Estrogen Receptor alphaSignal TransductionAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationDisease Models, AnimalFemaleHumansImmunohistochemistryMammary Glands, AnimalMiceMice, TransgenicPregnancyWnt ProteinsEstrogen Receptor alphaWnt Proteins

Identifiers

PMID19665836
PMCPMC2874254
OpenAlexW2097332180

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.