Evidence map›Paper›PMID 8825137›Full record

ArticleBreast cancer research and treatment1996

Characterization of the estrogen receptor transfected MCF10A breast cell line 139B6.

M J Pilat, J K Christman, S C Brooks

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Breast cancer research and treatment, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TARGETING THE GENOTOXIC EFFECTS OF ESTROGENS.Drug discovery today. Disease mechanisms · 2012
    Article
  8. Estrogens, regulation of p53 and breast cancer risk: a balancing act.Cellular and molecular life sciences : CMLS · 2010
    Review
  9. Article
  10. Article
  11. Progesterone receptor A-regulated gene expression in mammary organoid cultures.The Journal of steroid biochemistry and molecular biology · 2009
    Article
  12. Review
  13. Estrogen responsiveness and control of normal human breast proliferation.Journal of mammary gland biology and neoplasia · 1998
    Review
  14. 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

3 authors at 2 institutions in 1 country.

M J PilatDepartment of Biochemistry, Wayne State University School of Medicine, Detroit, MI 48201, USA.
J K Christman
S C Brooks
Wayne State University · USMolecular Oncology (United States) · US

Funding

ESTROGEN STRUCTURE/RECEPTOR FUNCTION RELATIONSHIPSR01CA044771 · NCI · WAYNE STATE UNIVERSITY · PI BROOKS, SAMUEL C · 1987 to 1994
–
NCI NIH HHS CA44771
6 · The paper itself

Abstract

There has been increasing evidence which suggests that abnormal expression of the estrogen receptor (ER) protein in nonmalignant breast tissue may be important in the carcinogenic process. To examine the effects of ER expression in immortalized nonmalignant mammary epithelial cells, an expression vector containing human ER cDNA was transfected into the ER negative human breast cells, MCF10A. Characterization of a clone stably expressing ER, 139B6, provided evidence for the regulated synthesis of a functional ER capable of binding estradiol-17 beta (E2) and undergoing processing. Expression of the ER gene did not enable E2 to stimulate endogenous genes [progesterone receptor (PgR), pS2, cathepsin D and TGF alpha] which normally respond to estrogens in breast cancer cells. The ER in 139B6 cells was, however, capable of inducing expression of an ERE-regulated reporter gene, indicating its ability to interact with transcriptional machinery. Furthermore, cultures in log growth displayed a slight increase in doubling time in the presence of E2. These results indicate that ER expression alone is not sufficient to induce a transformed phenotype. Thus, the 139B6 cell line should provide a new model for determining what additional changes lead to increased growth potential in response to E2 and for exploring how E2 itself may help bring about changes leading to progression of preneoplastic breast epithelial cells.

Indexed as

ActinsBreastBreast NeoplasmsCathepsin DCell LineEstradiolFemaleHumansReceptors, EstrogenRNA, MessengerTransfectionActinsCathepsin DEstradiolReceptors, EstrogenRNA, Messenger

Identifiers

PMID8825137
OpenAlexW2080872706

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.