Evidence map›Paper›PMID 17113977›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2006

The role of estrogen in the initiation of breast cancer.

J Russo, Irma H Russo

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
191citing papers in PubMed, 4 pooled it
14.4field-weighted citation impact, top 1% 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

191 citing papers in PubMed, 4 syntheses or guidelines pooled it, 566 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Single nucleotide polymorphism 6q25.1 rs2046210 and increased risk of breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  5. Estrogen plus progestin and risk of benign proliferative breast disease.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2008
    Trial
  6. Article
  7. Review
  8. Article
  9. Review
  10. PARP-1 as a novel target in endocrine-resistant breast cancer.Journal of experimental & clinical cancer research : CR · 2025
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Breast cancer screening for transgender individuals with breast cancer susceptibility genes.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Article

131 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

J RussoBreast Cancer Research Laboratory, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA. j_russo@fccc.edu
Irma H Russo
Fox Chase Cancer Center · US

Funding

Center for Environment and Mammary Gland DevelopmentU01ES012771 · NIEHS · FOX CHASE CANCER CENTER · PI RUSSO, JOSE · 2003 to 2009
$11.1M
NIEHS NIH HHS U01 ES012771
6 · The paper itself

Abstract

Estrogens are considered to play a major role in promoting the proliferation of both the normal and the neoplastic breast epithelium. Their role as breast carcinogens has long been suspected and recently confirmed by epidemiological studies. Three major mechanisms are postulated to be involved in their carcinogenic effects: stimulation of cellular proliferation through their receptor-mediated hormonal activity, direct genotoxic effects by increasing mutation rates through a cytochrome P450-mediated metabolic activation, and induction of aneuploidy. Recently it has been fully demonstrated that estrogens are carcinogenic in the human breast by testing in an experimental system the natural estrogen 17beta-estradiol (E(2)) by itself or its metabolites 2-hydroxy, 4-hydroxy, and 16-a-hydroxy-estradiol (2-OH-E(2), 4-OH-E(2), and 16-alpha-OH E(2)), respectively, by inducing neoplastic transformation of human breast epithelial cells (HBEC) MCF-10F in vitro to a degree at least similar to that induced by the chemical carcinogen benz(a)pyrene (BP). Neither Tamoxyfen (TAM) nor ICI-182,780 abrogated the transforming efficiency of estrogen or its metabolites. The E(2) induced expression of anchorage independent growth, loss of ductulogenesis in collagen, invasiveness in Matrigel, is associated with the loss of 9p11-13 and only invasive cells that exhibited a 4p15.3-16 deletion were tumorigenic. Tumors were poorly differentiated ER-alpha and progesterone receptor negative adenocarcinomas that expressed keratins, EMA and E-cadherin. The E(2) induced tumors and tumor-derived cell lines exhibited loss of chromosome 4, deletions in chromosomes 3p12.3-13, 8p11.1-21, 9p21-qter, and 18q, and gains in 1p, and 5q15-qter. The induction of complete transformation of the human breast epithelial cell MCF-10F in vitro confirms the carcinogenicity of E(2), supporting the concept that this hormone could act as an initiator of breast cancer in women. This model provides a unique system for understanding the genomic changes that intervene for leading normal cells to tumorigenesis and for testing the functional role of specific genomic events taking place during neoplastic transformation.

Indexed as

Breast NeoplasmsCell ProliferationCell Transformation, NeoplasticChromosome AberrationsEstrogensHumansNeoplasm InvasivenessEstrogens

Identifiers

PMID17113977
PMCPMC1832080
OpenAlexW2091340779

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.