Evidence map›Paper›PMID 20824048›Full record

ArticleNeoplasia (New York, N.Y.)2010

Somatic expression of PyMT or activated ErbB2 induces estrogen-independent mammary tumorigenesis.

Michael J Toneff, Zhijun Du, Jie Dong, Jian Huang, Parisa Sinai, James Forman, Susan Hilsenbeck, Rachel Schiff, Shixia Huang, Yi Li

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

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  16. The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011
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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.

Michael J ToneffLester & Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030, USA.
Zhijun Du
Jie Dong
Jian Huang
Parisa Sinai
James Forman
Susan Hilsenbeck
Rachel Schiff
Shixia Huang
Yi Li
Baylor College of Medicine · USThe University of Texas Southwestern Medical Center · US

Funding

IMMUNE POTENTIAL OF ANIMALS LACKING CLASS IA MOLECULESR01AI045764 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI FORMAN, JAMES M · 1999 to 2010
$2.8M
Oncogene susceptibility: physiological state & breast cell differentiationR01CA124820 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LI, YI · 2010 to 2014
$1.5M
PROGENITOR CELLS AND ONCOGENE TARGETS IN BREAST CANCERR01CA113869 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LI, YI · 2005 to 2009
$1.4M
NCI NIH HHS CA113869NCI NIH HHS CA124820NCI NIH HHS R01 CA113869NCI NIH HHS R01 CA124820NIAID NIH HHS AI45764NIAID NIH HHS R01 AI045764
6 · The paper itself

Abstract

Estrogen signaling is required for the proliferation of normal breast epithelial cells. However, prophylactic inhibition of estrogen signaling fails to prevent 56% of human breast cancer cases. The underlying mechanism is not well understood. Aberrant activation of growth factor signaling is known to provide alternative proliferation pathways in breast cells that are fully transformed, but it is not known whether activation of growth factor signaling can substitute for estrogen signaling in causing aberrant proliferation in the normal breast epithelium. Here, we report that in a retrovirus-based somatic mouse model (replication-competent ALV-LTR splice acceptor/tumor virus A) that closely mimics the evolution of sporadic human breast cancers, mammary epithelial cells harboring PyMT or activated ErbB2 evolve into tumors independent of estrogen or other ovarian functions in contrast to previous observations of estrogen-dependent cancer formation in germ line mouse models of ErbB2 activation. Importantly, ErbB2 activation in normal mammary cells causes estrogen-independent proliferation in both estrogen receptor (ER)-negative cells as well as in normally quiescent ER-positive cells. Therefore, aberrant activation of growth factor signaling contributes to estrogen-independent proliferation of both preneoplastic and cancerous mammary cells, and prophylactic therapy against both growth factor signaling and estrogen signaling may need to be considered in women with increased risk of breast cancer.

Indexed as

Genes, erbB-2AnimalsAntigens, Viral, TumorCarcinoma, Ductal, BreastCell Transformation, NeoplasticDrug Resistance, NeoplasmEnzyme ActivationErb-b2 Receptor Tyrosine KinasesEstrogensFemaleGene Expression Regulation, NeoplasticMammary Neoplasms, ExperimentalMiceMice, TransgenicPolyomavirusTransfectionAntigens, Viral, TumorErbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesEstrogens

Identifiers

PMID20824048
PMCPMC2933692
OpenAlexW1935043580

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.