Evidence map›Paper›PMID 21159643›Full record

ArticleCancer research2010

Tip30 deletion in MMTV-Neu mice leads to enhanced EGFR signaling and development of estrogen receptor-positive and progesterone receptor-negative mammary tumors.

Chengliang Zhang, Mikito Mori, Shenglan Gao, Aimin Li, Isamu Hoshino, Mark D Aupperlee, Sandra Z Haslam, Hua Xiao

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  15. Article
  16. TIP30: A Novel Tumor-Suppressor Gene.Oncology research · 2014
    Review
  17. Article
  18. Article
  19. Review
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 2 countries.

Chengliang ZhangDepartment of Biomedical and Integrative Physiology, College of Human Medicine, Michigan State University, 3193 Biomedical and Physical Sciences Building, East Lansing, MI 48824-3320, USA.
Mikito Mori
Shenglan Gao
Aimin Li
Isamu Hoshino
Mark D Aupperlee
Sandra Z Haslam
Hua Xiao
Southern Medical University · CNMichigan State University · USNanfang Hospital · CN

Funding

Breast Cancer and the Environment Research CenterU01ES012800 · NIEHS · MICHIGAN STATE UNIVERSITY · PI HASLAM, SANDRA Z · 2003 to 2009
$5.6M
The Role of A Transcription Cofactor in TumorigenesisR01DK066110 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIAO, HUA · 2004 to 2008
$1.3M
NCI NIH HHS U01 ES/CA 012800NIDDK NIH HHS R01 DK066110NIDDK NIH HHS R01 DK066110-01NIEHS NIH HHS U01 ES012800
6 · The paper itself

Abstract

Estrogen receptor-positive and progesterone receptor-negative (ER+/PR-) breast cancers account for 15% to 25% of all human breast cancers and display more aggressive malignant characteristics than ER+/PR+ cancers. However, the molecular mechanism underlying development of ER+/PR- breast cancers still remains elusive. We show here that Tip30 deletion dramatically accelerated the onset of mammary tumors in the MMTV-Neu mouse model of breast cancer. The mammary tumors arising in Tip30(-/-)/MMTV-Neu mice were exclusively ER+/PR-. The growth of these ER+/PR- tumors depends not only on estrogen but also on progesterone despite the absence of detectable PR. Tip30 is predominantly expressed in ER+ mammary epithelial cells, and its deletion leads to an increase in the number of phospho-ERα-positive cells in mammary glands and accelerated activation of Akt in MMTV-Neu mice. Moreover, we found that Tip30 regulates the EGFR pathway through controlling endocytic downregulation of EGFR protein level and signaling. Together, these findings suggest a novel mechanism in which loss of Tip30 cooperates with Neu activation to enhance the activation of Akt signaling, leading to the development of ER+/PR- mammary tumors.

Indexed as

AnimalsCell Transformation, NeoplasticErbB ReceptorsFemaleGenes, erbB-2Mammary Neoplasms, ExperimentalMammary Tumor Virus, MouseMiceMice, Inbred C57BLMice, NudeMice, TransgenicPhosphorylationProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, ProgesteroneRepressor ProteinsErbB ReceptorsProto-Oncogene Proteins c-aktReceptors, EstrogenReceptors, ProgesteroneRepressor ProteinsTip30 protein, mouseTumor Suppressor Proteins

Identifiers

PMID21159643
PMCPMC3074979
OpenAlexW2171841329

What OpenQuestion holds

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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.