Evidence map›Paper›PMID 22279420›Full record

ArticleJournal of carcinogenesis2011

Mouse models of estrogen receptor-positive breast cancer.

Shakur Mohibi, Sameer Mirza, Hamid Band, Vimla Band

Open access · goldAbstract read
In one paragraph

Article in Journal of carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Mouse ER+/PIK3CAOncogene · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. SRC IncreasesMolecular and cellular biology · 2018
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Shakur MohibiDepartment of Genetics, Cell Biology, and Anatomy, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska.
Sameer Mirza
Hamid Band
Vimla Band
University of Nebraska Medical Center · US

Funding

TYROSINE KINASE REGULATION VIA PROTEIN DEGRADATIONR01CA087986 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2000 to 2015
$4.2M
MOLECULAR CONTROL OF EGF RECEPTOR DOWN-REGULATIONR01CA099163 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2003 to 2012
$3.7M
Targeting Endocytic Recycling of EGF Receptor in Cancer R01CA105489 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2004 to 2014
$3.0M
A novel regulator of p53 functionR01CA096844 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2002 to 2011
$2.7M
High Capacity Nanocarriers for Cancer ChemotherapeuticsU01CA151806 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KABANOV, ALEXANDER V · 2010 to 2014
$2.0M
Ecd as a regulator of cell cycle and breast oncogenesisR01CA144027 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2011 to 2015
$1.6M
ErbB2 Downregulation Through HSP90 InhibitionR01CA116552 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2007 to 2011
$1.4M
NCI NIH HHS R01 CA087986NCI NIH HHS R01 CA096844NCI NIH HHS R01 CA099163NCI NIH HHS R01 CA105489NCI NIH HHS R01 CA116552NCI NIH HHS R01 CA144027NCI NIH HHS U01 CA151806
6 · The paper itself

Abstract

Breast cancer is the most frequent malignancy and second leading cause of cancer-related deaths among women. Despite advances in genetic and biochemical analyses, the incidence of breast cancer and its associated mortality remain very high. About 60 - 70% of breast cancers are Estrogen Receptor alpha (ER-α) positive and are dependent on estrogen for growth. Selective estrogen receptor modulators (SERMs) have therefore provided an effective targeted therapy to treat ER-α positive breast cancer patients. Unfortunately, development of resistance to endocrine therapy is frequent and leads to cancer recurrence. Our understanding of molecular mechanisms involved in the development of ER-α positive tumors and their resistance to ER antagonists is currently limited due to lack of experimental models of ER-α positive breast cancer. In most mouse models of breast cancer, the tumors that form are typically ER-negative and independent of estrogen for their growth. However, in recent years more attention has been given to develop mouse models that develop different subtypes of breast cancers, including ER-positive tumors. In this review, we discuss the currently available mouse models that develop ER-α positive mammary tumors and their potential use to elucidate the molecular mechanisms of ER-α positive breast cancer development and endocrine resistance.

Indexed as

Breast cancerestrogen receptor-αmouse models

Identifiers

PMID22279420
PMCPMC3263010
OpenAlexW2066166280

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.