Evidence map›Paper›PMID 22265958›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2012

The development, application and limitations of breast cancer cell lines to study tamoxifen and aromatase inhibitor resistance.

Cynthie Wong, Shiuan Chen

Abstract readReview
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-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

24 citing papers in PubMed, 42 citations in OpenAlex.

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  7. Exploration of targeted anti-tumor therapy · 2022
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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

2 authors at 1 institution in 1 country.

Cynthie WongDivision of Tumor Cell Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
Shiuan Chen
Beckman Research Institute

Funding

AROMATASE AND BREAST CANCERR01CA044735 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI CHEN, SHIUAN · 1988 to 2009
$4.0M
ENDOCRINE DISRUPTING CHEMICALS AND AROMATASER01ES008258 · NIEHS · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI CHEN, SHIUAN · 1996 to 2009
$2.6M
Mechanism of Aromatase Inhibitor ResistanceF31CA123691 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI MASRI, SELMA · 2006 to 2008
$80k
NCI NIH HHS CA123691NCI NIH HHS CA44735NCI NIH HHS F31 CA123691NCI NIH HHS R01 CA044735NIEHS NIH HHS ES08258NIEHS NIH HHS R01 ES008258
6 · The paper itself

Abstract

Estrogen plays important roles in hormone receptor-positive breast cancer. Endocrine therapies, such as the antiestrogen tamoxifen, antagonize the binding of estrogen to estrogen receptor (ER), whereas aromatase inhibitors (AIs) directly inhibit the production of estrogen. Understanding the mechanisms of endocrine resistance and the ways in which we may better treat these types of resistance has been aided by the development of cellular models for resistant breast cancers. In this review, we will discuss what is known thus far regarding both de novo and acquired resistance to tamoxifen or AIs. Our laboratory has generated a collection of AI- and tamoxifen-resistant cell lines in order to comprehensively study the individual types of resistance mechanisms. Through the use of microarray analysis, we have determined that our cell lines resistant to a particular AI (anastrozole, letrozole, or exemestane) or tamoxifen are distinct from each other, indicating that these mechanisms can be quite complex. Furthermore, we will describe two novel de novo AI-resistant cell lines that were generated from our laboratory. Initial characterization of these cells reveals that they are distinct from our acquired AI-resistant cell models. In addition, we will review potential therapies which may be useful for overcoming resistant breast cancers through studies using endocrine resistant cell lines. Finally, we will discuss the benefits and shortcomings of cell models. Together, the information presented in this review will provide us a better understanding of acquired and de novo resistance to tamoxifen and AI therapies, the use of appropriate cell models to better study these types of breast cancer, which are valuable for identifying novel treatments and strategies for overcoming both tamoxifen and AI-resistant breast cancers.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic Agents, HormonalAromatase InhibitorsBreast NeoplasmsCell Line, TumorFemaleHumansSelective Estrogen Receptor ModulatorsTamoxifenTranslational Research, BiomedicalAntineoplastic Agents, HormonalAromatase InhibitorsSelective Estrogen Receptor ModulatorsTamoxifen

Identifiers

PMID22265958
PMCPMC3369003
OpenAlexW2046448644

What OpenQuestion holds

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LicenceTDM
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.