Evidence map›Paper›PMID 24511377›Full record

ArticleInterface focus2013

Modelling the effect of GRP78 on anti-oestrogen sensitivity and resistance in breast cancer.

Jignesh H Parmar, Katherine L Cook, Ayesha N Shajahan-Haq, Pamela A G Clarke, Iman Tavassoly, Robert Clarke, John J Tyson, William T Baumann

Open access · bronzeAbstract read
In one paragraph

Article in Interface focus, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  14. Endocrine resistance in breast cancer--An overview and update.Molecular and cellular endocrinology · 2015
    Review
  15. 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

8 authors at 3 institutions in 1 country.

Jignesh H ParmarDepartment of Biological Sciences , Virginia Polytechnic Institute and State University , Blacksburg, VA 24061 , USA.
Katherine L CookDepartment of Oncology, Lombardi Comprehensive Cancer Center , Georgetown University Medical Center , Washington, DC 20057 , USA.
Ayesha N Shajahan-HaqDepartment of Oncology, Lombardi Comprehensive Cancer Center , Georgetown University Medical Center , Washington, DC 20057 , USA.
Pamela A G ClarkeDepartment of Oncology, Lombardi Comprehensive Cancer Center , Georgetown University Medical Center , Washington, DC 20057 , USA.
Iman TavassolyDepartment of Biological Sciences , Virginia Polytechnic Institute and State University , Blacksburg, VA 24061 , USA.
Robert ClarkeDepartment of Oncology, Lombardi Comprehensive Cancer Center , Georgetown University Medical Center , Washington, DC 20057 , USA.
John J TysonDepartment of Biological Sciences , Virginia Polytechnic Institute and State University , Blacksburg, VA 24061 , USA.
William T BaumannBradley Department of Electrical and Computer Engineering , Virginia Polytechnic Institute and State University , Blacksburg, VA 24061 , USA.
Virginia Tech · USGeorgetown University · USMedStar Washington Hospital Center · US

Funding

TRAINING GRANT IN TUMOR BIOLOGYT32CA009686 · NCI · GEORGETOWN UNIVERSITY · PI ANNA Tate RIEGEL, DAVID J ROBBINS · 1996 to 2026
$10.8M
Novel Targets in Endocrine ResponsivenessU54CA149147 · NCI · GEORGETOWN UNIVERSITY · PI MADHAVAN, SUBHA · 2010 to 2014
$6.9M
NCI NIH HHS T32 CA009686NCI NIH HHS U54 CA149147
6 · The paper itself

Abstract

Understanding the origins of resistance to anti-oestrogen drugs is of critical importance to many breast cancer patients. Recent experiments show that knockdown of GRP78, a key gene in the unfolded protein response (UPR), can re-sensitize resistant cells to anti-oestrogens, and overexpression of GRP78 in sensitive cells can cause them to become resistant. These results appear to arise from the operation and interaction of three cellular systems: the UPR, autophagy and apoptosis. To determine whether our current mechanistic understanding of these systems is sufficient to explain the experimental results, we built a mathematical model of the three systems and their interactions. We show that the model is capable of reproducing previously published experimental results and some new data gathered specifically for this paper. The model provides us with a tool to better understand the interactions that bring about anti-oestrogen resistance and the effects of GRP78 on both sensitive and resistant breast cancer cells.

Indexed as

anti-oestrogen resistanceautophagybreast cancerGRP78mathematical modellingunfolded protein response

Identifiers

PMID24511377
PMCPMC3915832
OpenAlexW2114456941

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.