Evidence map›Paper›PMID 32842890›Full record

ArticleJournal of the Royal Society, Interface2020

Mathematical modelling of breast cancer cells in response to endocrine therapy and Cdk4/6 inhibition.

Wei He, Diane M Demas, Isabel P Conde, Ayesha N Shajahan-Haq, William T Baumann

Open access · hybridAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  8. OvercomingFrontiers in microbiology · 2024
    Article
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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

5 authors at 2 institutions in 1 country.

Wei HeProgram in Genetics, Bioinformatics, and Computational Biology, VT BIOTRANS, Virginia Tech, Blacksburg, VA, USA.
Diane M DemasDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Isabel P CondeDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Ayesha N Shajahan-HaqDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
William T BaumannDepartment of Electrical and Computer Engineering, Virginia Tech, Blacksburg, VA, USA.
Georgetown University · USVirginia Tech · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI STEPHEN W BYERS · 1990 to 2026
$71.5M
Optimizing Targeted Breast Cancer Therapy by Mathematical Modeling and Experimental StudiesR01CA201092 · NCI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI BAUMANN, WILLIAM THOMAS, SHAJAHAN-HAQ, AYESHA N. · 2016 to 2020
$2.0M
NCI NIH HHS P30 CA051008NCI NIH HHS R01 CA201092
6 · The paper itself

Abstract

Oestrogen receptor (ER)-positive breast cancer is responsive to a number of targeted therapies used clinically. Unfortunately, the continuous application of any targeted therapy often results in resistance to the therapy. Our ultimate goal is to use mathematical modelling to optimize alternating therapies that not only decrease proliferation but also stave off resistance. Toward this end, we measured levels of key proteins and proliferation over a 7-day time course in ER+ MCF-7 breast cancer cells. Treatments included endocrine therapy, either oestrogen deprivation, which mimics the effects of an aromatase inhibitor, or fulvestrant, an ER degrader. These data were used to calibrate a mathematical model based on key interactions between ER signalling and the cell cycle. We show that the calibrated model is capable of predicting the combination treatment of fulvestrant and oestrogen deprivation. Further, we show that we can add a new drug, palbociclib, to the model by measuring only two key proteins, cMyc and hyperphosphorylated RB1, and adjusting only parameters associated with the drug. The model is then able to predict the combination treatment of oestrogen deprivation and palbociclib. We illustrate the model's potential to explore protocols that limit proliferation and hold off resistance by not depending on any one therapy.

Indexed as

Breast NeoplasmsCyclin-Dependent Kinase 4Drug Resistance, NeoplasmFemaleFulvestrantHumansMCF-7 CellsModels, TheoreticalReceptors, EstrogenCDK4 protein, humanCyclin-Dependent Kinase 4FulvestrantReceptors, Estrogenbreast cancerendocrine therapymathematical modellingpalbociclibtherapy optimization

Identifiers

PMID32842890
PMCPMC7482571
OpenAlexW3080736866

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.