ArticleTrends in molecular medicine2014
Simplifying the complexity of resistance heterogeneity in metastasis.
Article in Trends in molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed.
- Female breast cancer classification using immunohistochemistry biomarkers staining in Botswana.BMC cancer · 2025Article
- Radial Data Visualization-Based Step-by-Step Eliminative Algorithm to Predict Colorectal Cancer Patients' Response to FOLFOX Therapy.International journal of molecular sciences · 2024Article
- Mitogen signaling strength and duration can control cell cycle decisions.Science advances · 2024Review
- Interplay of Darwinian Selection, Lamarckian Induction and Microvesicle Transfer on Drug Resistance in Cancer.Scientific reports · 2019Article
- Review: Precision medicine and driver mutations: Computational methods, functional assays and conformational principles for interpreting cancer drivers.PLoS computational biology · 2019Review
- Redundancy: a critical obstacle to improving cancer therapy.Cancer research · 2015Article
- Niche inheritance: a cooperative pathway to enhance cancer cell fitness through ecosystem engineering.Journal of cellular biochemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The main goal of treatment regimens for metastasis is to control growth rates, not eradicate all cancer cells. Mathematical models offer methodologies that incorporate high-throughput data with dynamic effects on net growth. The ideal approach would simplify, but not over-simplify, a complex problem into meaningful and manageable estimators that predict the response of a patient to specific treatments. We explore here three fundamental approaches with different assumptions concerning resistance mechanisms in which the cells are categorized into either discrete compartments or described by a continuous range of resistance levels. We argue in favor of modeling resistance as a continuum, and demonstrate how integrating cellular growth rates, density-dependent versus exponential growth, and intratumoral heterogeneity improves predictions concerning the resistance heterogeneity of metastases.
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Registered trials
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.