ArticleOncotarget2016
Drug resistance in cancer: molecular evolution and compensatory proliferation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed.
- Docetaxel Resistance in Breast Cancer: Current Insights and Future Directions.International journal of molecular sciences · 2025Review
- Resistance to FLT3 inhibitors involves different molecular mechanisms and reduces new DNA synthesis.Biochemistry and biophysics reports · 2025Article
- The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers.International journal of molecular sciences · 2024Review
- Advancements in precision nanomedicine design targeting the anoikis-platelet interface of circulating tumor cells.Acta pharmaceutica Sinica. B · 2024Review
- An evolutionary differential game for regulating the role of monoclonal antibodies in treating signalling pathways in oesophageal cancer.Royal Society open science · 2024Article
- Potts Hamiltonian Models and Molecular Dynamics Free Energy Simulations for Predicting the Impact of Mutations on Protein Kinase Stability.The journal of physical chemistry. B · 2024Article
- Modeling the Effect of Spatial Structure on Solid Tumor Evolution and Circulating Tumor DNA Composition.Cancers · 2024Article
- Modeling the effect of spatial structure on solid tumor evolution and ctDNA composition.bioRxiv : the preprint server for biology · 2023Article
- The design of TOPK inhibitors using structure-based pharmacophore modeling and molecular docking based on an MD-refined homology model.Molecular diversity · 2022Article
- Drug Metabolism for the Identification of Clinical Biomarkers in Breast Cancer.International journal of molecular sciences · 2022Review
- Evaluation of a CD13 and Integrin αFrontiers in oncology · 2022Article
- Anticancer drug resistance: An update and perspective.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2021Review
- Activation of Abl1 Kinase Explored Using Well-Tempered Metadynamics Simulations on an Essential Dynamics Sampled Path.Journal of chemical theory and computation · 2021Article
- Clinical utility of circulating tumor cells: an update.Molecular oncology · 2021Review
- Combating drug resistance in acute myeloid leukaemia by drug rotations: the effects of quizartinib and pexidartinib.Cancer cell international · 2021Article
- Isolating live cell clones from barcoded populations using CRISPRa-inducible reporters.Nature biotechnology · 2021Article
- The ovarian carcinoma risk with the polymorphisms of CYP1B1 come from the positive selection.American journal of translational research · 2021Article
- Extracellular Vesicle-Mediated Chemoresistance in Oral Squamous Cell Carcinoma.Frontiers in molecular biosciences · 2021Review
- 'What I cannot create, I do not understand': functionally validated synergism of metabolic and target site insecticide resistance.Proceedings. Biological sciences · 2020Article
- APOBEC3B-mediated corruption of the tumor cell immunopeptidome induces heteroclitic neoepitopes for cancer immunotherapy.Nature communications · 2020Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted therapies have revolutionized cancer treatment. Unfortunately, their success is limited due to the development of drug resistance within the tumor, which is an evolutionary process. Understanding how drug resistance evolves is a prerequisite to a better success of targeted therapies. Resistance is usually explained as a response to evolutionary pressure imposed by treatment. Thus, evolutionary understanding can and should be used in the design and treatment of cancer. In this article, drug-resistance to targeted therapies is reviewed from an evolutionary standpoint. The concept of apoptosis-induced compensatory proliferation (AICP) is developed. It is shown that AICP helps to explain some of the phenomena that are observed experimentally in cancers. Finally, potential drug targets are suggested in light of AICP.
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What OpenQuestion holds
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.