ReviewNature reviews. Clinical oncology2011
Targeted therapy in GIST: in silico modeling for prediction of resistance.
Review in Nature reviews. Clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 72 citations in OpenAlex.
- Mutational landscape of gastrointestinal stromal tumors using next-generation sequencing of a 73-gene panel.World journal of surgical oncology · 2025Article
- Computed tomography radiogenomics: A potential tool for prediction of molecular subtypes in gastric stromal tumor.World journal of gastrointestinal oncology · 2024Article
- Molecular Mechanisms of Gastrointestinal Stromal Tumors and Their Impact on Systemic Therapy Decision.Cancers · 2023Review
- Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022Review
- Molecular rationale for SARS-CoV-2 spike circulating mutations able to escape bamlanivimab and etesevimab monoclonal antibodies.Scientific reports · 2021Article
- Computational Alanine Scanning and Structural Analysis of the SARS-CoV-2 Spike Protein/Angiotensin-Converting Enzyme 2 Complex.ACS nano · 2020Article
- HIF-1α regulates cellular metabolism, and Imatinib resistance by targeting phosphogluconate dehydrogenase in gastrointestinal stromal tumors.Cell death & disease · 2020Article
- Molecular modelling evaluation of exon 18 His845_Asn848delinsPro PDGFRα mutation in a metastatic GIST patient responding to imatinib.Scientific reports · 2019Article
- Dichloro-Phenyl-Benzotriazoles: A New Selective Class of Human Respiratory Syncytial Virus Entry Inhibitors.Frontiers in chemistry · 2019Article
- β-Catenin in desmoid-type fibromatosis: deep insights into the role of T41A and S45F mutations on protein structure and gene expression.Molecular oncology · 2017Article
- Molecular and functional characterization of a new 3' end KIT juxtamembrane deletion in a duodenal GIST treated with neoadjuvant Imatinib.Oncotarget · 2017Article
- The Role of Mast Cells in Molding the Tumor Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2015Article
- Killing two birds with one stone: a case of GIST and supervening CML.BMJ case reports · 2015Article
- Role of genetic and molecular profiling in sarcomas.Current treatment options in oncology · 2015Review
- Smoothened (SMO) receptor mutations dictate resistance to vismodegib in basal cell carcinoma.Molecular oncology · 2015Article
- Insight into molecular dynamics simulation of BRAF(V600E) and potent novel inhibitors for malignant melanoma.International journal of nanomedicine · 2015Article
- Molecular dynamics reveal BCR-ABL1 polymutants as a unique mechanism of resistance to PAN-BCR-ABL1 kinase inhibitor therapy.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Through the open door: Preferential binding of dasatinib to the active form of BCR-ABL unveiled by in silico experiments.Molecular oncology · 2013Article
- Are two better than one? A novel double-mutant KIT in GIST that responds to Imatinib.Molecular oncology · 2013Article
- Comprehensive Analysis of ETS Family Members in Melanoma by Fluorescence In Situ Hybridization Reveals Recurrent ETV1 Amplification.Translational oncology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elucidation of the genetic processes leading to neoplastic transformation has identified cancer-promoting molecular alterations that can be selectively targeted by rationally designed therapeutic agents. Protein kinases are druggable targets and have been studied intensively. New methodologies--including crystallography and three-dimensional modeling--have allowed the rational design of potent and selective kinase inhibitors that have already reached the clinical stage. However, despite the clinical success of kinase-targeted therapies, most patients that respond eventually relapse as a result of acquired resistance. Darwinian-type selection of secondary mutations seems to have a major role in this resistance. The emergence and/or expansion of tumor clones containing new mutations in the target kinase and that are drug-insensitive have been observed after chronic treatment. The resistance mechanisms to tyrosine kinase inhibitors, in particular secondary resistant mutations as a consequence of treatment, will be discussed in detail. In particular, this Review will focus on KIT and PDGFRA mutations, which are involved in the pathogenesis of gastrointestinal stromal tumors. Harnessing the selection of mutated variants developed to overcome these resistance mechanisms is an ongoing goal of current research and new strategies to overcome drug resistance is being envisaged.
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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.