ReviewCancer letters2009
Cancer driver mutations in protein kinase genes.
Review in Cancer letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled 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.
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
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- A meta-analysis of somatic mutations from next generation sequencing of 241 melanomas: a road map for the study of genes with potential clinical relevance.Molecular cancer therapeutics · 2014Pooled it
- Paradoxical non-catalytic kinase functions are driven by inhibitor-induced displacement of autoinhibitory domains.Molecular systems biology · 2026Article
- Uncovering the molecular basis of kinase activity and substrate recognition with phospho-PCA.bioRxiv : the preprint server for biology · 2025Article
- Exploring the mutational spectrum of key kinase genes PIK3CA, BRAF, EGFR, ALK and ROS1 in oral squamous cell carcinoma.BMC cancer · 2025Article
- Insight into the inhibitory activity of mangiferin and Silybin against HER2 and EGFR using theoretical and experimental approaches.Scientific reports · 2025Article
- MultiplexedbioRxiv : the preprint server for biology · 2025Article
- Report of an Extremely Rare Case of BRCA-Positive Head and Neck Cancer: A New Disease on the Horizon?Cureus · 2025Article
- Article
- An allosteric switch between the activation loop and a c-terminal palindromic phospho-motif controls c-Src function.Nature communications · 2023Article
- Pathogenic mutation hotspots in protein kinase domain structure.Protein science : a publication of the Protein Society · 2023Article
- Evaluating the ability of end-point methods to predict the binding affinity tendency of protein kinase inhibitors.RSC advances · 2023Article
- Antitumor activity of triazine mimic antibiotics for DNA-binding implications (impressive activity in vitro against a variety of tumor types in the NCI-60 screen): NSC 710607 to fight HCT-116 human colon carcinoma cell lines in vivo using the hollow fiber assay and xenograft mouse models.Journal of cancer research and clinical oncology · 2023Article
- Large-scale pathogenicity prediction analysis of cancer-associated kinase mutations reveals variability in sensitivity and specificity of computational methods.Cancer medicine · 2023Article
- APOBECs: Our fickle friends?PLoS pathogens · 2023Article
- Unveiling pathogenic mutations in BRCA1 and BRCA2 genes across head and neck squamous cell carcinoma patients via next generation sequencing.American journal of cancer research · 2023Article
- Article
- Known allosteric proteins have central roles in genetic disease.PLoS computational biology · 2022Article
- Article
- How Far Are We from the Rapid Prediction of Drug Resistance Arising Due to Kinase Mutations?ACS omega · 2021Article
- The Clinical Kinase Index: A Method to Prioritize Understudied Kinases as Drug Targets for the Treatment of Cancer.Cell reports. Medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Recent studies investigating the genetic determinants of cancer suggest that some of the genetic alterations contributing to tumorigenesis may be inherited, but the vast majority is somatically acquired during the transition of a normal cell to a cancer cell. A systematic understanding of the genetic and molecular determinants of cancers has already begun to have a transformative effect on the study and treatment of cancer, particularly through the identification of a range of genetic alterations in protein kinase genes, which are highly associated with the disease. Since kinases are prominent therapeutic targets for intervention within the cancer cell, studying the impact that genomic alterations within them have on cancer initiation, progression, and treatment is both logical and timely. In fact, recent sequencing and resequencing (i.e., polymorphism identification) efforts have catalyzed the quest for protein kinase 'driver' mutations (i.e., those genetic alterations which contribute to the transformation of a normal cell to a proliferating cancerous cell) in distinction to kinase 'passenger' mutations which reflect mutations that merely build up in course of normal and unchecked (i.e., cancerous) somatic cell replication and proliferation. In this review, we discuss the recent progress in the discovery and functional characterization of protein kinase cancer driver mutations and the implications of this progress for understanding tumorigenesis as well as the design of 'personalized' cancer therapeutics that target an individual's unique mutational profile.
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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.