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- W2205815637 abstract "The emergence of drug resistance is a recurrent theme in targeted cancer therapies; thus, the understanding and conquering of drug resistance have become focal points in precision cancer medicine. While the biochemical and genetic mechanisms underlying drug resistance are diverse and complex, the state-of-art technologies (high-throughput sequencing, functional genomics, model systems, etc.) leading to the understanding of such mechanisms have been a consistent force driving the advancement of this field. Although many genes have been found to impact drug resistance, the limited convergence from multiple studies indicates that we are still at the beginning stage of unearthing the entire drug-resistance repertoire. New genomic technologies, preclinical models, and computational methodologies are poised to further accelerate the development of this new field. A major obstacle in precision cancer medicine is the inevitable resistance to targeted therapies. Tremendous effort and progress has been made over the past few years to understand the biochemical and genetic mechanisms underlying drug resistance, with the goal to eventually overcome such daunting challenges. Diverse mechanisms, such as secondary mutations, oncogene bypass, and epigenetic alterations, can all lead to drug resistance, and the number of known involved genes is growing rapidly, thus providing many possibilities to overcome resistance. The finding of these mechanisms and genes invariably requires the application of genomic and functional genomic approaches to tumors or cancer models. In this review, we briefly highlight the major drug-resistance mechanisms known today, and then focus primarily on the technological approaches leading to the advancement of this field. A major obstacle in precision cancer medicine is the inevitable resistance to targeted therapies. Tremendous effort and progress has been made over the past few years to understand the biochemical and genetic mechanisms underlying drug resistance, with the goal to eventually overcome such daunting challenges. Diverse mechanisms, such as secondary mutations, oncogene bypass, and epigenetic alterations, can all lead to drug resistance, and the number of known involved genes is growing rapidly, thus providing many possibilities to overcome resistance. The finding of these mechanisms and genes invariably requires the application of genomic and functional genomic approaches to tumors or cancer models. In this review, we briefly highlight the major drug-resistance mechanisms known today, and then focus primarily on the technological approaches leading to the advancement of this field. the CRISPR-Cas system functions as an adaptive immune system in bacteria and has been adapted to engineer mammalian genomes in an efficient manner. The CRISPR-Cas9 screen has become a powerful functional genetic screening approach suitable for mammalian genetic models, including human cancer cells and mouse models. a human cancer cell line panel established by the NCI Developmental Therapeutics Program to discover novel anticancer drugs; they are frequently studied cancer cell lines. a collection of ORF sequences are introduced into cancer cells through transfection in a multiwell format, and the cells are then exposed to single or combinatory agents before being tested for changes in their viability. an organ-bud grown in vitro, based on stem cells from a particular organ to form a 3D epithelial structure while retaining its tissue identity. a xenograft created when cancerous tissue from a patient's primary tumor is implanted directly into an immunodeficient mouse. These models avoid prior selection in tissue culture and may more closely mimic human cancer compared with cell line-derived xenografts. a member of the protein tyrosine kinases family, containing high-affinity cell surface receptors for many polypeptide growth factors, cytokines, and hormones. similar to an ORF screen, but with the ORF libraries replaced by siRNA or shRNA libraries. a situation in which cells can tolerate the loss of one of two genes but their simultaneous inactivation causes lethality. Chemical synthetic lethality screens, drug enhancer screens, or ‘drop out’ screens are all intended to identify ways to achieve synthetic lethality. small-molecule drugs that inhibit tyrosine kinases. Tyrosine kinases are enzymes responsible for the activation of many proteins that can be regulated by phosphorylation in signal transduction cascades." @default.
- W2205815637 created "2016-06-24" @default.
- W2205815637 creator A5060146570 @default.
- W2205815637 creator A5082995478 @default.
- W2205815637 date "2016-02-01" @default.
- W2205815637 modified "2023-10-17" @default.
- W2205815637 title "Understanding the Genetic Mechanisms of Cancer Drug Resistance Using Genomic Approaches" @default.
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