Defective cell cycle checkpoints as targets for anti-cancer therapies.
Abstract
Conventional chemotherapeutics target the proliferating fraction of cells in the patient's body, which will include the tumor cells, but are also toxic to actively proliferating normal tissues. Cellular stresses, such as those imposed by chemotherapeutic drugs, induce cell cycle checkpoint arrest, and currently approaches targeting these checkpoints are being explored to increase the efficacy and selectivity of conventional chemotherapeutic treatments. Loss of a checkpoint may also make cancer cells more reliant on other mechanisms to compensate for the loss of this function, and these compensatory mechanisms may be targeted using synthetic lethal approaches. Here we will discuss the utility of targeting checkpoint defects as novel anti-cancer therapies.
Citations
Identifying CDKN3 Gene Expression as a Prognostic Biomarker in Lung Adenocarcinoma via Meta-analysis
CHK1 Inhibition Synergizes with Gemcitabine Initially by Destabilizing the DNA Replication Apparatus
Tyrosine Threonine Kinase Inhibition Eliminates Lung Cancers by Augmenting Apoptosis and Polyploidy.
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Cell Checkpoints & Regulators
Cell cycle checkpoints are a series of complex checkpoint mechanisms that detect DNA abnormalities and ensure that DNA replication and repair are complete before cell division. They are primarily regulated by cyclins, cyclin-dependent kinases, and the anaphase-promoting complex/cyclosome. Here is the latest research.