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| http://dx.doi.org/10.18632/oncoscience.325 | DOI Listing |
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DNA damage and its links to neuronal aging and degeneration.
Neuron
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Departments of Psychiatry, Neuroscience, and Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Peter O' Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
DNA damage is a major risk factor for the decline of neuronal functions with age and in neurodegenerative diseases. While how DNA damage causes neurodegeneration is still being investigated, innovations over the past decade have provided significant insights into this issue. Breakthroughs in next-generation sequencing methods have begun to reveal the characteristics of neuronal DNA damage hotspots and the causes of DNA damage.
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Cross Cancer Institute, University of Alberta, Edmonton, AB, Canada.
Non-small-cell lung cancer (NSCLC) is a highly heterogeneous disease that is frequently associated with a host of known oncogenic alterations. Advances in molecular diagnostics and drug development have facilitated the targeting of novel alterations such that the majority of NSCLC patients have driver mutations that are now clinically actionable. The goal of this review is to gain insights into clinical research and development principles by summary, analysis, and discussion of data on agents targeting known alterations in oncogene-driven, advanced NSCLC beyond those in the and the .
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Research Group in Biological Anthropology, Biological Anthropology Unit, Department of Animal Biology, Vegetal Biology and Ecology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Mitochondrial DNA (mtDNA) analysis is crucial for understanding human population structure and genetic diversity. However, post-mortem DNA damage poses challenges, that make analysis difficult. DNA preservation is affected by environmental conditions which, among other factors, complicates the differentiation of endogenous variants from artefacts in ancient mtDNA mix profiles.
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The course of evolution is strongly shaped by interaction between mutations. Such epistasis can yield rugged sequence-function maps and constrain the availability of adaptive paths. While theoretical intuition is often built on global statistics of large, homogeneous model landscapes, mutagenesis measurements necessarily probe a limited neighborhood of a reference genotype.
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