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Andrew Collins
Researcher at University of Oslo
Publications - 733
Citations - 44066
Andrew Collins is an academic researcher from University of Oslo. The author has contributed to research in topics: Comet assay & DNA damage. The author has an hindex of 100, co-authored 684 publications receiving 40634 citations. Previous affiliations of Andrew Collins include Norwegian University of Life Sciences & Pontifical Xavierian University.
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Establishing the background level of base oxidation in human lymphocyte DNA: results of an interlaboratory validation study
TL;DR: The ESCODD consortium of mainly European laboratories has attempted to minimize this artifact and to provide standard, reliable protocols for sample preparation and analysis as mentioned in this paper. But the accuracy of low levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in DNA is hampered by the ease with which guanine is oxidized during preparation of DNA for analysis.
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The essential comet assay: a comprehensive guide to measuring DNA damage and repair
Amaya Azqueta,Andrew Collins +1 more
TL;DR: The comet assay has been modified to detect various base alterations, by including digestion of nucleoids with a lesion-specific endonuclease, and modifications to measure cellular antioxidant status and different types of DNA repair.
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Extended tracts of homozygosity in outbred human populations
TL;DR: The results suggest that multiple-megabase-scale ancestral haplotypes persist in outbred human populations in broad genomic regions which have lower than average recombination rates.
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JAK2 haplotype is a major risk factor for the development of myeloproliferative neoplasms.
Amy V. Jones,Andrew Chase,Richard T. Silver,David Oscier,Katerina Zoi,Y. Lynn Wang,Holger Cario,Heike L. Pahl,Andrew Collins,Andreas Reiter,Francis H. Grand,Nicholas C.P. Cross +11 more
TL;DR: It is reported here that JAK2V617F-associated disease is strongly associated with a specific constitutional Jak2 haplotype, designated 46/1, in all three disease entities compared to healthy controls and provides a model whereby a constitutional genetic factor is associated with an increased risk of acquiring a specific somatic mutation.
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Oxidative DNA damage, antioxidants, and cancer.
TL;DR: It seems that efficient antioxidant defences together with DNA repair maintain a steady‐state level of damage representing minimal risk to cell or organism.