FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2546056126> ?p ?o ?g. }

• W2546056126 endingPage "230" @default.
• W2546056126 startingPage "214" @default.
• W2546056126 abstract "Overlaying different genetic tests for association, selection, and linkage can increase the likelihood of identifying genetic variants responsible for drug resistance. Artemisinin resistance is mediated by mutations in the kelch13 locus, but other interacting partners or pathways may be involved in modulating this resistance. Genetic variants responsible for resistance to partner drugs paired with artemisinin-based compounds in combination therapy are a growing concern and may involve multiple loci and copy-number variations as well as nucleotide changes. Technological advances in generating and analyzing genome sequences to identify copy-number variations as well as SNPs directly from patient isolates promise to aid the discovery of drug-resistance loci. Increasing use of drugs for malaria elimination campaigns will likely alter parasite population structure and increase drug resistance, and it will be a challenge for genome-wide association studies to identify drug-resistance loci from among a largely shared genetic background. Increasing awareness of ‘anti-correlated’ drug combinations that are active against alternative allelic versions of the target locus are changing the way drug combinations may be deployed and provide opportunities for novel combination therapies or strategies to offset or reduce the risk of emerging drug resistance. Population genetic strategies that leverage association, selection, and linkage have identified drug-resistant loci. However, challenges and limitations persist in identifying drug-resistance loci in malaria. In this review we discuss the genetic basis of drug resistance and the use of genome-wide association studies, complemented by selection and linkage studies, to identify and understand mechanisms of drug resistance and response. We also discuss the implications of nongenetic mechanisms of drug resistance recently reported in the literature, and present models of the interplay between nongenetic and genetic processes that contribute to the emergence of drug resistance. Throughout, we examine artemisinin resistance as an example to emphasize challenges in identifying phenotypes suitable for population genetic studies as well as complications due to multiple-factor drug resistance. Population genetic strategies that leverage association, selection, and linkage have identified drug-resistant loci. However, challenges and limitations persist in identifying drug-resistance loci in malaria. In this review we discuss the genetic basis of drug resistance and the use of genome-wide association studies, complemented by selection and linkage studies, to identify and understand mechanisms of drug resistance and response. We also discuss the implications of nongenetic mechanisms of drug resistance recently reported in the literature, and present models of the interplay between nongenetic and genetic processes that contribute to the emergence of drug resistance. Throughout, we examine artemisinin resistance as an example to emphasize challenges in identifying phenotypes suitable for population genetic studies as well as complications due to multiple-factor drug resistance." @default.
• W2546056126 created "2016-11-04" @default.
• W2546056126 creator A5027581906 @default.
• W2546056126 creator A5061240448 @default.
• W2546056126 creator A5080134164 @default.
• W2546056126 creator A5081926124 @default.
• W2546056126 date "2017-03-01" @default.
• W2546056126 modified "2023-09-23" @default.
• W2546056126 title "Genome-Wide Association Studies of Drug-Resistance Determinants" @default.
• W2546056126 cites W1499342446 @default.
• W2546056126 cites W1694215848 @default.
• W2546056126 cites W1782975369 @default.
• W2546056126 cites W1865107143 @default.
• W2546056126 cites W1893108453 @default.
• W2546056126 cites W1922669960 @default.
• W2546056126 cites W1961772435 @default.
• W2546056126 cites W1966054814 @default.
• W2546056126 cites W1966124517 @default.
• W2546056126 cites W1967215049 @default.
• W2546056126 cites W1969571661 @default.
• W2546056126 cites W1973235308 @default.
• W2546056126 cites W1974313358 @default.
• W2546056126 cites W1976176203 @default.
• W2546056126 cites W1977845940 @default.
• W2546056126 cites W1980975034 @default.
• W2546056126 cites W1985812034 @default.
• W2546056126 cites W1993347313 @default.
• W2546056126 cites W2001761048 @default.
• W2546056126 cites W2004803790 @default.
• W2546056126 cites W2008166606 @default.
• W2546056126 cites W2009259923 @default.
• W2546056126 cites W2010485888 @default.
• W2546056126 cites W2015791647 @default.
• W2546056126 cites W2016102145 @default.
• W2546056126 cites W2019851585 @default.
• W2546056126 cites W2022803608 @default.
• W2546056126 cites W2023639417 @default.
• W2546056126 cites W2025946325 @default.
• W2546056126 cites W2026791163 @default.
• W2546056126 cites W2033314986 @default.
• W2546056126 cites W2035826427 @default.
• W2546056126 cites W2036512457 @default.
• W2546056126 cites W2037350416 @default.
• W2546056126 cites W2037542225 @default.
• W2546056126 cites W2038945865 @default.
• W2546056126 cites W2040110445 @default.
• W2546056126 cites W2042345412 @default.
• W2546056126 cites W2043458699 @default.
• W2546056126 cites W2047009134 @default.
• W2546056126 cites W2049016946 @default.
• W2546056126 cites W2050052884 @default.
• W2546056126 cites W2055730063 @default.
• W2546056126 cites W2057943518 @default.
• W2546056126 cites W2061649602 @default.
• W2546056126 cites W2062095500 @default.
• W2546056126 cites W2064792211 @default.
• W2546056126 cites W2066343605 @default.
• W2546056126 cites W2067958295 @default.
• W2546056126 cites W2069047837 @default.
• W2546056126 cites W2074875016 @default.
• W2546056126 cites W2075152545 @default.
• W2546056126 cites W2075935548 @default.
• W2546056126 cites W2076050649 @default.
• W2546056126 cites W2076086908 @default.
• W2546056126 cites W2077046573 @default.
• W2546056126 cites W2078889551 @default.
• W2546056126 cites W2079127050 @default.
• W2546056126 cites W2079451231 @default.
• W2546056126 cites W2081078606 @default.
• W2546056126 cites W2081729133 @default.
• W2546056126 cites W2082456955 @default.
• W2546056126 cites W2082680042 @default.
• W2546056126 cites W2086702905 @default.
• W2546056126 cites W2088967867 @default.
• W2546056126 cites W2089884239 @default.
• W2546056126 cites W2092116492 @default.
• W2546056126 cites W2094260046 @default.
• W2546056126 cites W2097263871 @default.
• W2546056126 cites W2099198335 @default.
• W2546056126 cites W2100013190 @default.
• W2546056126 cites W2101546138 @default.
• W2546056126 cites W2102343384 @default.
• W2546056126 cites W2104355399 @default.
• W2546056126 cites W2104700616 @default.
• W2546056126 cites W2108932995 @default.
• W2546056126 cites W2110994467 @default.
• W2546056126 cites W2113516463 @default.
• W2546056126 cites W2115787721 @default.
• W2546056126 cites W2121485644 @default.
• W2546056126 cites W2122534122 @default.
• W2546056126 cites W2122652489 @default.
• W2546056126 cites W2123390069 @default.
• W2546056126 cites W2123470783 @default.
• W2546056126 cites W2124634096 @default.
• W2546056126 cites W2126938337 @default.
• W2546056126 cites W2127733438 @default.
• W2546056126 cites W2127754721 @default.
• W2546056126 cites W2129174519 @default.

• next