ArticlePloS one2012
Genome wide adaptations of Plasmodium falciparum in response to lumefantrine selective drug pressure.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- AbioRxiv : the preprint server for biology · 2026Article
- Plasmodium falciparum isolates: ex vivo drug response.The Journal of antimicrobial chemotherapy · 2025Article
- Unravelling the mode of action of the Tres Cantos Antimalarial Set (TCAMS): investigating the mechanism of potent antimalarial compounds potentially targeting the human serotonin receptor.Malaria journal · 2025Article
- Changes in KInternational journal of molecular sciences · 2023Review
- Decreased susceptibility of Plasmodium falciparum to both dihydroartemisinin and lumefantrine in northern Uganda.Nature communications · 2022Article
- Mechanistic basis for multidrug resistance and collateral drug sensitivity conferred to the malaria parasite by polymorphisms in PfMDR1 and PfCRT.PLoS biology · 2022Article
- The Knockout for G Protein-Coupled Receptor-Like PfSR25 Increases the Susceptibility of Malaria Parasites to the Antimalarials Lumefantrine and Piperaquine but Not to Medicine for Malaria Venture Compounds.Frontiers in microbiology · 2021Article
- Antimalarial Drug Resistance and Novel Targets for Antimalarial Drug Discovery.Infection and drug resistance · 2020Review
- Resistance to Artemisinin Combination Therapies (ACTs): Do Not Forget the Partner Drug!Tropical medicine and infectious disease · 2019Review
- Genetic resistance to purine nucleoside phosphorylase inhibition inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Plasmodium falciparum GPCR-like receptor SR25 mediates extracellular KScientific reports · 2017Article
- Amodiaquine resistance inWellcome open research · 2017Article
- Plasmodium Helical Interspersed Subtelomeric (PHIST) Proteins, at the Center of Host Cell Remodeling.Microbiology and molecular biology reviews : MMBR · 2016Review
- Article
- Chemogenomic profiling of Plasmodium falciparum as a tool to aid antimalarial drug discovery.Scientific reports · 2015Article
- Piperaquine and Lumefantrine resistance in Plasmodium berghei ANKA associated with increased expression of Ca2+/H+ antiporter and glutathione associated enzymes.Experimental parasitology · 2014Article
- Comparative impacts over 5 years of artemisinin-based combination therapies on Plasmodium falciparum polymorphisms that modulate drug sensitivity in Ugandan children.The Journal of infectious diseases · 2014Article
- Temporal changes in prevalence of molecular markers mediating antimalarial drug resistance in a high malaria transmission setting in Uganda.The American journal of tropical medicine and hygiene · 2014Article
- Role of Different Pfcrt and Pfmdr-1 Mutations in Conferring Resistance to Antimalaria Drugs in Plasmodium falciparum.Malaria research and treatment · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The combination therapy of the Artemisinin-derivative Artemether (ART) with Lumefantrine (LM) (Coartem®) is an important malaria treatment regimen in many endemic countries. Resistance to Artemisinin has already been reported, and it is feared that LM resistance (LMR) could also evolve quickly. Therefore molecular markers which can be used to track Coartem® efficacy are urgently needed. Often, stable resistance arises from initial, unstable phenotypes that can be identified in vitro. Here we have used the Plasmodium falciparum multidrug resistant reference strain V1S to induce LMR in vitro by culturing the parasite under continuous drug pressure for 16 months. The initial IC(50) (inhibitory concentration that kills 50% of the parasite population) was 24 nM. The resulting resistant strain V1S(LM), obtained after culture for an estimated 166 cycles under LM pressure, grew steadily in 378 nM of LM, corresponding to 15 times the IC(50) of the parental strain. However, after two weeks of culturing V1S(LM) in drug-free medium, the IC(50) returned to that of the initial, parental strain V1S. This transient drug tolerance was associated with major changes in gene expression profiles: using the PFSANGER Affymetrix custom array, we identified 184 differentially expressed genes in V1S(LM). Among those are 18 known and putative transporters including the multidrug resistance gene 1 (pfmdr1), the multidrug resistance associated protein and the V-type H+ pumping pyrophosphatase 2 (pfvp2) as well as genes associated with fatty acid metabolism. In addition we detected a clear selective advantage provided by two genomic loci in parasites grown under LM drug pressure, suggesting that all, or some of those genes contribute to development of LM tolerance--they may prove useful as molecular markers to monitor P. falciparum LM susceptibility.
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