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edensity F98Y

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Molecular Biology and Evolution 2009 26(9):2041-2046; doi:10.1093/molbev/msp111
Thomas E. Keller, Ian J. Molineux, and James J. Bull

Abstract

Viruses are notoriously capable of evolving resistance to drugs. However, if the endpoint of resistance evolution is only partial escape, a feasible strategy should be to stack drugs, so the combined effect of partial inhibition by several drugs results in net inhibition.

by Benoit Witkowski, Antoine Berry, Françoise Benoit-Vical
Drug Resistance Updates (Vol. 12, Issue 1, Pages 42-50)

Abstract

Considerable progress has been made in antimalarial research; however, much more effort is required to develop new antimalarials which overcome plasmodial resistance to clinically available drugs and limit the emergence of resistance.

by Annamaria Rapisarda, Giovanni Melillo
Drug Resistance Updates (Vol. 12, Issue 3, Pages 74-80)

Abstract

Angiogenesis, a key process for the growth of human cancers, has recently been exploited for the development of a novel class of cancer therapeutics that was thought to have wide applications and not to induce resistance in the clinical setting. Indeed, anti-angiogenic therapy has become an important option for the management of several human malignancies. However, a significant number of patients either do not respond to anti-angiogenic agents or fairly rapidly develop resistance.

by Jordan P. Volpato, Joelle N. Pelletier
Drug Resistance Updates (Vol. 12, Issue 1, Pages 28-41)

Abstract

Human dihydrofolate reductase (DHFR) is a primary target for antifolate drugs in cancer treatment, while DHFRs from Plasmodium falciparum, Plasmodium vivax and various bacterial species are primary targets in the treatment of malaria and bacterial infections. Mutations in each of these DHFRs can result in resistance towards clinically relevant antifolates.

by Ellen Weisberg, Rosemary Barrett, Qingsong Liu, Richard Stone, Nathanael Gray, James D. Griffin
Drug Resistance Updates (Vol. 12, Issue 3, Pages 81-89)

Abstract

An appealing therapeutic target in AML is constitutively activated, mutant FLT3, which is expressed in a subpopulation of AML patients and is generally a poor prognostic indicator in patients under the age of 65. There are currently several FLT3 inhibitors that are undergoing clinical investigation. However, the discovery of drug-resistant leukemic blast cells in FLT3 inhibitor-treated AML patients has prompted the search for novel, structurally diverse FLT3 inhibitors that could be alternatively used to circumvent drug resistance.