scholarly journals The Molecular Basis of Anti-HCV Drug Resistance

2017 ◽  
Author(s):  
Shaina M. Lynch ◽  
George Y. Wu
Keyword(s):  
Drug Resistance ◽  
Molecular Basis

Molecular Basis of Drug Resistance in Mycobacterium tuberculosis

2014 ◽  
Vol 2 (3) ◽  
Author(s):  
Keira A. Cohen ◽  
William R. Bishai ◽  
Alexander S. Pym
Keyword(s):  
Drug Resistance ◽  
Mycobacterium Tuberculosis ◽  
Molecular Basis

scholarly journals Plasmodium vivax and Drug Resistance

2021 ◽  
Author(s):  
Puji Budi Setia Asih ◽  
Din Syafruddin
Keyword(s):  
Drug Resistance ◽  
Molecular Basis ◽  
Indirect Evidence ◽  
Antimalarial Drugs ◽  
In Vivo Studies ◽  
In Vitro Cultivation ◽  
Radical Cure ◽  
The Status

Resistance to antimalarial drugs is a threat to global efforts to eliminate malaria by 2030. Currently, treatment for vivax malaria uses chloroquine or ACT for uncomplicated P. vivax whereas primaquine is given to eliminate latent liver stage infections (a method known as radical cure). Studies on P. vivax resistance to antimalarials and the molecular basis of resistance lags far behind the P. falciparum as in vitro cultivation of the P. vivax has not yet been established. Therefore, data on the P. vivax resistance to any antimalarial drugs are generated through in vivo studies or through monitoring of antimalarial treatments in mixed species infection. Indirect evidence through drug selective pressure on the parasites genome, as evidenced by the presence of the molecular marker(s) for drug resistance in areas where P. falciparum and P. vivax are distributed in sympatry may reflect, although require validation, the status of P. vivax resistance. This review focuses on the currently available data that may represent the state-of-the art of the P. vivax resistance status to antimalarial to anticipate the challenge for malaria elimination by 2030.

Molecular Basis and Evolution of Multiple Drug Resistance in the Foodborne PathogenSalmonella entericaSerovar Ohio

2010 ◽  
Vol 7 (2) ◽  
pp. 189-198 ◽  
Author(s):  
Noelia Martínez ◽  
Irene Rodríguez ◽  
Rosaura Rodicio ◽  
María del Carmen Mendoza ◽  
María del Rosario Rodicio
Keyword(s):  
Drug Resistance ◽  
Molecular Basis ◽  
Multiple Drug Resistance ◽  
Multiple Drug

HIV Drug Resistance: Molecular Basis and Clinical Significance

2015 ◽  
pp. 179-190
Author(s):  
Mark A. Wainberg ◽  
Marilyn Smith ◽  
Julio S. G. Montaner ◽  
Kazushige Nagai ◽  
Avrum Spira ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Clinical Significance ◽  
Molecular Basis ◽  
Hiv Drug Resistance

c-Abl Kinase Inhibitors Overcome CD40-Mediated Drug Resistance in CLL.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3078-3078 ◽  
Author(s):  
Delfine Y. Hallaert ◽  
Annelieke Jaspers ◽  
Carel J. van Noesel ◽  
Marinus H.J. Van Oers ◽  
Arnon P. Kater ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Molecular Basis ◽  
Kinase Inhibitors ◽  
Lymphocytic Leukemia ◽  
Recent Analysis ◽  
Combination Strategies ◽  
Cd40 Stimulation ◽  
Erk Inhibition ◽  
Erk Activity

Abstract In chronic lymphocytic leukemia (CLL), proliferation centers reside in lymph node (LN) and possibly also bone marrow, where the environment protects CLL cells from apoptotic and cytotoxic triggers. This protective milieu may well contribute to the lack of curative chemotherapy in CLL, and our recent analysis of the distinct profiles of apoptosis regulators in CLL LN versus peripheral blood supports this notion (Smit et al., Blood 2007, 109: 1660). The aim of the present study was to define the molecular basis for the increased drug resistance and to search for novel strategies to circumvent it. To mimic the situation in CLL LN, we applied prolonged in vitro CD40 stimulation of CLL cells, which results in strong upregulation of anti-apoptotic Bcl-xL and Mcl-1. Moreover, we now also report a gradual reduction of Bim at the protein level, further contributing to the anti-apoptotic profile. Using specific inhibitors (PD98059 and MG132), we found that the decrease in Bim is due to ERK-mediated phosporylation and subsequent proteasomal degradation. ERK inhibition during CD40 triggering abrogated the decrease in Bim levels, but did however not re-establish sensitivity to various drugs (fludarabine, Velcade, Roscovitine). In chronic myeloid leukemia (CML), changes in Bcl-xL, Mcl-1 and Bim levels similar to those observed in our CLL/CD40 system are known to depend on BCR-Abl signaling. Therefore, we next applied c-Abl inhibitors Gleevec or Dasatinib in conjunction with CD40. Both drugs caused a profound reversal of most protective CD40 effects; ERK activity, Bim, Bcl-xL and Mcl-1 levels as well as sensitivity to subsequent drug treatment were restored to pre-CD40 values. These effects also occurred in CLL samples with dysfunctional p53 (n=3). Importantly, in CLL LN samples we also found strong ERK activation together with high Bcl-xL and Mcl-1 but low Bim levels, suggesting that there might be a c-Abl dependent survival pathway in proliferation centers. These data provide a molecular basis for combination strategies that could target refractory niches in CLL, using therapeutics that function independently of p53.

scholarly journals The Molecular Basis of Drug Resistance against Hepatitis C Virus NS3/4A Protease Inhibitors

2012 ◽  
Vol 8 (7) ◽  
pp. e1002832 ◽  
Author(s):  
Keith P. Romano ◽  
Akbar Ali ◽  
Cihan Aydin ◽  
Djade Soumana ◽  
Ayşegül Özen ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Protease Inhibitors ◽  
Molecular Basis

THE MOLECULAR BASIS OF DRUG RESISTANCE IN FAMILIAL HYPERINSULINISM: FROM BEDSIDE TO PETRI DISH.

1997 ◽  
Vol 24 (4) ◽  
pp. 477
Author(s):  
K. J. Lindley ◽  
M. J. Dunne ◽  
C. Kane ◽  
R. M. Shepherd ◽  
R. F.L. James ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Molecular Basis ◽  
Petri Dish
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