scholarly journals Drug Sensitization

2020 ◽  
Author(s):  
Keyword(s):  
2017 ◽  
Vol 3 (4) ◽  
pp. 301-305 ◽  
Author(s):  
Yumi Aoyama ◽  
Fumihisa Sawada ◽  
Eiichi Makino ◽  
Tetsuo Shiohara

Author(s):  
Mateusz Rytelewski ◽  
Adrian Buensuceso ◽  
Hon S. Leong ◽  
Bonnie J. Deroo ◽  
Ann F. Chambers ◽  
...  

2015 ◽  
Vol 11 (1) ◽  
Author(s):  
Katinka Ónodi-Nagy ◽  
Ágnes Kinyó ◽  
Angéla Meszes ◽  
Edina Garaczi ◽  
Lajos Kemény ◽  
...  

1986 ◽  
Vol 44 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Jean Louis Bec ◽  
Pascal Delrieu ◽  
Gérard Abravanel ◽  
Nicole Paillous

PEDIATRICS ◽  
1957 ◽  
Vol 19 (1) ◽  
pp. 84-87
Author(s):  
Alvin M. Mauer ◽  
William DeVaux ◽  
M. E. Lahey

A case of quinine induced thrombocytopenic purpura in a mother and her newborn born infant is presented. In-vitro confirmation of the presence of quinine-platelet "antibodies" in the plasma of both mother and infant was obtained just after delivery. Five months later the "antibody" was still demonstrable in the mother, though backing in the infant. It is suggested that the neonatal thrombocytopenic purpura in this infant resulted from transplacental passage of antibody and quinine from the mother. A careful search for possible drug sensitization seems warranted in other cases of neonatal thrombocytopenia not explained by other means.


Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1468-1468
Author(s):  
Gabriel G Vega ◽  
Luz A Franco-Cea ◽  
Sara Huerta-Yepez ◽  
Hector Mayani ◽  
Otoniel Martinez-Maza ◽  
...  

Abstract Introduction: The standard treatment of B-NHL consists of rituximab in combination with CHOP (RCHOP) and results in a significant clinical response. Rituximab inhibits cell-proliferation and inhibits cell survival/anti-apoptic signaling pathways. A subset of patients does not initially respond and a subset of responding patients develops resistance to RCHOP. The genetic engineering of a fusion protein, α-CD20-hIFN-α, was found to be active in the rituximab-resistant B-NHL cell lines. Objective: To investigate the underlying mechanism by which α-CD20-hIFN-α signals in the resistant lines. Hypothesis: We hypothesized that the treatment with the α-CD20-hIFN-α may result in the cooperation of both α-CD20 and hIFN-α and their interactions with corresponding receptors that will result in overriding α-CD20 blocked cell signaling. Methods: Rituximab-resistant cell lines, R-2F7 and R-Ramos, were used as models. Cell signaling was determined by western. Sensitivity to drug-induced apoptosis was done by activation of caspase 3 by flow cytometry. Results: Treatment of the R lines with α-CD20-hIFN-α resulted in the inhibition of cell growth and sensitization to doxorubicin-induced apoptosis. Treatment with single agents alone or combination was not effective. Treatment with the α-CD20-hIFN-α resulted in the inhibition of the NFκB and the p38 MAPK pathways. In addition, the hIFN-mediated signaling pathway, namely, PKC-d, was also inhibited by the α-CD20-hIFN-α.The role of PKC-d in drug sensitization was corroborated by the use of the specific inhibitor, Rotterin, which reversed the drug sensitization by α-CD20-hIFN-α and doxorubicin Conclusion: The ability of the α-CD20-hIFN-α to inhibit cell survival and anti-apoptotic pathways, that was not achieved with single agents or combination, suggested that there may be a crosslinking of the CD20 and hIFN-α receptors by α-CD20-hIFN-α and results in triggering the cells via both receptors and inhibiting intracellular survival pathways and sensitization to drug apoptosis. Clinical Implication: The findings also suggest the potential therapeutic application of the combination of α-CD20-hIFN-α and drugs for the treatment of patients resistant to RCHOP. Disclosures No relevant conflicts of interest to declare.


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