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Development of Hif1α pharmacogenomic mutation models to study individual variations in drug action for tumor hypoxia: An in silico approach
Author(s) -
P. K. Krishnan Namboori,
Vaisali Balasubramaniam
Publication year - 2021
Publication title -
journal of pharmacy and bioallied sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.268
H-Index - 36
eISSN - 0976-4879
pISSN - 0975-7406
DOI - 10.4103/jpbs.jpbs_766_21
Subject(s) - in silico , computational biology , pharmacogenomics , population , biology , drug , homology modeling , tirapazamine , genetics , drug resistance , docking (animal) , gene , mutation , drug action , hypoxia (environmental) , bioinformatics , pharmacology , medicine , chemistry , biochemistry , nursing , environmental health , organic chemistry , cytotoxicity , oxygen , in vitro , enzyme
Tumor hypoxia, a predominant feature of solid tumor produces drug resistance that significantly impacts a patient's clinical outcomes. Hypoxia-inducible factor 1-alpha (HIF1α) is the major mutation involved in establishing the microenvironment. As a consequence of its involvement in pathways that enable rapid tumor growth, it creates resistance to chemotherapeutic treatments. The propensity of medications to demonstrate drug action often diverges according to the genetic composition. The aim of this study is therefore to examine the effect of population-dependent drug response variations using mutation models.