2013
DOI: 10.1186/1472-6947-13-s1-s4
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Rule-based multi-scale simulation for drug effect pathway analysis

Abstract: BackgroundBiological systems are robust and complex to maintain stable phenotypes under various conditions. In these systems, drugs reported the limited efficacy and unexpected side-effects. To remedy this situation, many pharmaceutical laboratories have begun to research combination drugs and some of them have shown successful clinical results. Complementary action of multiple compounds could increase efficacy as well as reduce side-effects through pharmacological interactions. However, experimental approach … Show more

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Cited by 14 publications
(6 citation statements)
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“…This constitutes the main obstacle for anticancer therapeutic success [72]. There are four major mechanisms that contribute to drug resistance in cancer cells: 1) Decreased uptake of water soluble drugs [73]; 2) changes in intracellular pathways that affect the potential of cytotoxic drugs to kill cells, including alterations in the cell cycle, DNA repair, apoptosis pathways, metabolism/elimination of drugs, or others [73][74][75]; 3) increased energy-dependent efflux of hydrophobic drugs mediated via overexpression of a family of energy-dependent transporters (known as ATP-binding cassette transporters) such as P-glycoprotein 1 (P-gp, ABCB1) or breast cancer resistance protein (ABCG2) amongst others [73]; and 4) intracellular detoxifiers such as antioxidants (e.g., glutathione) [76,77]. Multiple signaling pathways have been implicated in resistance to chemotherapy, and innovative therapeutic strategies to overcome these are urgently needed [78].…”
Section: Fucoidans and Drug Resistance In Cancermentioning
confidence: 99%
“…This constitutes the main obstacle for anticancer therapeutic success [72]. There are four major mechanisms that contribute to drug resistance in cancer cells: 1) Decreased uptake of water soluble drugs [73]; 2) changes in intracellular pathways that affect the potential of cytotoxic drugs to kill cells, including alterations in the cell cycle, DNA repair, apoptosis pathways, metabolism/elimination of drugs, or others [73][74][75]; 3) increased energy-dependent efflux of hydrophobic drugs mediated via overexpression of a family of energy-dependent transporters (known as ATP-binding cassette transporters) such as P-glycoprotein 1 (P-gp, ABCB1) or breast cancer resistance protein (ABCG2) amongst others [73]; and 4) intracellular detoxifiers such as antioxidants (e.g., glutathione) [76,77]. Multiple signaling pathways have been implicated in resistance to chemotherapy, and innovative therapeutic strategies to overcome these are urgently needed [78].…”
Section: Fucoidans and Drug Resistance In Cancermentioning
confidence: 99%
“…Molecular targets of phytochemicals were collected from the DrugBank, the Drug Combination Database (DCDB) [ 26 ], the Comparative Toxicogenomics Database (CTD) [ 27 ], MATADOR [ 28 ], STITCH [ 29 ] and TTD [ 30 ] databases, and gene-phenotype associations were collected from the CTD database. A protein-protein interaction (PPI) network, including 19,093 nodes and 270,970 edges, was obtained from BioGrid version 3.4.136 [ 31 ] and the Context-Oriented Directed Associations (CODA) system [ 32 ]. A phenotypic network was collected from UMLS in the 2017AA version [ 33 ].…”
Section: Methodsmentioning
confidence: 99%
“…In addition, we used the integrated PPI network (12,492 proteins and 82,694 interactions) by HPRD, I2D, and IntAct from HIPPIE [ 21 – 24 , 26 ]. A rule format based on our previous work was used to describe the PPI network [ 29 ]. The DDI side effects were downloaded from TWOSIDES ( http://www.pharmgkb.org/downloads/ ) [ 15 ].…”
Section: Methodsmentioning
confidence: 99%