Any advice on Cytochromes P450 (CYP) panel on chemotherapy? What's your gene list? Clinically, Roche got an FDA-approved panel but is outdated and limited - do you have an updated list?
Cytochromes P450 (CYP) are a major source of variability in drug pharmacokinetics and response. Of 57 putatively functional human CYPs only about a dozen enzymes, belonging to the CYP1, 2, and 3 families, are responsible for the biotransformation of most foreign substances including 70–80% of all drugs in clinical use. The highest expressed forms in liver are CYPs 3A4, 2C9, 2C8, 2E1, and 1A2, while 2A6, 2D6, 2B6, 2C19 and 3A5 are less abundant and CYPs 2J2, 1A1, and 1B1 are mainly expressed extrahepatically.http://www.sciencedirect.com/science/article/pii/S0163725813000065
Dear Chengwen,
This paper may shed some light on your question:
Enzyme and Microbial Technology 60 (2014) 24–31. Chemotherapy pro-drug activation by biocatalytic virus-like nanoparticles containing cytochrome P450
Lorena Sánchez-Sánchez et al.
Hi Shengwen,
Replying to your question regarding CYP panel on chemotherapy, it's very important to keep in mind that even within an FDA-approved panel one must operate with pre-assessment of, say, each individual intra-tumor expression of CYP and its monooxygenase activity towards the drug used. The latter pattern is major source of variability in drug pharmacokinetics and response. For instance, early studies by Patterson et al. (1995) identifying P450R as a key player in tirapazamine bioactivation. This evidence came from studying the in vitro sensitivity of breast tumor cell lines to tirapazamine that exhibited an inherent 6-fold range in the CYP activity. Using short exposures (3 h) to tirapazamine, the level of P450R correlated strongly with the extent of tirapazamine toxicity in hypoxic conditions. However, aerobic sensitivity was also measured following both short-term (3 h) and prolonged (96 h) exposures to tirapazamine and was also shown to be dependent on P450R activity.
Besy wishes,
Ilya
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