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2. Supplementary Table 1 from CYP3A4*22 Genotype and Systemic Exposure Affect Paclitaxel-Induced Neurotoxicity

Author

de Graan, Anne-Joy M., primary, Elens, Laure, primary, Sprowl, Jason A., primary, Sparreboom, Alex, primary, Friberg, Lena E., primary, van der Holt, Bronno, primary, de Raaf, Pleun J., primary, de Bruijn, Peter, primary, Engels, Frederike K., primary, Eskens, Ferry A.L.M., primary, Wiemer, Erik A.C., primary, Verweij, Jaap, primary, Mathijssen, Ron H.J., primary, and van Schaik, Ron H.N., primary

Published
2023
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3. Supplementary Figure 1 from CYP3A4*22 Genotype and Systemic Exposure Affect Paclitaxel-Induced Neurotoxicity

Author

de Graan, Anne-Joy M., primary, Elens, Laure, primary, Sprowl, Jason A., primary, Sparreboom, Alex, primary, Friberg, Lena E., primary, van der Holt, Bronno, primary, de Raaf, Pleun J., primary, de Bruijn, Peter, primary, Engels, Frederike K., primary, Eskens, Ferry A.L.M., primary, Wiemer, Erik A.C., primary, Verweij, Jaap, primary, Mathijssen, Ron H.J., primary, and van Schaik, Ron H.N., primary

Published
2023
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4. Primary cardioprotection with dexrazoxane in patients with childhood cancer who are expected to receive anthracyclines: recommendations from the International Late Effects of Childhood Cancer Guideline Harmonization Group

Author

de Baat, Esmée C, primary, van Dalen, Elvira C, additional, Mulder, Renée L, additional, Hudson, Melissa M, additional, Ehrhardt, Matthew J, additional, Engels, Frederike K, additional, Feijen, Elizabeth A M, additional, Grotenhuis, Heynric B, additional, Leerink, Jan M, additional, Kapusta, Livia, additional, Kaspers, Gertjan J L, additional, Merkx, Remy, additional, Mertens, Luc, additional, Skinner, Roderick, additional, Tissing, Wim J E, additional, de Vathaire, Florent, additional, Nathan, Paul C, additional, Kremer, Leontien C M, additional, Mavinkurve-Groothuis, Annelies M C, additional, and Armenian, Saro, additional

Published
2022
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10. CYP3A4*22 Genotype and Systemic Exposure Affect Paclitaxel-Induced Neurotoxicity

Author

de Graan, Anne-Joy M., Elens, Laure, Sprowl, Jason A., Sparreboom, Alex, Friberg, Lena E., van der Holt, Bronno, de Raaf, Pleun J., de Bruijn, Peter, Engels, Frederike K., Eskens, Ferry A. L. M., Wiemer, Erik A. C., Verweij, Jaap, Mathijssen, Ron H. J., van Schaik, Ron H. N., de Graan, Anne-Joy M., Elens, Laure, Sprowl, Jason A., Sparreboom, Alex, Friberg, Lena E., van der Holt, Bronno, de Raaf, Pleun J., de Bruijn, Peter, Engels, Frederike K., Eskens, Ferry A. L. M., Wiemer, Erik A. C., Verweij, Jaap, Mathijssen, Ron H. J., and van Schaik, Ron H. N.

Abstract

Purpose: Paclitaxel is used for the treatment of several solid tumors and displays a high interindividual variation in exposure and toxicity. Neurotoxicity is one of the most prominent side effects of paclitaxel. This study explores potential predictive pharmacokinetic and pharmacogenetic determinants for the onset and severity of neurotoxicity. Experimental Design: In an exploratory cohort of patients (n = 261) treated with paclitaxel, neurotoxicity incidence, and severity, pharmacokinetic parameters and pharmacogenetic variants were determined. Paclitaxel plasma concentrations were measured by high-performance liquid chromatography or liquid chromatography/tandem mass spectrometry, and individual pharmacokinetic parameters were estimated from previously developed population pharmacokinetic models by nonlinear mixed effects modeling. Genetic variants of paclitaxel pharmacokinetics tested were CYP3A4*22, CYP2C8*3, CYP2C8*4, and ABCB1 3435 C>T. The association between CYP3A4*22 and neurotoxicity observed in the exploratory cohort was validated in an independent patient cohort (n = 239). Results: Exposure to paclitaxel ((log)AUC) was correlated with severity of neurotoxicity (P < 0.00001). Female CYP3A4*22 carriers were at increased risk of developing neurotoxicity (P = 0.043) in the exploratory cohort. CYP3A4*22 carrier status itself was not associated with pharmacokinetic parameters (CL, AUC, C-max, or T->0.05) of paclitaxel in males or females. Other genetic variants displayed no association with neurotoxicity. In the subsequent independent validation cohort, CYP3A4*22 carriers were at risk of developing grade 3 neurotoxicity (OR = 19.1; P = 0.001). Conclusions: Paclitaxel exposure showed a relationship with the severity of paclitaxel-induced neurotoxicity. In this study, female CYP3A4*22 carriers had increased risk of developing severe neurotoxicity during paclitaxel therapy. These observations may guide future individualization of paclitaxel treatment.

Published
2013
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11. CYP3A4*22 genotype and systemic exposure affect paclitaxel-induced neurotoxicity.

Author

UCL - SSS/LDRI - Louvain Drug Research Institute, de Graan, Anne-Joy M, Elens, Laure, Sprowl, Jason A, Sparreboom, Alex, Friberg, Lena E, van der Holt, Bronno, de Raaf, Pleun J, de Bruijn, Peter, Engels, Frederike K, Eskens, Ferry A L M, Wiemer, Erik A C, Verweij, Jaap, Mathijssen, Ron H J, van Schaik, Ron H N, UCL - SSS/LDRI - Louvain Drug Research Institute, de Graan, Anne-Joy M, Elens, Laure, Sprowl, Jason A, Sparreboom, Alex, Friberg, Lena E, van der Holt, Bronno, de Raaf, Pleun J, de Bruijn, Peter, Engels, Frederike K, Eskens, Ferry A L M, Wiemer, Erik A C, Verweij, Jaap, Mathijssen, Ron H J, and van Schaik, Ron H N

Abstract

Paclitaxel is used for the treatment of several solid tumors and displays a high interindividual variation in exposure and toxicity. Neurotoxicity is one of the most prominent side effects of paclitaxel. This study explores potential predictive pharmacokinetic and pharmacogenetic determinants for the onset and severity of neurotoxicity.

Published
2013

12. CYP3A4*22 Genotype and Systemic Exposure Affect Paclitaxel-Induced Neurotoxicity

Author

de Graan, Anne-Joy M., primary, Elens, Laure, additional, Sprowl, Jason A., additional, Sparreboom, Alex, additional, Friberg, Lena E., additional, van der Holt, Bronno, additional, de Raaf, Pleun J., additional, de Bruijn, Peter, additional, Engels, Frederike K., additional, Eskens, Ferry A.L.M., additional, Wiemer, Erik A.C., additional, Verweij, Jaap, additional, Mathijssen, Ron H.J., additional, and van Schaik, Ron H.N., additional

Published
2013
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15. Medicinal cannabis in oncology

Author

Engels, Frederike K., primary, de Jong, Floris A., additional, Mathijssen, Ron H.J., additional, Erkens, Joëlle A., additional, Herings, Ron M., additional, and Verweij, Jaap, additional

Published
2007
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20. In Reply

Author

de Jong, Floris A., primary, Engels, Frederike K., additional, Mathijssen, Ron H.J., additional, van Zuylen, Lia, additional, Verweij, Jaap, additional, Peters, Remco P.H., additional, and Sparreboom, Alex, additional

Published
2005
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22. Neuropsychiatric side effects of interferon-alfa therapy.

Author

Van Gool AR, Kruit WH, Engels FK, Stoter G, Bannink M, and Eggermont AM

Subjects
Clinical Trials as Topic, Depressive Disorder chemically induced, Depressive Disorder psychology, Dose-Response Relationship, Drug, Humans, Immunologic Factors administration & dosage, Immunologic Factors therapeutic use, Interferon-alpha administration & dosage, Interferon-alpha therapeutic use, Mental Disorders psychology, Syndrome, Immunologic Factors adverse effects, Interferon-alpha adverse effects, Mental Disorders chemically induced
Abstract

Aim: Immunotherapy with interferon-alfa (IFN-alfa) is used in a variety of diseases in- and outside clinical trials (e.g., chronic hepatitis, melanoma, chronic myelogenous leukemia, renal cell carcinoma, multiple myeloma). Treatment with IFN-alfa can cause (severe) neuropsychiatric side effects. The purpose of this article is to give an updated review of data on the incidence, manifestations and prediction of psychiatric side effects of immunotherapy with IFN-alfa. Furthermore, the article gives an overview of the management strategies and of the various theories on the pathophysiology of behavioural effects induced by cytokines., Methods: Use was made of computerized searches and of checking cross-references of articles and book chapters. The data on the incidence, manifestations and prediction are arranged by source of information, by target symptoms and by method of ascertainment., Results: Different sources of information exist, e.g. adverse event reports of clinical trials, case descriptions and research specifically targeted on neuropsychiatric side effects. IFN-alfa is capable of inducing depressive symptoms and syndromes; the evidence for the induction of other psychiatric side effects is weaker. The depressive syndromes induced by IFN-alfa are in need of a more precise characterization. The results of studies on prediction of side effects are contradictory. Guidelines on managing psychiatric side effects predominantly arise from practical experience and common sense. Patient education plays a pivotal role. At this moment, there is no comprehensive theory on the pathophysiology of cytokine-induced psychiatric side effects., Conclusion: There is sufficient empirical support for a causal relation between IFN-alfa and the development of depressive symptoms and syndromes. Practical management of neuropsychiatric side effects begins before the start of therapy and should consist of repeated patient education, drug treatment and supportive measures. There are diverging theories on the pathophysiological backgrounds.

Published
2003
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