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Mitotane Therapy in Adrenocortical Cancer Induces CYP3A4 and Inhibits 5α-Reductase, Explaining the Need for Personalized Glucocorticoid and Androgen Replacement
Author(s) -
Vasileios Chortis,
Angela E. Taylor,
Petra Schneider,
Jeremy Tomlinson,
Beverly Hughes,
Donna O’Neil,
Rossella Libé,
Bruno Allolio,
Xavier Bertagna,
Jérôme Bertherat,
Felix Beuschlein,
Martin Faßnacht,
Niki Karavitaki,
Massimo Mannelli,
Franco Mantero,
Giuseppe Opocher,
Emilio Porfiri,
Marcus Quinkler,
Mark Sherlock,
Massimo Terzolo,
Peter Nightingale,
Cedric Shackleton,
Paul M. Stewart,
Stefanie Hahner,
Wiebke Arlt
Publication year - 2012
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2012-2851
Subject(s) - mitotane , adrenocortical carcinoma , medicine , endocrinology , glucocorticoid , cyp3a4 , context (archaeology) , interquartile range , chemistry , cytochrome p450 , biology , metabolism , paleontology
Mitotane [1-(2-chlorophenyl)-1-(4-chlorophenyl)-2,2-dichloroethane] is the first-line treatment for metastatic adrenocortical carcinoma (ACC) and is also regularly used in the adjuvant setting after presumed complete removal of the primary tumor. Mitotane is considered an adrenolytic substance, but there is limited information on distinct effects on steroidogenesis. However, adrenal insufficiency and male hypogonadism are widely recognized side effects of mitotane treatment.

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