High-dose itraconazole as a noncastrating therapy for a patient with biochemically recurrent prostate cancer

Daniel L. Suzman; Emmanuel S. Antonarakis

doi:10.1016/j.clgc.2013.11.015

High-dose itraconazole as a noncastrating therapy for a patient with biochemically recurrent prostate cancer

Daniel L. Suzman, Emmanuel S. Antonarakis

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

The role of androgen deprivation therapy (ADT) in biochemically recurrent prostate cancer is unclear and is associated with significant adverse events. Itraconazole has demonstrated clinical activity in castration-resistant prostate cancer (CRPC) and does not appear to mediate its activity by androgen suppression. In this patient with biochemically recurrent prostate cancer, off-label treatment with itraconazole 600 mg/d resulted in a > 50% decline in prostatespecific antigen (PSA) levels, without evidence of testosterone suppression. Inhibition of the Hedgehog (Hh) pathway may mediate the clinical activity of itraconazole. Clinical trials are ongoing to further elucidate this mechanism in men ith biochemically recurrent and castration-resistant prostate cancer.

Original language	English (US)
Pages (from-to)	e51-e53
Journal	Clinical Genitourinary Cancer
Volume	12
Issue number	2
DOIs	https://doi.org/10.1016/j.clgc.2013.11.015
State	Published - Apr 2014
Externally published	Yes

Bibliographical note

Funding Information:
ESA is partially funded by NIH grant P30 CA006973 .

Keywords

Biochemical recurrence
Hedgehog pathway
Itraconazole
Prostate cancer

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.clgc.2013.11.015

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title = "High-dose itraconazole as a noncastrating therapy for a patient with biochemically recurrent prostate cancer",

abstract = "The role of androgen deprivation therapy (ADT) in biochemically recurrent prostate cancer is unclear and is associated with significant adverse events. Itraconazole has demonstrated clinical activity in castration-resistant prostate cancer (CRPC) and does not appear to mediate its activity by androgen suppression. In this patient with biochemically recurrent prostate cancer, off-label treatment with itraconazole 600 mg/d resulted in a > 50% decline in prostatespecific antigen (PSA) levels, without evidence of testosterone suppression. Inhibition of the Hedgehog (Hh) pathway may mediate the clinical activity of itraconazole. Clinical trials are ongoing to further elucidate this mechanism in men ith biochemically recurrent and castration-resistant prostate cancer.",

keywords = "Biochemical recurrence, Hedgehog pathway, Itraconazole, Prostate cancer",

author = "Suzman, {Daniel L.} and Antonarakis, {Emmanuel S.}",

note = "Funding Information: ESA is partially funded by NIH grant P30 CA006973 .",

year = "2014",

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doi = "10.1016/j.clgc.2013.11.015",

language = "English (US)",

volume = "12",

pages = "e51--e53",

journal = "Clinical Genitourinary Cancer",

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T1 - High-dose itraconazole as a noncastrating therapy for a patient with biochemically recurrent prostate cancer

AU - Suzman, Daniel L.

AU - Antonarakis, Emmanuel S.

N1 - Funding Information: ESA is partially funded by NIH grant P30 CA006973 .

PY - 2014/4

Y1 - 2014/4

N2 - The role of androgen deprivation therapy (ADT) in biochemically recurrent prostate cancer is unclear and is associated with significant adverse events. Itraconazole has demonstrated clinical activity in castration-resistant prostate cancer (CRPC) and does not appear to mediate its activity by androgen suppression. In this patient with biochemically recurrent prostate cancer, off-label treatment with itraconazole 600 mg/d resulted in a > 50% decline in prostatespecific antigen (PSA) levels, without evidence of testosterone suppression. Inhibition of the Hedgehog (Hh) pathway may mediate the clinical activity of itraconazole. Clinical trials are ongoing to further elucidate this mechanism in men ith biochemically recurrent and castration-resistant prostate cancer.

AB - The role of androgen deprivation therapy (ADT) in biochemically recurrent prostate cancer is unclear and is associated with significant adverse events. Itraconazole has demonstrated clinical activity in castration-resistant prostate cancer (CRPC) and does not appear to mediate its activity by androgen suppression. In this patient with biochemically recurrent prostate cancer, off-label treatment with itraconazole 600 mg/d resulted in a > 50% decline in prostatespecific antigen (PSA) levels, without evidence of testosterone suppression. Inhibition of the Hedgehog (Hh) pathway may mediate the clinical activity of itraconazole. Clinical trials are ongoing to further elucidate this mechanism in men ith biochemically recurrent and castration-resistant prostate cancer.

KW - Biochemical recurrence

KW - Hedgehog pathway

KW - Itraconazole

KW - Prostate cancer

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High-dose itraconazole as a noncastrating therapy for a patient with biochemically recurrent prostate cancer

Abstract

Bibliographical note

Keywords

UN SDGs

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