scholarly journals High dose androgen therapy in male pseudohermaphroditism due to 5 alpha-reductase deficiency and disorders of the androgen receptor.

1984 ◽  
Vol 74 (4) ◽  
pp. 1496-1508 ◽  
Author(s):  
P Price ◽  
J A Wass ◽  
J E Griffin ◽  
M Leshin ◽  
M O Savage ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Male Pseudohermaphroditism ◽  
High Dose ◽  
Androgen Therapy ◽  
Reductase Deficiency

scholarly journals Dual Functions of SPOP and ERG Dictate Androgen Therapy Responses in Prostate Cancer

2020 ◽  
Author(s):  
Tiziano Bernasocchi ◽  
Geniver El Tekle ◽  
Marco Bolis ◽  
Azzurra Mutti ◽  
Arianna Vallerga ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Therapeutic Interventions ◽  
High Dose ◽  
Wild Type ◽  
Driver Genes ◽  
Androgen Therapy ◽  
Cancer Driver ◽  
Cancer Pathways ◽  
Mutation Pattern

Driver genes with a mutually exclusive mutation pattern across tumor genomes are thought to have overlapping roles in tumorigenesis. In contrast, we show here that mutually-exclusive prostate cancer driver alterations involving the ERG transcription factor and the ubiquitin ligase adaptor SPOP are synthetic sick. At the molecular level, the incompatible cancer pathways are driven by opposing functions in SPOP. ERG up-regulates wild type SPOP to dampen androgen receptor (AR) signaling and sustain ERG activity through degradation of the bromodomain histone reader ZMYND11. Conversely, SPOP-mutant tumors stabilize ZMYND11 to repress ERG-function and enable oncogenic androgen receptor signaling. This dichotomy regulates the response to therapeutic interventions in the AR pathway. While mutant SPOP renders tumor cells susceptible to androgen deprivation therapies, ERG promotes sensitivity to high-dose androgen therapy and pharmacological inhibition of wild type SPOP. More generally, these results define a distinct class of antagonistic cancer drivers and a blueprint toward their therapeutic exploitation.

scholarly journals Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tiziano Bernasocchi ◽  
Geniver El Tekle ◽  
Marco Bolis ◽  
Azzurra Mutti ◽  
Arianna Vallerga ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Therapeutic Interventions ◽  
High Dose ◽  
Wild Type ◽  
Driver Genes ◽  
Androgen Therapy ◽  
Cancer Driver ◽  
Cancer Pathways ◽  
Mutation Pattern

AbstractDriver genes with a mutually exclusive mutation pattern across tumor genomes are thought to have overlapping roles in tumorigenesis. In contrast, we show here that mutually exclusive prostate cancer driver alterations involving the ERG transcription factor and the ubiquitin ligase adaptor SPOP are synthetic sick. At the molecular level, the incompatible cancer pathways are driven by opposing functions in SPOP. ERG upregulates wild type SPOP to dampen androgen receptor (AR) signaling and sustain ERG activity through degradation of the bromodomain histone reader ZMYND11. Conversely, SPOP-mutant tumors stabilize ZMYND11 to repress ERG-function and enable oncogenic androgen receptor signaling. This dichotomy regulates the response to therapeutic interventions in the AR pathway. While mutant SPOP renders tumor cells susceptible to androgen deprivation therapies, ERG promotes sensitivity to high-dose androgen therapy and pharmacological inhibition of wild type SPOP. More generally, these results define a distinct class of antagonistic cancer drivers and a blueprint toward their therapeutic exploitation.

scholarly journals Molecular basis of androgen resistance in a family with a qualitative abnormality of the androgen receptor and responsive to high-dose androgen therapy.

1991 ◽  
Vol 87 (4) ◽  
pp. 1413-1421 ◽  
Author(s):  
M J McPhaul ◽  
M Marcelli ◽  
W D Tilley ◽  
J E Griffin ◽  
R F Isidro-Gutierrez ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Molecular Basis ◽  
High Dose ◽  
Androgen Therapy ◽  
Androgen Resistance

Androgen Resistance Associated With a Qualitative Abnormality of the Androgen Receptor and Responsive to High Dose Androgen Therapy*

1989 ◽  
Vol 68 (3) ◽  
pp. 578-584 ◽  
Author(s):  
PLACIDO B. GRINO ◽  
ROSARIO F. ISIDRO-GUTIERREZ ◽  
JAMES E. GRIFFIN ◽  
JEAN D. WILSON
Keyword(s):  
Androgen Receptor ◽  
High Dose ◽  
Androgen Therapy ◽  
Androgen Resistance

scholarly journals 5-alpha-Reductase deficiency causing male pseudohermaphroditism.

1978 ◽  
Vol 53 (9) ◽  
pp. 751-753 ◽  
Author(s):  
S A Greene ◽  
E Symes ◽  
C G Brook
Keyword(s):  
Male Pseudohermaphroditism ◽  
Reductase Deficiency
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