scholarly journals Aberrant TGF-β Signaling Drives Castration-Resistant Prostate Cancer in a Male Mouse Model of Prostate Tumorigenesis

Endocrinology ◽  
2017 ◽  
Vol 158 (6) ◽  
pp. 1612-1622 ◽  
Author(s):  
Hong Pu ◽  
Diane E. Begemann ◽  
Natasha Kyprianou
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Male Mouse ◽  
Castration Resistant Prostate Cancer ◽  
Prostate Tumorigenesis ◽  
Castration Resistant

scholarly journals Exercise Training Attenuates Tumor Growth In A Mouse Model Of Castration-Resistant Prostate Cancer

2021 ◽  
Vol 53 (8S) ◽  
pp. 475-475
Author(s):  
Benjamin A. Kugler ◽  
Dong Hang ◽  
Muqing Li ◽  
Meaghan Anderson ◽  
Paul Nguyen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Exercise Training ◽  
Mouse Model ◽  
Tumor Growth ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant

Enzalutamide, an androgen receptor signaling inhibitor, induces tumor regression in a mouse model of castration-resistant prostate cancer

The Prostate ◽  
2013 ◽  
Vol 73 (12) ◽  
pp. 1291-1305 ◽  
Author(s):  
Javier Guerrero ◽  
Iván E. Alfaro ◽  
Francisco Gómez ◽  
Andrew A. Protter ◽  
Sebastián Bernales
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Mouse Model ◽  
Tumor Regression ◽  
Receptor Signaling ◽  
Castration Resistant Prostate Cancer ◽  
Androgen Receptor Signaling ◽  
Castration Resistant

scholarly journals Axitinib and crizotinib combination therapy inhibits bone loss in a mouse model of castration resistant prostate cancer

BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Jeetendra Eswaraka ◽  
Anand Giddabasappa ◽  
Guangzhou Han ◽  
Kush Lalwani ◽  
Koleen Eisele ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Loss ◽  
Combination Therapy ◽  
Mouse Model ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant

SPOP mutation as a predictive marker for treatment of metastatic castration-resistant prostate cancer.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 160-160
Author(s):  
Andrew Stangl ◽  
Christopher Willner ◽  
Lucas Maahs ◽  
Charlotte Burmeister ◽  
Clara Hwang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Metastatic Disease ◽  
Dna Analysis ◽  
Bone Lesion ◽  
Next Generation ◽  
Castration Resistant Prostate Cancer ◽  
Wild Type ◽  
Prostate Tumorigenesis ◽  
Castration Resistant ◽  
Psa Progression

160 Background: Predictive markers linking molecular background to treatment response and clinical outcomes are currently lacking in prostate cancer. Missense mutations in SPOP (speckle-type POZ protein) define a distinct molecular subtype, occurring in about 12% of both clinically localized and metastatic disease. SPOP mutations occur early in prostate tumorigenesis and facilitate dysregulation of the androgen-receptor (AR) signaling network, suggesting mutant SPOP can impact response to AR-directed therapies. We hypothesized that SPOP mutation will be associated with superior response to next-generation AR inhibitors in metastatic castration-resistant prostate cancer (mCRPC). Methods: This is a retrospective study to evaluate patients who progressed to mCRPC and were treated with AR-targeted therapy (i.e. enzalutamide, abiraterone acetate). Eligibility criteria inlcuded androgen deprivation therapy, metastatic disease documented by bone lesion or soft tissue identified on imaging, castrate testosterone level ( < 50g/dL), and evaluable tissue for DNA analysis. SPOP status was determined by next-generation sequencing. Time to PSA progression (PSA TTP) was defined per PCWG2 as PSA increase of 25% from nadir and a minimum of 2 ng/ml calculated from date of primary treatment initiation to the date of PSA progression. Overall survival (OS) was calculated from start of treatment to date of death. Statisitcal comparision of the SPOP mutant or wild-type was determined using Kaplan-Meier and independent t-test analysis. Results: The analysis included 69 men with mCRPC with previous or ongoing ADT and receipt of AR-directed therapy (aberaterone acetate, enzalutamide). SPOP status was determined for all patients: 7 patients SPOP mutant, 62 patients SPOP wild-type. Mutant SPOP was associated with significantly longer PSA TTP (22.5 vs. 9.7 months, p = 0.031) and improved OS (21 vs. 29 months, p = 0.12) with enzalutamide or abiraterone as compared to SPOP wild-type patients. Conclusions: Our data demonstrate that SPOP mutations predict for better outcomes with next-generation AR inhibitors in men with mCRPC. SPOP mutations are a prominent molecular sub-type with potential to impact clinical management in men with metastatic, therapy resistant prostate cancer.

scholarly journals Transdifferentiation as a Mechanism of Treatment Resistance in a Mouse Model of Castration-Resistant Prostate Cancer

2017 ◽  
Vol 7 (7) ◽  
pp. 736-749 ◽  
Author(s):  
Min Zou ◽  
Roxanne Toivanen ◽  
Antonina Mitrofanova ◽  
Nicolas Floch ◽  
Sheida Hayati ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Treatment Resistance ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant
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