Multivariate analysis of plasma hormones in patients with metastatic prostate cancer receiving combined LHRH-analog and antiandrogen therapy

The Prostate ◽  
1993 ◽  
Vol 23 (4) ◽  
pp. 291-313 ◽  
Author(s):  
Jean Fiet ◽  
Jean-Christophe Doré ◽  
Alice Le G?? ◽  
Tiiu Ojasoo ◽  
Jean-Pierre Raynaud
Keyword(s):  
Prostate Cancer ◽  
Multivariate Analysis ◽  
Metastatic Prostate Cancer ◽  
Plasma Hormones ◽  
Antiandrogen Therapy ◽  
Lhrh Analog

Prognostic value of anemia in untreated metastatic prostate cancer: a multivariate analysis of SWOG 8894

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 4574-4574
Author(s):  
L. B. Bland ◽  
C. M. Tangen ◽  
I. M. Thompson ◽  
E. D. Crawford ◽  
T. M. Beer
Keyword(s):  
Prostate Cancer ◽  
Multivariate Analysis ◽  
Prognostic Value ◽  
Metastatic Prostate Cancer

Imaging metastatic prostate cancer with 18F-DCFBC PET/CT (DCFBC) and 18F-NaF PET/CT (NaF).

2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 231-231
Author(s):  
Farhad Fakhrejahani ◽  
Maria Liza Lindenberg ◽  
Ethan S. Bargvall ◽  
Esther Mena ◽  
Baris Turkbey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Soft Tissue ◽  
Functional Imaging ◽  
Metastatic Prostate Cancer ◽  
Whole Body ◽  
Inverse Association ◽  
Non Invasive ◽  
Imaging Results ◽  
Pet Ct ◽  
Antiandrogen Therapy

231 Background: Conventional imaging of advanced prostate cancer (computerized tomography and nuclear bone scintigraphy) is limited and indicates a need for a more specific molecular imaging probe. DCFBC is a radiolabeled PET agent that binds with high affinity to prostate specific membrane antigen (PSMA), which is overexpressed in almost all prostate cancers and through whole-body non-invasive functional imaging, may provide new information on the expression of PSMA. We compare the uptake of DCFBC in bone with respect to NaF PET/CT in metastatic prostate cancer patients. DCFBC has added capability to detect soft tissue metastasis whereas NaF is confined to secondary effects of bone disease. Methods: Subjects with known or suspected prostate cancer metastasis underwent DCFBC PET/CT imaging performed at 1 hour and 2 hours after IV bolus injection of 8 mCi of DCFBC. Patients also underwent a whole body NaF PET/CT scan within 3 weeks of DCFBC PET/CT to assess for bone metastases. Patients received 3 mCi of NaF IV bolus and then were imaged 1hour post injection. PSA levels and antiandrogen therapy status were obtained at the time of DCFBC imaging. Results: Fifteen patients have been preliminarily analyzed. PSA ranged from < .01 to 4379 ng/mL. NaF identified bone lesions in 10 patients but matching focal DCFBC uptake was only seen in 3 patients. DCFBC additionally showed lymph node metastasis in 1of these 3 patient. There were 5 patients without focal abnormal bone uptake on NaF or DCFBC. In this group, 4 of 5 patients had focal DCFBC uptake in lymph nodes or soft tissue lesions. Ten patients were on some form of androgen deprivation therapy (ADT). For those on ADT, 7 of 10 patients had positive findings on NaF, compared to 2 of 10 patients on DCFBC. Conclusions: DCFBC uptake in bone metastasis does not routinely correspond to focal NaF uptake which could be due to distinct mechanisms of tracer uptake and tumor biology. There is an inverse association in focal bone findings when comparing each tracer on antiandrogen therapy. Through whole-body non-invasive functional imaging and further study, DCFBC may prove useful in characterizing prostate cancer based on PSMA expression. Clinical trial information: NCT02190279.

Cytology of metastatic prostate cancer following orchiectomy and antiandrogen therapy: A diagnostic challenge

2008 ◽  
Vol 36 (7) ◽  
pp. 499-502 ◽  
Author(s):  
Amy Rapkiewicz ◽  
Rimma Gorokhovsky ◽  
Eduardo Farcon ◽  
Kasturi Das
Keyword(s):  
Prostate Cancer ◽  
Metastatic Prostate Cancer ◽  
Diagnostic Challenge ◽  
Antiandrogen Therapy

Prognostic value of anemia in untreated metastatic prostate cancer: a multivariate analysis of SWOG 8894

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 4574-4574
Author(s):  
L. B. Bland ◽  
C. M. Tangen ◽  
I. M. Thompson ◽  
E. D. Crawford ◽  
T. M. Beer
Keyword(s):  
Prostate Cancer ◽  
Multivariate Analysis ◽  
Prognostic Value ◽  
Metastatic Prostate Cancer

scholarly journals Targeting glucocorticoid metabolism in prostate cancer

Endocrinology ◽  
2021 ◽  
Author(s):  
Shelley Valle ◽  
Nima Sharifi
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Metastatic Prostate Cancer ◽  
Tumor Tissue ◽  
Resistance Mechanism ◽  
Therapeutic Benefit ◽  
Cancer Resistance ◽  
Primary Driver ◽  
Glucocorticoid Metabolism ◽  
Antiandrogen Therapy

Abstract In the treatment of metastatic prostate cancer, resistance to hormonal therapy is a major obstacle. With antiandrogen therapies that suppress androgen signaling through the androgen receptor (AR), the primary driver of prostate cancer, some malignancies are able take advantage of the closely related glucocorticoid receptor (GR). Escape from AR-dependency often involves a simple functional switch from one steroid receptor to another. Recent research efforts have outlined the mechanism enabling this switch, which involves alterations in glucocorticoid metabolism that occur with antiandrogen therapy to increase tumor tissue glucocorticoids and enable GR signaling. Targeting this mechanism pharmacologically by blocking hexose-6-phosphate dehydrogenase shows promise in normalizing glucocorticoid metabolism and restoring responsiveness to antiandrogen therapy. This perspective reviews what we have learned about this resistance mechanism, examines potential implications, and considers how this knowledge might be harnessed for therapeutic benefit.

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