scholarly journals Marginal improvement in survival among patients diagnosed with metastatic prostate cancer in the second‐line antiandrogen therapy era

2021 ◽  
Author(s):  
Isaac E. Kim ◽  
Thomas L. Jang ◽  
Sinae Kim ◽  
David Y. Lee ◽  
Daniel D. Kim ◽  
...  
2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 173-173
Author(s):  
U. B. McGovern ◽  
S. J. Harland

173 Background: ECarboF chemotherapy is an active first line chemotherapy treatment for metastatic prostate cancer. We have now investigated its efficacy and toxicity in patients who have progressed during or after docetaxel chemotherapy. Methods: 37 patients with metastatic prostate cancer who had received ECarboF chemotherapy were retrospectively reviewed from a five year period (2005-2010). All patients had previously received first-line docetaxel chemotherapy and had either progressed following treatment (n=17) or were docetaxel refractory (n=20). Patients received epirubicin 50mg/m2 iv d1, carboplatin (AUC 5) d1, fluorouracil 440mg/m2 d1, d15 and folinic acid 20mg/m2 d1, d15 on a q4w cycle. 20% dose reductions were made for the first cycle in patients with poorer performance status. PSA was measured before each cycle of treatment and all patients were assessed for toxicity. Results: Patients had a median age of 70 years (range 48-77), median baseline PSA of 226.5 ng/mL (range 9.6-1,580) and the median number of ECarboF chemotherapy cycles received was 6 (range 1-10). 65% (n=24) of patients were ECOG 0-1, the remaining 35% (n=13) were ECOG 2-3. 16% (n=6) patients had a ≥ 30% decline in PSA and 16% (n=6) patients had a ≥ 50% decline in PSA. 35% (n=13) of patients experienced grade 3/4 toxicity, most commonly anaemia (13.5%), neutropenia (13.5%) and thrombocytopenia (8.1%) with one treatment related death (neutropenic sepsis) during the five year period analysed. Median time to PSA progression was 5.1 months. Conclusions: ECarboF has activity with acceptable toxicity post docetaxel in the treatment of metastatic castration resistant prostate cancer. Although PSA response rates are modest, the time to progression is comparable to that of more toxic regimens. ECarboF should be considered as an active second-line chemotherapy regimen. No significant financial relationships to disclose.


2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 231-231
Author(s):  
Farhad Fakhrejahani ◽  
Maria Liza Lindenberg ◽  
Ethan S. Bargvall ◽  
Esther Mena ◽  
Baris Turkbey ◽  
...  

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.


2008 ◽  
Vol 36 (7) ◽  
pp. 499-502 ◽  
Author(s):  
Amy Rapkiewicz ◽  
Rimma Gorokhovsky ◽  
Eduardo Farcon ◽  
Kasturi Das

2005 ◽  
Vol 23 (16_suppl) ◽  
pp. 4659-4659 ◽  
Author(s):  
K. W. Beekman ◽  
M. T. Fleming ◽  
H. I. Scher ◽  
M. Warren ◽  
N. Ishill ◽  
...  

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e15193-e15193
Author(s):  
Hongwei Wang ◽  
Laura Liao ◽  
Eliot Obi-Tabot ◽  
Robert Sands ◽  
Mathieu Rose ◽  
...  

e15193 Background: Patients with prostate cancer progressing from first-line (1L) docetaxel have limited approved treatment options available. Study is to evaluate patterns of second-line (2L) chemotherapy in a US managed care between 2004 and 2010. Methods: Patients with metastatic prostate cancer (mPC) and treated with docetaxel as 1L chemotherapy after July 1, 2004 were ascertained from the OptumInsight database. We evaluated type and timing of chemotherapy and relationships between patient characteristics, physician specialty, healthcare costs and geographic region, 6 months prior to 1L docetaxel and choice of 2L chemotherapy. Results: Patients (N=1,173) were on average 71 yrs old at onset of 1L docetaxel. During a mean follow-up period of 18 months, 38% of patients received 2L treatment. Out of the patients received 2L therapy, 32% received mitoxantrone (MITO), 24% with docetaxel rechallenge (RECH), 14% carboplatin (CARB), and 12% paclitaxel (PAC), plus 11% on Combo therapy. Examination of the 2L treatment groups showed that during the 6 months prior to 1L docetaxel, the RECH group (n=101) was older (73yrs), had fewer hospital admissions (12%), lower comorbidity burden [Charlson Comorbidity Index (CCI)=7.4], lower total healthcare costs ($10,083), and 78% seeing an oncologist; relative to MITO group (n=143) with 70 yrs, 16% hospital admissions, CCI of 7.5, total healthcare costs of $12,074, and 80% seeing an oncologist. The combo group (n=52) was 66 years old, with 19% hospital admissions, CCI of 8, total healthcare costs of $20,505, and 92% seeing an oncologist. Median time to MITO from the start of 1L docetaxel was 184 days, 309 days to RECH and 223 days to Combo therapy. Midwest (36%) and West (37%) were more frequently using MITO than Northeast (26%) and South (31%), while RECH was more frequently used in Northeast. Conclusions: Patients with mPC in US were most frequently treated with MITO or RECH as 2L chemotherapy after 1L docetaxel. MITO was also given sooner than RECH, hence a valid comparator for comparative effectiveness evaluation on new 2L therapy. Rechallenge with docetaxel increased with time and was given to patients with lower disease burden and healthcare costs than the MITO or Combo group.


The Prostate ◽  
1993 ◽  
Vol 23 (4) ◽  
pp. 291-313 ◽  
Author(s):  
Jean Fiet ◽  
Jean-Christophe Doré ◽  
Alice Le G?? ◽  
Tiiu Ojasoo ◽  
Jean-Pierre Raynaud

Endocrinology ◽  
2021 ◽  
Author(s):  
Shelley Valle ◽  
Nima Sharifi

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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