Efficacy and toxicity of docetaxel in elderly men with castrate-resistant metastatic prostate cancer.

2010 ◽  
Vol 28 (15_suppl) ◽  
pp. 4687-4687 ◽  
Author(s):  
D. R. Shepard ◽  
A. Weil ◽  
J. A. Garcia ◽  
R. Dreicer ◽  
D. Raghavan
2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Ayun Cassell ◽  
Bashir Yunusa ◽  
Mohamed Jalloh ◽  
Medina Ndoye ◽  
Mouhamadou M. Mbodji ◽  
...  

The estimated incidence rate of prostate cancer in Africa was 22.0/100,000 in 2016. The International Agency for Research on Cancer (IARC) has cited prostate cancer as a growing health threat in Africa with approximated 28,006 deaths in 2010 and estimated 57,048 deaths in 2030. The exact incidence of advanced and metastatic prostate cancer is not known in sub-Saharan Africa. Hospital-based reports from the region have shown a rising trend with most patients presenting with advanced or metastatic disease. The management of advanced and metastatic prostate cancer is challenging. The available international guidelines may not be cost-effective for an African population. The most efficient approach in the region has been surgical castration by bilateral orchidectomy or pulpectomy. Medical androgen deprivation therapy is expensive and may not be available. Patients with metastatic castrate-resistant prostate cancer tend to be palliated due to the absence or cost of chemotherapy or second-line androgen deprivation therapy in most of Africa. A cost-effective guideline for developing nations to address the rising burden of advanced prostate cancer is warranted at this moment.


Oncotarget ◽  
2016 ◽  
Vol 7 (11) ◽  
pp. 12477-12488 ◽  
Author(s):  
Hojjat Ahmadzadehfar ◽  
Elisabeth Eppard ◽  
Stefan Kürpig ◽  
Rolf Fimmers ◽  
Anna Yordanova ◽  
...  

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 324-324
Author(s):  
Matthew Keating ◽  
Lisa Giscombe ◽  
Andre Desouza ◽  
Shiva Kumar Reddy Mukkamalla ◽  
Ritesh Rathore

324 Background: Androgen deprivation therapy (ADT) remains a standard of care in the treatment of locally advanced prostate cancer. But thanks to a few key trials (STAMPEDE, CHAARTED, and LATITUDE) reported within the past three years, docetaxel and abiraterone now have roles in extending overall survival in a patient population traditionally treated with ADT alone. These treatments when combined with ADT have been shown to extend overall survival in metastatic hormone-sensitive prostate cancer patients. The role of ADT in relation to other therapies continues to evolve rapidly. We intend to revisit ADT’s longstanding role in prostate cancer treatment using a national cancer database. Our aim is to look beyond traditional standards of care to identify patients more likely to have overall survival benefit from ADT. Are there any subgroups of patients with intermediate or high risk disease that have improved survival outcomes with androgen deprivation therapy, besides patients with localized disease that underwent radiation? Could there be other variables besides PSA and localization of the prostate cancer that should be considered when identifying ADT treatment candidates, or identifying survival trends in these groups? Methods: We are currently analyzing variables present in the National Cancer Database to retrospectively identify predictive factors for overall survival and progression to metastatic castrate resistant prostate cancer in locally advanced prostate cancers treated with ADT. We will evaluate time-to-death from the initiation of ADT and from the diagnosis of metastatic castrate resistant prostate cancer. The following variables in localized, locally advanced, and metastatic prostate cancer will be analyzed with Statistical Analysis Software: age, locally advanced, site-specific metastasis (M1a, M1b, M1c), Gleason score, local treatment (radical prostatectomy or radiation), stage (T, N, and M), prostate lobe (one vs. both; T2a/b vs. T2c), chemotherapy (date, time from M1 stage), comorbidity score, ethnicity, facility type, insurance, and risk groups (low/intermediate/high as per NCCN guidelines).


2014 ◽  
Vol 32 (2) ◽  
pp. 173-191 ◽  
Author(s):  
J. Jayasekera ◽  
E. Onukwugha ◽  
K. Bikov ◽  
C. D. Mullins ◽  
B. Seal ◽  
...  

2008 ◽  
Vol 26 (36) ◽  
pp. 5936-5942 ◽  
Author(s):  
Randall E. Millikan ◽  
Sijin Wen ◽  
Lance C. Pagliaro ◽  
Melissa A. Brown ◽  
Brenda Moomey ◽  
...  

Purpose We conducted a phase III trial in patients with previously untreated metastatic prostate cancer to test the hypothesis that three 8-week cycles of ketoconazole and doxorubicin alternating with vinblastine and estramustine, given in addition to standard androgen deprivation, would delay the appearance of castrate-resistant disease. Patients and Methods Eligible patients had metastatic prostate cancer threatening enough to justify sustained androgen ablation and were fit enough for chemotherapy. The primary end point was time to castrate-resistant progression as shown by increasing prostate-specific antigen, new radiographic lesions, worsening cancer-related symptoms, or receipt of any other systemic therapy. Results Three hundred six patients were registered; 286 are reported. Median time to progression was 24 months (95% CI, 18 to 39 months) in the standard therapy arm, and 35 months (95% CI, 26 to 44 months) in the chemohormonal group (P = .39). At median follow-up of 6.4 years, overall survival was 5.4 years (95% CI, 4.7 to 7.8 years) in the standard therapy arm versus 6.1 years (95% CI, 5.1 to 10.1 years; P = .41). Prostate-specific antigen kinetics at the time of androgen ablation and the nadir after hormone treatment were strongly correlated with survival. Chemotherapy significantly increased the burden of therapy, with 51% of patients experiencing an adverse event of grade 3 or worse, especially thromboembolic events. Conclusion There is no role for ketoconazole and doxorubicin alternating with vinblastine and estramustine before emergence of a castrate-resistant phenotype.


2021 ◽  
Vol 50 (1) ◽  
pp. 71
Author(s):  
Božo Krušlin ◽  
Lucija Škara ◽  
Tonći Vodopić ◽  
Borna Vrhovec ◽  
Jure Murgić ◽  
...  

<p>The aim of this review is to provide a brief overview of some current approaches regarding diagnostics, pathologic features, treatment, and genetics of prostate carcinoma (PCa). Prostate carcinoma is the most common visceral tumor and the second most common cancer-related cause of death in males. Clinical outcomes for patients with localized prostate cancer are excellent, but despite advances in prostate cancer treatments, castrate-resistant prostate cancer and metastatic prostate cancer patients have a poor prognosis. Advanced large-scale genomic studies revealed a large number of genetic alterations in prostate cancer. The meaning of these alterations needs to be validated in the specific prostate cancer molecular subtype context. Along these lines, there is a critical need for establishing genetically engineered mouse models, which would include speckle type BTB/POZ protein and isocitrate Dehydrogenase (NADP (+)) 1 mutant, as well as androgen receptor neuroendocrine subtypes of prostate cancer. Another urgent need is developing highly metastatic prostate cancer models, as only up to 17% of available models dis- play bone metastases and exhibit a less typical neuroendocrine prostate cancer or sarcomatoid carcinoma. Moreover, androgen deprivation and relapse should be mimicked in the genetically engineered mouse models, as androgen independence may yield a better model for metastatic castrate-resistant prostate cancer. The development of such refined animal models should be guid- ed by comparative genomics of primary versus corresponding metastatic tumors. Such an approach will have the potential to illuminate the key genetic events associated with specific molecular prostate cancer subsets and indicate directions for effective therapy.</p><p><strong>Conclusion</strong>. Despite excellent results in the treatment of localized prostatic carcinoma, castrate-resistant prostate can- cer and metastatic prostate cancer have a poor prognosis. Advanced large-scale genomic studies revealed a large number of ge- netic alterations in PCa. Experimental models of prostate carcinoma in genetically modified mice could provide new data about the genetic changes in such cancers and help in developing better animal models for treatment resistant prostate carcinomas.</p>


2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 187-187 ◽  
Author(s):  
Frances May Mark ◽  
Adam Pollard ◽  
Alastair H Thomson

187 Background: Docetaxel use has led to a significant prolongation in overall survival in metastatic prostate cancer (MPC). There is however limited information on treatment tolerance and outcomes in patients 80 years old and over in routine clinical practice. With the ever aging population it is becoming more important to assess outcomes in this age group. Methods: Patients diagnosed with MPC and treated with docetaxel from 2006 to 2016 were identified and their records retrospectively reviewed via electronic clinical and prescribing systems in a single centre in the UK. Data was assessed for prostate specific antigen (PSA) response, number of cycles and dosing of docetaxel and castrate resistant overall survival (OS). Results: 209 consecutive patients with MPC receiving docetaxel were reviewed. Three patient groups were identified; younger than 75 years old (n = 150, 37 early (as part of initial therapy) docetaxel), 75-79 years (n = 40, 2 early docetaxel) and 80 years or over (n = 19, no early docetaxel). When comparing mean OS excluding early docetaxel treatment, respective mean survival times for each of the three age groups, younger to older were 1001, 1045 and 1294 days, with between class difference being insignificant. The PSA response rates to docetaxel excluding first line use were compared between the age groups and did not show a significant difference at 39% in the youngest group, 38% in the intermediate age group and 42% for the oldest patients. There was a trend that the older the patient, the more likely docetaxel was the final systemic treatment given at 42% (80 years or over), 32% (75-79 years) and 23% (younger than 75 years). The 80 years or over group received fewer docetaxel cycles (3.8, p = 0.006) and less dose per course (226mg/m2, p = 0.004) than the group less than 75 years (5.8 cycles, 409mg/m2) and 75-79 years (5.1 cycles, 341mg/m2). Conclusions: In this group of patients, in routine clinical practice, the 80 years and over age group received fewer cycles of docetaxel in MPC and less dose per course, but nevertheless achieved similar PSA response rates and castrate resistant OS. Given these results, docetaxel should be considered as a treatment option in suitable patients of 80 years and over.


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