A Phase II Study of Weekly Paclitaxel/Estramustine/Carboplatin in Hormone-Refractory Prostate Cancer

Berry, William R.; Friedland, David; Fleagle, John; Jackson, Don V.; Ilegbodu, D.; Boehm, Kristi A.; Asmar, Lina

doi:10.3816/cgc.2006.n.029

Cited by 25 publications

(12 citation statements)

References 16 publications

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“…For each group, the median and interquartile range (IQR) of nomogram-predicted 12-and 18-month OS probabilities were calculated, and the Kaplan-Meier estimates of 12-and 18-month OS probabilities were calculated along with 95% confidence intervals (CIs). Trials were excluded from this analysis if no laboratory data were available (Berry et al [17] and Kikuno et al [18]); otherwise, to maximize the number of analyzable patients, the occasional missing values were imputed with the mean value (LDH in the Oh et al DF/HCC trial and 5.6% of all other values) and a sensitivity analysis repeated the analyses by excluding these patients to ensure consistent conclusions.…”

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confidence: 99%

Efficacy of carboplatin–taxane combinations in the management of castration-resistant prostate cancer: a pooled analysis of seven prospective clinical trials

et al. 2010

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Background: Docetaxel is associated with prolonged survival in castration-resistant prostate cancer (CRPC).Platinum compounds have modest but distinct single-agent activity. Carboplatin may have greatest potential for benefit when combined with taxanes. We investigated whether there is a subset of patients with CRPC for whom the efficacy of combination taxane-estramustine-carboplatin (TEC) chemotherapy may be greatest.Patients and methods: Individual patient data (n = 310) were obtained from seven trials using TEC chemotherapy.Prostate-specific antigen (PSA) response was defined as ‡50% post-therapy decline from baseline. Overall survival was defined from baseline to death from any cause. Logistic and Cox regression were used to investigate heterogeneity in outcome to TEC by patient and disease characteristics. Predicted survival probabilities were calculated from the Halabi Cancer and Leukemia Group B (CALGB) nomogram. Results:The pooled PSA response proportion was 69% [95% confidence interval (CI) 56% to 80%]. There was no evidence of differential PSA response by disease characteristics. Established prognostic factors were associated with survival. The pooled 12-month survival estimate of 79% (95% CI 71% to 84%) was higher than the median 59% 12-month nomogram-predicted survival.Conclusions: TEC chemotherapy has significant clinical activity in CRPC. A randomized, controlled trial evaluating the addition of carboplatin to taxane-based chemotherapy is needed to elucidate the value of carboplatin in CRPC.

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confidence: 99%

Efficacy of carboplatin–taxane combinations in the management of castration-resistant prostate cancer: a pooled analysis of seven prospective clinical trials

et al. 2010

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“…In a randomized phase II study in patients with castration-resistant prostate cancer, the 3-week administration of paclitaxel/carboplatin combination was well tolerated and resulted in a greater and more durable PSA response than did mitoxantrone [15]. In addition, several phase I and II trials, evaluating the efficacy of a taxane and carboplatin combination in patients with castration-resistant prostate cancer, reported a C50 % decrease in the serum levels of PSA in 60-100 % of patients and an objective response rate up to 45-65 % [1,[16][17][18][19][20][21]. However, a meta-analysis failed to clearly demonstrate a substantial effect of platinum-based regimens on the patients' overall survival [22].…”

Section: Introductionmentioning

confidence: 96%

Paclitaxel in combination with carboplatin as salvage treatment in patients with castration-resistant prostate cancer: a Hellenic oncology research group multicenter phase II study

Kentepozidis

Soultati

Giassas

et al. 2012

Cancer Chemother Pharmacol

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“…21 Efficacy of paclitaxel specifically for TNBC (compared with non-TNBC) has been observed in subtype analyses within clinical trials. 24,25 However, these associations between TNBC and taxanes have not been consistent; a meta-analysis has shown benefit for taxane in the adjuvant setting independent of ER status. 26 Ixabepilone is an epothilone B analogue that stabilizes microtubules and has activity in patients with TNBC as a monotherapy.…”

Section: Microtubule-targeting Agentsmentioning

confidence: 99%

Treating Triple-Negative Breast Cancer: Where Are We?

Morikawa

Seidman

2015

J Natl Compr Canc Netw

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Unlike estrogen receptor (ER)-positive and HER2-positive breast cancer, triple-negative breast cancer (TNBC) lacks a repertoire of targeted therapies. Hence, chemotherapy is the only available systemic option in current clinical practice. In general, survival of patients with TNBC is worse than that for those with ER-positive and HER2-positive breast cancer, especially for advanced-stage disease. Thus, a great unmet need exists. Conventional chemotherapeutic agents such as platinumsalts have been examined for specific benefit in TNBC; however, no one agent has yet been shown to offer a differential incremental benefit in metastatic TNBC. The hope is that ongoing research in targetable molecular pathways will lead to new therapeutic options for TNBC. Because these patients are likely to be increasingly subcategorized using potentially targetable molecular alterations, investigators will need to be mindful of the challenges in designing and conducting clinical trials in smaller subpopulations. The successful incorporation of targeted therapies in routine clinical practice for TNBC, which mirrors the success achieved by anti-HER2 and endocrine therapies, is awaited. (J Natl Compr Canc Netw 2015;13:(e8-e18) and rare types, such as adenoid cystic, metaplastic, apocrine, and neuroendocrine carcinoma.3 Nevertheless, the clinical utility of this categorization has been robust as a prognostic and predictive biomarker.Patients with TNBC are more likely to have a poor prognosis than those with estrogen receptor (ER)/ progesterone receptor (PR)-positive and/or HER2-positive breast cancer.4 This is likely partially attributable to a dearth of novel therapeutic options for TNBC, in contrast to the recent expansion of endocrine and anti-HER2 therapies (eg, ado-trastuzumab-emtansine, pertuzumab, everolimus with exemestane).5-7 Therefore, great interest has been shown in exploring potential biomarkers (prognostic and predictive) and developing new therapeutic options. This article reviews current treatment options ("where are we now?") and ongoing therapeutic research ("where are we going?") for TNBC. Heterogeneity of TNBCBecause the utilitarian definition of TNBC is simply based on the exclusion of ER/PR/HER2 expression, it is not unexpected that this clinical subtype remains biologically heterogeneous. Studies examining tumor characteristics have found correlations between TNBC and certain molecular genomic features, such as basal cytokeratin (eg, CK5/6) and epidermal growth factor receptor (EGFR) expression, checkpoint kinase (Chk1), p53 alterations, and BRCA1 germline mutations.8-13 TNBC has also been shown to have overlapping features with the basal-like subtype (intrinsic breast cancer classification), 14,15 including a high frequency of poorly differentiated tumors, expression of cytokeratins and EGFR, and p53 mutations. Although the basal-like-subtypes are most often triple-negative, they are not equivalent groups.16

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A Phase II Study of Weekly Paclitaxel/Estramustine/Carboplatin in Hormone-Refractory Prostate Cancer

Cited by 25 publications

References 16 publications

Efficacy of carboplatin–taxane combinations in the management of castration-resistant prostate cancer: a pooled analysis of seven prospective clinical trials

Efficacy of carboplatin–taxane combinations in the management of castration-resistant prostate cancer: a pooled analysis of seven prospective clinical trials

Paclitaxel in combination with carboplatin as salvage treatment in patients with castration-resistant prostate cancer: a Hellenic oncology research group multicenter phase II study

Treating Triple-Negative Breast Cancer: Where Are We?

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