SEARCH

SEARCH BY CITATION

Keywords:

  • castration-resistant prostate cancer;
  • docetaxel;
  • docetaxel-sensitive;
  • docetaxel reintroduction

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

OBJECTIVE

To investigate the potential benefit of reintroducing docetaxel chemotherapy in patients with progressive metastatic castration-resistant prostate cancer (mCRPC) who had initially responded to first-line docetaxel-based regimen.

PATIENTS AND METHODS

Records were evaluated retrospectively from French patients with mCRPC who had been included in seven controlled clinical studies of docetaxel as first-line treatment. We identified patients who were confirmed as responders to first-line treatment, discontinued for reasons other than disease progression or unacceptable toxicity, and who received further docetaxel chemotherapy for disease progression. The primary objective was to assess efficacy in terms of the prostate-specific antigen (PSA) response after resuming a docetaxel-based chemotherapy. Secondary objectives were overall survival and tolerance.

RESULTS

Of the 148 patients who responded to first-line docetaxel, 50 received further therapy with docetaxel and were analysed. The median (range) response duration to first-line docetaxel was 10.3 (4.6–45.7) months and the median docetaxel-free interval was 18.4 (5.0–46.7) months. Docetaxel was reintroduced as second-line therapy in 52% of patients and as further lines in 48%. After docetaxel reintroduction, 24 patients (48%) had a 50% decrease in PSA level (95% confidence interval, CI, 34.1–61.8%). The median (95% CI) overall survival from docetaxel reintroduction was 16 (13–20) months. Re-treatment was well tolerated (6% of grade 3–4 haemotoxicity).

CONCLUSION

Docetaxel reintroduction appears to be effective, with favourable tolerance profiles, in patients with mCRPC having responded to first-line docetaxel, and should be prospectively assessed in clinical trials against alternative therapies or investigational agents given alone or in combination, to define further management.


Abbreviations
(m)CRPC

(metastatic) castration-resistant prostate cancer

AE

adverse event.

INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

Prostate cancer is the second most common cancer in men worldwide, with an estimated incidence of 25.3 per 100 000, and is one of the most common lethal malignancies in men [1]. Docetaxel was approved by the European Medicine Agency and the US Food and Drug Administration in 2004 for the first-line treatment of patients with metastatic castration-resistant prostate cancer (mCRPC) and is now the only standard of care in this setting. Two large randomized phase III studies (Southwest Oncology Group 99–16 and TAX 327) showed that docetaxel, combined with either estramustine phosphate or prednisone, significantly prolongs overall survival in men with mCRPC compared with the former standard treatment [2–4]. No other drug has been shown to influence survival in advanced CRPC [5]. However, all patients eventually discontinue docetaxel therapy after disease progression, unacceptable toxicity, or maximum response [4]. Indeed, the optimum treatment duration in cases of clinical benefit is not established [6] and docetaxel is sometimes discontinued after confirming the maximal response.

In the case of progression after initial docetaxel-based chemotherapy, treatment options for mCRPC are limited. Mitoxantrone is the only other chemotherapeutic agent to be approved in symptomatic mCRPC. In combination with a steroid, it was shown to achieve palliation better than steroid alone for symptomatic patients in two independent studies [7,8]. In studies where survival was the primary endpoint, there was no difference in metastatic patients whether symptomatic [8] or not [9]. Mitoxantrone is commonly used in patients with CRPC and who show progression after docetaxel in clinical practice, but its activity as a second-line treatment is modest, with PSA response rates of 10–20%[10–12]. Consequently, there is no standard treatment for the growing proportion of patients with mCRPC whose disease progresses despite previous benefit from docetaxel.

In this context, the reintroduction of docetaxel represents a pragmatic approach for patients who benefited from first-line docetaxel with manageable adverse events (AEs), and had disease progression after a reasonably long docetaxel-free interval.

Thus, we conducted this retrospective analysis to assess the status of docetaxel re-treatment in common practice, and to evaluate the efficacy and safety of this approach in patients with mCRPC who had an objective response and acceptable tolerance to first-line docetaxel therapy.

PATIENTS AND METHODS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

The primary objective was to retrospectively evaluate the efficacy, in terms of PSA response, of reintroducing a docetaxel-based chemotherapy in patients with CRPC who had an objective response to first-line docetaxel and remained potentially docetaxel-sensitive. The secondary objectives were to assess the safety profile and overall survival.

The original population consisted of patients with mCRPC from participating French institutions who were enrolled in seven prospective phase II and III clinical trials testing docetaxel as first-line chemotherapy for CRPC [3,13–18]. In participating centres, all patients who were enrolled in these first-line studies were considered for this retrospective analysis. Patients were considered as eligible for our retrospective analysis if they had experienced a confirmed response according to the first-line protocol criteria, discontinued first-line docetaxel for reasons other than tumour progression or unacceptable toxicity, and had progression after docetaxel discontinuation. The medical charts of recorded patients sharing these selection criteria were made available by the investigators and could be followed for treatment response to subsequent docetaxel-based chemotherapy when this occurred. Finally the population of interest was represented by patients responding to a first-line docetaxel treatment in a controlled trial, who were given one further docetaxel-based chemotherapy regimen. Re-treatments with either the standard 3-week schedule or an adapted weekly regimen of docetaxel (Taxotere®, Sanofi-Aventis, Paris, France) were considered for this population in the context of practical management.

The investigators retrospectively collected the following data from case report forms: initial study identification, patient’s demographic data, prostate cancer history, docetaxel first-line schedule and number of cycles delivered, PSA values during first-line treatment, best response to first-line docetaxel, date of progression, type of rescue treatment, and date of last follow-up or death. For re-treatment with docetaxel-based chemotherapy, line of treatment, dates of first and last cycles, PSA values, rates of febrile neutropenia and grade 3–4 haematological, gastrointestinal, neurological, renal, or hepatic toxicities, and grade 3–4 oedema, weight gain, and nail disorders were recorded. A biochemical response to docetaxel reintroduction was defined as a ≥50% reduction of baseline PSA in patients with a baseline PSA level of ≥5 ng/mL using the criteria of Bubley et al.[19]. Analysis of a ≥30% decrease in PSA level within 3 months of treatment initiation was also carried out according to the definition of Petrylak et al.[20] and Armstrong et al.[21]. Case report forms were checked against medical charts by independent monitors.

Based on various assumptions of docetaxel reintroduction rates of 30%, 40% or 50% in patients responding to first-line docetaxel, and response rates of 35%, 50% or 65% to docetaxel re-treatment, it was calculated that ≈150 responders to first-line docetaxel should be reviewed to properly assess the response rate to docetaxel reintroduction, with a precision of 10.8–14.6%.

Purely descriptive analyses, with no statistical comparisons, were planned using percentages and 95% CI. Descriptive statistics were used for qualitative and quantitative data. Survival function was assessed using the Kaplan-Meier method.

RESULTS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

In all, 148 patients were identified as responders at first-line docetaxel-based chemotherapy among seven prospective controlled trials conducted in 18 French centres. The median (range) PSA level at the end of the first-line treatment was 6.5 (0.5–2995) ng/mL. At relapse, treatment included at least a chemotherapy regimen for 100 patients and among them, 50 (33.8%) received one further docetaxel-based chemotherapy regimen, constituting the study population of interest.

The characteristics of the 50 patients reintroduced to docetaxel are shown in Table 1; the median age at docetaxel reintroduction was 67 years and the median Gleason score at diagnosis was 7. The initial docetaxel regimen was monotherapy in 32% and combined therapy (either estramustine or capecitabine) in 68%, with a weekly schedule in 40% and an ‘every 3-week’ schedule in 60%, according to initial study designs. Initially, 43 patients (86%) had an elevated PSA level, two were evaluable based on measurable lesions only, and the data were unknown in five patients. The median (range) duration of the initial response until documented progression was 10.3 (4.6–45.7) months. The median (range) time between the last first-line docetaxel perfusion and the first docetaxel reintroduction perfusion was 18.4 (5.0–46.7) months.

Table 1.  The characteristics of the 50 patients at docetaxel re-treatment
CharacteristicMedian (range) or n (%)
  • *

    Time from first day of first-line treatment to first documentation of disease progression;

  • †time from last day of first-line treatment to first day of further docetaxel treatment.

Age, years67 (52–80)
Gleason score at diagnosis 7 (3–9)
Castration 
 Surgical 6 (12)
 Medical44 (88)
First-line docetaxel regimen 
 Monotherapy ± steroids16 (32)
 Combined with estramustine ± steroids24 (48)
 Combined with capecitabine10 (20)
 Total with steroids25 (50)
First-line docetaxel schedule of administration 
 Weekly20 (40)
 Every 3 weeks30 (60)
Duration of response to first-line therapy, months*10.3 (4.6–45.7)
Docetaxel-free interval, months18.4 (5.0–46.7)
PSA level at baseline, ng/mL74.5 (2–1609)
Evaluable patients with baseline PSA level46 (92)
of ≥5 ng/mL at reintroduction 
Line of docetaxel reintroduction 
 2nd26 (52)
 3rd17 (34)
 4th 7 (14)

At the time of docetaxel reintroduction, 46 patients (92%) had an elevated serum PSA level of ≥5 ng/mL and were evaluable for biochemical response. Twenty-six patients (52%) received docetaxel reintroduction as second-line treatment, and 24 (48%) as a further line. Thirty patients were given docetaxel as a single agent (60%) and 20 (40%) in combination (estramustine in 18, capecitabine in one, and investigational agent in one). The median (range) duration of treatment was 3.7 (0.5–11.5) months.

Among the 50 patients, four were not evaluable due to a baseline PSA level of <5 ng/mL; 24 (48%, 95% CI 34.1–61.8%) achieved a confirmed biochemical response, defined by a ≥50 (52–98)% decrease in PSA level (Table 2). In addition, 62% of patients (95% CI 48.5–75.4%) had a mean (range) decline in PSA level of ≥30 (35.5–97.9%) within 3 months of starting re-treatment. Among them, 12 (half the responders) achieved a ≥75% reduction in baseline PSA level. Eighteen patients (36%) had a stable PSA level and only four (8%) had a biochemical progression (>25% increase in PSA level). A waterfall plot (Fig. 1) shows that most patients had some reduction in PSA level. Among the 26 patients who received docetaxel as a second-line, 12 had a PSA response (46%), vs 12 of the 24 re-treated in the third or fourth line (50%). Thirty-two patients died; the median (95% CI) overall survival was 16 (13–20) months and the 2-year survival rate was 28.9% (Fig. 2).

Table 2.  The PSA response rate to docetaxel reintroduction for all 50 patients
Responsen (%)
  • *

    Within 3 months of treatment initiation.

PSA decrease ≥30%*31 (62)
Partial response (≥50% decrease)24 (48)
PSA decrease ≥75%12 (24)
Stable disease18 (36)
Progressive disease 4 (8)
Not evaluable 4 (8)
image

Figure 1. A waterfall plot of variation in PSA level on docetaxel reintroduction, for the 46 patients evaluable for PSA response (baseline PSA ≥5 ng/mL).

Download figure to PowerPoint

image

Figure 2. Overall survival of the 50 patients (32 events; 18 censored).

Download figure to PowerPoint

Twenty-two grade 3 or 4 AEs were reported in 50 patients. The most frequent grade 3 or 4 nonhaematological AEs were nail disorders in 12% of patients, followed by oedema/weight gain in 8%, skin toxicity in 6%, and asthenia in 4% (Table 3). Grade 3–4 haematotoxicity was found in three patients (6%) and one episode of febrile neutropenia was reported.

Table 3.  Patients with grade 3–4 AEs
Any grade 3–4 AEn (%)
Nail disorders6 (12)
Oedema/weight gain4 (8)
Skin3 (6)
Asthenia2 (4)
Febrile neutropenia1 (2)
Infection3 (6)
Neuropathy0

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

There are no guidelines for the optimum duration of docetaxel treatment in patients with mCRPC who respond to chemotherapy [6]. Rather than treating until progression or cumulative toxicity, a common practice in the first-line setting is to administer docetaxel up to a maximum of 10 cycles, as planned in the TAX 327 study [3], leading to treatment discontinuation in the absence of evidence that continuing treatment would benefit the patients. In such patients, docetaxel reintroduction at the time of disease progression is justified by the very limited alternative therapeutic options. Several drugs have been tested, with discouraging results. Oral satraplatin delayed progression of disease and pain in patients progressing after initial chemotherapy, but with no significant survival benefit [22]. The novel taxane, cabazitaxel (XRP-6258), currently in development for patients previously treated with docetaxel, might address the medical need of second-line chemotherapy in mCRPC. However, without an established standard of care after first-line chemotherapy, the current therapeutic strategy remains dependent on the possibility of docetaxel reintroduction, but this clinical practice has not yet been properly evaluated [23].

We therefore undertook this retrospective analysis to gather preliminary evidence on the outcomes of docetaxel re-treatment in patients with mCRPC. Only patients receiving first-line treatment for CRPC in the context of prospective clinical studies were considered, to minimize the usual selection biases associated with retrospective analyses (i.e. heterogeneity of the population and incomplete collection of all cases actually treated). Of note, the selection of patients according to first-line treatment response was not biased, as the response rate was well established and responding patients were identified from trial documents. Using this method, we were able to identify, in several institutions, patients who shared similar and confirmed characteristics at the start of their docetaxel-based therapy, including mCPRC with a documented disease progression, adequate renal, hepatic and haematological function, as well as an Eastern Cooperative Oncology Group performance status of 0–2; most of all, response to first-line docetaxel was confirmed and controlled. Thus 148 patients responding to first-line docetaxel in seven prospective studies conducted at participating French institutions were included and analysed. This sample was consistent with the planned number of 150 that was prospectively calculated to assess the response rate to docetaxel reintroduction with acceptable precision. Moreover, this sample represents an exhaustive collection of all patients corresponding to selection criteria in the 27 centres that participated in this retrospective study. Furthermore, considering that most patients with mCRPC discontinue first-line docetaxel because of tumour progression or unacceptable toxicity [22], and that we included only patients not discontinuing docetaxel for these reasons, this population provides a representative ‘snapshot’ of docetaxel reintroduction in daily practice, suitable for a retrospective hypothesis-generating study. To our knowledge, it is the largest series published to date [23,24].

Our data show that docetaxel reintroduction is a common routine medical practice outside of clinical trials. Fifty of 148 patients (34%) with mCRPC potentially sensitive to docetaxel were given further docetaxel therapy at the time of tumour progression, and 48% of these patients had a second biochemical response to docetaxel re-treatment. These results were achieved at the expense of known docetaxel-induced toxicity. Other trials have reported similar results with docetaxel reintroduction [23,24]. Our results also compare favourably with other therapeutic options after docetaxel failure [22,25,26]. This approach appears to be similar to the reintroduction of a platinum salt for patients with advanced ovarian cancer, who are not initially resistant and relapse after a platinum-free interval [27]. These patients are recognized as ‘potentially platinum-sensitive’. Similarly, oxaliplatin reintroduction in potentially sensitive patients with metastatic colorectal cancer seems to be beneficial in terms of overall survival [28].

In conclusion, although it was limited by the retrospective nature of the study, these encouraging data, in terms of efficacy and acceptable tolerance, suggest that docetaxel reintroduction in potentially sensitive patients is a therapeutic option whose role, compared with other therapeutic alternatives, should be confirmed further in prospective studies after first-line chemotherapy. Docetaxel re-treatment in combination with new targeted agents could also be investigated in clinical settings, to define an active combination in these potentially docetaxel-sensitive pretreated patients. One alternative to resuming docetaxel in patients whose disease is progressing is to deliver intermittent docetaxel as long as the disease is sensitive [6]. This concept has been validated with hormone therapy of prostate cancer, allowing for a reduction of time on treatment, incidence of AEs, with improvement of quality of life and finally reduced healthcare costs [29–31]. Such studies would help to define the subsets of patients more likely to benefit from docetaxel re-treatment.

ACKNOWLEDGEMENTS

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

We thank the other investigators: Eric Voog, Clinique Victor Hugo, Le Mans; Sabine Rieul, Centre Azuréen de Cancérologie, Mougins; Emanuel Achille, Clinique Claude Bernard, Metz; Claude Linassier, CHU Bretonneau, Tours; Daniel Lepillé, Clinique Pasteur, Evreux; Brigitte Duclos, Hôpitaux Civils, Strasbourg; Philippe Laplaige, Polyclinique de Blois, La Chaussée-Saint-Victor; Denis Langlois, Centre Saint-Michel, La Rochelle; Brigitte Laguerre, Centre Eugène Marquis, Rennes; Didier Kamioner, Hôpital Privé de l’Ouest Parisien, Trappes; Anne-Claire Hardy-Bessard, Clinique Armoricaine de Radiologie, Saint-Brieuc; Pascal Demolis, Institut Bergonié, Bordeaux; Xavier Muracciole, CHU la Timone, Marseille; Gérard Lesbats, Clinique Saint-Laurent-du-Var, Saint-Laurent-du-Var; Alain Goupil, Centre René-Huguenin, Saint-Cloud; François Guinet, Hôpital Européen La Roseraie, Aubervilliers and Mireille Mousseau, CHU A. Michalon, Grenoble. We are particularly grateful to G. Hayward for her technical assistance.

CONFLICT OF INTEREST

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES

None of the clinical trials investigators and authors of this study have any conflict of interest to declare. L. Thill is an employee of Sanofi-Aventis; she has refrained from undue influence throughout the project and manuscript preparation. This study was supported by a grant from Sanofi-Aventis, France.

REFERENCES

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. PATIENTS AND METHODS
  5. RESULTS
  6. DISCUSSION
  7. ACKNOWLEDGEMENTS
  8. CONFLICT OF INTEREST
  9. REFERENCES
  • 1
    Nelen V. Epidemiology of prostate cancer. Recent Results Cancer Res 2007; 175: 18
  • 2
    Petrylak DP, Tangen CM, Hussain MH et al. Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. N Engl J Med 2004; 351: 151320
  • 3
    Tannock IF, De Wit R, Berry WR et al. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer. N Engl J Med 2004; 351: 150212
  • 4
    Berthold DR, Pond GR, Soban F, De Wit R, Eisenberger M, Tannock IF. Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer: updated survival in the TAX 327 study. J Clin Oncol 2008; 26: 2425
  • 5
    Mike S, Harrison C, Coles B, Staffurth J, Wilt TJ, Mason MD. Chemotherapy for hormone-refractory prostate cancer. Cochrane Database Syst Rev 2006; (18): CD005247
  • 6
    Lin AM, Ryan CJ, Small EJ. Intermittent chemotherapy for metastatic hormone refractory prostate cancer. Crit Rev Oncol Hematol 2007; 61: 24354
  • 7
    Tannock IF, Osoba D, Stockler MR et al. Chemotherapy with mitoxantrone plus prednisone or prednisone alone for symptomatic hormone-resistant prostate cancer: a Canadian randomized trial with palliative end points. J Clin Oncol 1996; 14: 175664
  • 8
    Kantoff PW, Halabi S, Conaway M et al. Hydrocortisone with or without mitoxantrone in men with hormone-refractory prostate cancer: results of the cancer and leukaemia group B 9182 study. J Clin Oncol 1999; 17: 250613
  • 9
    Berry W, Dakhil S, Modiano M, Gregurich M, Asmar L. Phase III study of mitoxantrone plus low dose prednisone versus low dose prednisone alone in patients with asymptomatic hormone refractory prostate cancer. J Urol 2002; 168: 243943
  • 10
    Michels JE, Montemurro T, Murray N, Kollmannsberger C, Nguyen Chi K. First- and second-line chemotherapy with docetaxel or mitoxantrone in patients with hormone-refractory prostate cancer (HRPC): does sequence matter? Cancer 2006; 106: 10416
  • 11
    Oh WK, Manola J, Babcic V, Harnam N, Kantoff PW. Response to second-line chemotherapy in patients with hormone refractory prostate cancer receiving two sequences of mitoxantrone and taxanes. Urology 2006; 67: 123540
  • 12
    Berthold DR, Pond G, De Witt R, Eisenberger M, Tannock IF, TAX 327 Investigators. Survival and PSA response of patients in the TAX 327 study who crossed over to receive docetaxel after mitoxantrone or vice versa. Ann Oncol 2008; 19: 174953
  • 13
    Gravis G, Bladou F, Salem N et al. Weekly administration of docetaxel for symptomatic metastatic hormone-refractory prostate carcinoma. Cancer 2003; 98: 162734
  • 14
    Ferrero JM, Foa C, Thezenas S et al. A weekly schedule of docetaxel for metastatic hormone-refractory prostate cancer. Oncology 2004; 66: 2817
  • 15
    Eymard JC, Priou F, Zannetti A et al. Randomized phase II study of docetaxel plus estramustine and single-agent docetaxel in patients with metastatic hormone-refractory prostate cancer. Ann Oncol 2007; 18: 106470
  • 16
    Oudard S, Banu E, Beuzeboc P et al. Multicenter randomized phase II study of two schedules of docetaxel, estramustine, and prednisone versus mitoxantrone plus prednisone in patients with metastatic hormone-refractory prostate cancer. J Clin Oncol 2005; 23: 334351
  • 17
    Gravis G, Protiere C, Salem N et al. Weekly administration of docetaxel and estramustine for symptomatic metastatic hormone-refractory prostate cancer. Prostate Cancer Symp 2006; Abstract 244
  • 18
    Ferrero JM, Chamorey E, Oudard S et al. Phase II trial evaluating a docetaxel-capecitabine combination as treatment for hormone refractory prostate cancer. Cancer 2006; 107: 73845
  • 19
    Bubley GJ, Carducci M, Dahut W et al. Eligibility and response guidelines for phase II clinical trials in androgen-independent prostate cancer: recommendations from the Prostate-Specific Antigen Working Group. J Clin Oncol 1999; 17: 34617
  • 20
    Petrylak DP, Ankerst DP, Jiang CS et al. Evaluation of prostate-specific antigen declines for surrogacy in patients treated on SWOG 99–16. J Natl Cancer Inst 2006; 98: 51621
  • 21
    Armstrong AJ, Garrett-Mayer E, Ou Yang YC et al. Prostate-specific antigen and pain surrogacy analysis in metastatic hormone-refractory prostate cancer. J Clin Oncol 2007; 25: 396570
  • 22
    Sternberg CN, Petrylak DP, Sartor O et al. Multinational, double-blind, phase III study of prednisone and either satraplatin or placebo in patients with castrate-refractory prostate cancer progressing after prior chemotherapy: the SPARC trial. J Clin Oncol 2009; 27: 54318
  • 23
    Berthold DR, Sternberg CN, Tannock IF. Management of advanced prostate cancer after first-line chemotherapy. J Clin Oncol 2005; 23: 824752
  • 24
    Ansari J, Hussain SA, Zarkar A, Tanguay JS, Bliss J, Glaholm J. Docetaxel chemotherapy for metastatic hormone refractory prostate cancer as first-line palliative chemotherapy and subsequent re-treatment: Birmingham experience. Oncol Rep 2008; 20: 8916
  • 25
    Jankovic B, Beardsley E, Chi KN. Rechallenge with docetaxel as second-line chemotherapy in patients with metastatic hormone refractory prostate cancer (HRPC) after previous docetaxel: a population based analysis. Genitourinary Cancers Symp 2008; Abstract 196
  • 26
    Aragon-Ching JB, Dahut WL. Chemotherapy in Androgen-Independent Prostate Cancer (AIPC): what’s next after taxane progression? Cancer Ther 2007; 5A: 15160
  • 27
    Rosenberg JE, Weinberg VK, Kelly WK et al. Activity of second-line chemotherapy in docetaxel-refractory hormone-refractory prostate cancer patients: randomized phase2 study of ixabepilone or mitoxantrone and prednisone. Cancer 2007; 110: 55663
  • 28
    Fung-Kee-Fung M, Oliver T, Elit L, Oza A, Hirte HW, Bryson P. Optimal chemotherapy treatment for women with recurrent ovarian cancer. Curr Oncol 2007; 14: 195208
  • 29
    De Gramont A, Buyse M, Abrahantes JC et al. Reintroduction of oxaliplatin is associated with improved survival in advanced colorectal cancer. J Clin Oncol 2007; 25: 32249
  • 30
    Tunn UW, Kurek R, Kienle E et al. Intermittent is as effective as continuous androgen deprivation in patients with PSA-relapse after radical prostatectomy. J Urol 2004; 171: 384, Abstract 1458
  • 31
    Calais da Silva FE, Bono AV, Whelan P et al. Intermittent androgen deprivation for locally advanced and metastatic prostate cancer: results from a randomised phase 3 study of the South Uroncological Group. Eur Urol 2009; 55: 126977