Journal of Clinical Oncology, Vol 17, Issue 11
(November), 1999: 3461-3467
© 1999 American Society for Clinical Oncology
Eligibility and Response Guidelines for Phase II Clinical Trials in Androgen-Independent Prostate Cancer: Recommendations From the Prostate-Specific Antigen Working Group
Glenn J. Bubley,
Michael Carducci,
William Dahut,
Nancy Dawson,
Danai Daliani,
Mario Eisenberger,
William D. Figg,
Boris Freidlin,
Susan Halabi,
Gary Hudes,
Maha Hussain,
Richard Kaplan,
Charles Myers,
William Oh,
Daniel P. Petrylak,
Eddie Reed,
Bruce Roth,
Oliver Sartor,
Howard Scher,
Jonathan Simons,
Vickie Sinibaldi,
Eric J. Small,
Matthew R. Smith,
Donald L. Trump,
Robin Vollmer,
George Wilding
From the Beth Israel Deaconess Medical CenterDana Farber Cancer Center, and Massachusetts General Hospital, Boston, MA; Johns Hopkins University, Baltimore, MD, National Cancer Institute, Bethesda, MD, University of Maryland, Baltimore, MD, MD Anderson Cancer Center, Houston, TX, Duke University, Durham, NC, Fox Chase Cancer Center, Philadelphia, PA, Wayne State University, Detroit, MI, University of Virginia, Charlottesville, VA, Columbia University, New York, NY, Vanderbilt University, Louisiana State Medical Center, New Orleans, LA, Memorial Sloan Kettering Cancer Center, New York, NY, University of California at San Francisco, San Francisco, CA, Massachusetts General Hospital, Boston, MA, University of Pittsburgh, Pittsburgh, PA, and University of Wisconsin, Madison, WI.
Address reprint requests to William D. Figg, PharmD, Bldg 10, Room 5A01, Medicine Branch, National Cancer Institute, 9000 Rockville Pike, Bethesda, MD 20892; email wdfigg{at}helix.nih.gov
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ABSTRACT
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PURPOSE: Prostate-specific antigen (PSA) is a glycoprotein that is found almost exclusively in normal and neoplastic prostate cells. For patients with metastatic disease, changes in PSA will often antedate changes in bone scan. Furthermore, many but not all investigators have observed an association between a decline in PSA levels of 50% or greater and survival. Since the majority of phase II clinical trials for patients with androgen-independent prostate cancer (AIPC) have used PSA as a marker, we believed it was important for investigators to agree on definitions and values for a minimum set of parameters for eligibility and PSA declines and to develop a common approach to outcome analysis and reporting. We held a consensus conference with 26 leading investigators in the field of AIPC to define these parameters.
RESULT: We defined four patient groups: (1) progressive measurable disease, (2) progressive bone metastasis, (3) stable metastases and a rising PSA, and (4) rising PSA and no other evidence of metastatic disease. The purpose of determining the number of patients whose PSA level drops in a phase II trial of AIPC is to guide the selection of agents for further testing and phase III trials. We propose that investigators report at a minimum a PSA decline of at least 50% and this must be confirmed by a second PSA value 4 or more weeks later. Patients may not demonstrate clinical or radiographic evidence of disease progression during this time period. Some investigators may want to report additional measures of PSA changes (ie, 75% decline, 90% decline). Response duration and the time to PSA progression may also be important clinical end point.
CONCLUSION: Through this consensus conference, we believe we have developed practical guidelines for using PSA as a measurement of outcome. Furthermore, the use of common standards is important as we determine which agents should progress to randomized trials which will use survival as an end point.
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INTRODUCTION
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PROSTATE CANCER IS THE most commonly diagnosed malignancy among males in the U.S. and the second leading cause of cancer-related mortality. It is estimated that 39,000 men will die of prostate cancer in 1999.1 Androgen ablation has been the cornerstone for the treatment of metastatic disease for more than 50 years,2 but ultimately, almost all patients with distant metastasis will develop androgen-independent cancer and succumb to their disease. In addition, no therapeutic regimen has been shown to prolong survival in this setting.3 The difficulties in determining the activity of new agents in androgen-independent prostate cancer (AIPC) are well documented (especially the slow resolution of bone lesions on bone scan). Most patients have disease limited to the bone, which is notoriously difficult to assess for response, with a small subset having soft tissue lesions. To limit trials to only patients with bidimensionally measurable disease would eliminate 70% to 80% of patients who would otherwise be eligible.4 Lack of consensus on response criteria further complicates the evaluation of new treatments. A review of recently completed trials suggest that, even within one cooperative group, there is a wide variation in both the eligibility and response criteria used (N. Dawson, personal communication, February, 1999). These differences can impede the development of new agents (or regimens) and hinder the comparison between therapies.
Prostate-specific antigen (PSA) is a 34 kD glycoprotein that is found almost exclusively in normal and neoplastic prostate cells and seminal fluid.5-8 Changes in PSA will often antedate changes on bone scan, and its use could theoretically permit new agents to be screened more rapidly for activity.9-11 In 1989, Ferro et al12 were the first to report PSA changes as an indicator of response in patients enrolled onto a trial for AIPC. Since then, the majority of phase II trials have used PSA as a marker.13-15 However, some of the data currently available suggests that serum PSA cannot serve as a reliable surrogate end point.14-17 Indeed, clinical experience has provided some settings in which PSA changes and "hard" end points, such as survival, were demonstrated not to correspond.11,18 The use of PSA as a surrogate for benefit would require specific validation for the clinical setting and agents under investigation.
Published data lend support to the assumption that, for many agents, a decline in serum PSA may be a useful indicator of outcome in AIPC. This has been put forward by several groups as a potential outcome measure for survival in patients with AIPC.14,17,19 Approximately 95% of patients with advanced metastatic cancer of the prostate have an elevated PSA.4 Several investigators have attempted to correlate a decrease in PSA with clinical benefit and survival.14-17,19,20 Most have noted that a posttherapy decline of 50% has been associated with a prolonged survival. Kelly et al16 reported a statistically significant survival advantage in 110 patients if they had a posttherapy decline in PSA of 50% as opposed to those who did not (8.6 months v >25 months, respectively). Likewise, Smith et al14 reported a significant increase in survival if the PSA decreased by 50% or greater at 8 weeks (median survival from a landmark analysis was 91 weeks in patients with a 50% or greater decrease v 38 weeks in those without this decrease). More recently, Scher et al17 reported a multivariate analysis in which a posttherapy decline in PSA level of 50% achieved at both 8 and 12 weeks was a statistically significant factor associated with survival.
For the purpose of this discussion, we assume that guidelines can be established under which serum PSA can play a valuable role in pilot studies of new therapeutic approaches in androgen-independent disease purely as a tool for determining which approaches warrant selection for more definitive testing. The only underlying assumptions are that observed major decreases in PSA in association with a new treatment imply some biologic effect that encourages further evaluation and that lack of effect on an increasing PSA is likely to indicate an approach of little interest (unless preclinical testing has suggested the likelihood of a confounding effect on PSA gene expression, synthesis, or release). Used in this way, no assumption or claims of clinical benefit can or should be made; however, screening of new therapies could proceed much more quickly, and a larger number of patients would have the opportunity to participate in clinical research.
To use PSA most effectively, investigators must agree on definitions and values for a minimal set of parameters such as eligibility criteria, criteria for PSA response, and approach to outcome analysis and reporting. For many of these criteria, existing data does not permit an unequivocal determination of the "right" approach, but use of serum PSA for the limited purpose does not require that we begin with validated surrogacy data. All that is required is that investigators agree to use some standardized criteria, which can and should be updated as better data become available. In addition, these criteria for PSA response may require future validation.
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Standardization of Terms
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Unfortunately, even among investigators who have reported a decline in serum PSA as an end point, there is no consistency in how a PSA decline is measured and reported. Moreover, divergent criteria for treatment eligibility have been used. Trials have required different minimum PSA values and different criteria for biochemical progression after a previous treatment. In fact, a survey published in 1998 reported that among 35 leading investigators in the field, the response duration for a hypothetical patient varied by as much as 77 days (range, 49 to 126 days) because of differences in the calculation of response.21 These data emphasize the need to standardize eligibility and response criteria to advance the field and develop new therapies.
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EFFECT OF DRUGS ON PSA EXPRESSION
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It is important to recognize that some agents may modulate PSA (either up- or downregulation) independent of their effect on cell growth.22 The majority of those agents identified to date are not conventional cytotoxic agents. It is also important to emphasize that the models currently used to evaluate these changes have not been validated. Nonetheless, we would recommend that attempts be made to prospectively evaluate the effects of novel anticancer agents on PSA as an aid to interpreting clinical studies using PSA as an end point. For example, a phase II clinical trial in patients with AIPC was conducted using carboxyamido-triazole inhibitor, an agent that had been shown to downregulate the expression of PSA.18,23 Therefore, the trial was limited to those with measurable soft tissue lesions. A large percent of patients were found to have decreases in their PSA, but their soft tissue lesions continued to grow, as demonstrated by serial radiographic studies.18 These data emphasize the importance of understanding the effect of new agents on PSA expression.
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RECOMMENDATIONS FOR ELIGIBILITY CRITERIA
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For the purpose of this discussion, we have defined four groups of patients: 1) progressive measurable disease, 2) progressive bone metastasis, 3) stable metastases and an increasing PSA, and 4) increasing PSA and no other evidence of metastatic disease. Although performance status, weight change, and pain may be valid eligibility and response criteria for some clinical studies, they are not addressed in this manuscript.
Progressive Disease
Patients who are entered onto clinical trials of AIPC must have demonstrated evidence of progressive disease. Patients may have progressive measurable disease, worsening disease on bone scan, or an increasing PSA (as defined below).
Progressive measurable disease.
Progressive measurable disease (changes in size of lymph nodes or parenchymal masses on physical examination or x-rays), regardless of changes in PSA, bone scan, or performance status, is adequate for protocol eligibility using conventional solid tumor criteria. Approximately 20% of patients with radiographic evidence of disease will have measurable soft tissue disease. In addition to PSA criteria, these patients may be evaluated using more traditional phase II criteria. For agents that seem to be promising based on PSA criteria, it may make sense to accrue additional patients with measurable disease to increase the understanding of the drug's activity.
Bone scan progression.
Most investigators believe that a worsening bone scan is adequate evidence of progressive disease, regardless of changes in PSA. However, it is well known that bone scans may worsen ("flare") with the initiation of hormonal ablation and even chemotherapy.24 This is manifested by dramatic serologic and clinical improvement at the same time a bone scan shows more intense lesions and occasionally even new lesions. Bone scans that worsen because of hormonal ablation or chemotherapy generally occur at the commencement of treatment and have not been difficult to detect clinically.
Patients who do not fit into this clinical scenario may have bone scans that demonstrate larger lesions, new lesions, or a combination of larger lesions and new lesions. Changes in the intensity or the size of a lesion may be difficult to interpret. Thus, we would suggest that at least one new lesion be evident before placing a patient onto a clinical trial based on progression in bone scan alone. In those patients entered onto clinical trials on the basis of nonmeasurable but assessable disease progression and who will subsequently be observed with PSA as an end point, the PSA level at trial entry should be greater than or equal to 5 ng/mL.
PSA progression.
An increasing PSA, in some patients, may be the only evidence of progressive disease. Investigators have defined PSA progression in a variety of different ways, with variability concerning the amount of increase, number of required consecutive increasing values, and the time interval between the values. There is a theoretical conflict between easing requirements to allow more patients on phase II trials and using more stringent criteria for better accuracy in selecting which drug will undergo phase III testing. There are no randomized data that one can use to define PSA progression, so all criteria are somewhat arbitrary.
In those patients entering onto a clinical trial and having PSA progression as the only evidence of progressive disease, we suggest that two consecutive increases in PSA be documented over a previous reference value (see Fig 1). The first increase in PSA (no. 2) should occur a minimum of 1 week from the reference value. This increase in PSA should be confirmed (no. 3A). It is recognized that PSA fluctuations are such that the confirmatory PSA value (no. 3B) might be less than the previous value. In these cases, the patient would still be eligible provided the next PSA (no. 4) was found to be greater than the second PSA (no. 2 in the above sequence). We believe that a patient whose only evidence of progressive disease is an increasing PSA should have a value of at least 5 ng/mL before entering onto a clinical trial. Unfortunately, at lower values it is much more difficult to interpret changes in PSA. We believe this is problematic and, thus, a minimum PSA level is required.
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Fig 1. For defining eligibility, the reference value (no. 1) is the last PSA level before a sequence of increases. The interval between the reference value and time point no. 2 must be a minimum of 1 week. If the PSA at time point no. 3 (value no. 3A) is greater than at time point no. 2, then the requirement for a sequence of three increases has been met. If the third value is not greater than value no. 2, but value no. 4 is, then increasing PSA has been confirmed, and the patient can be eligible. In all cases, value no. 3A or no. 4 must be greater than or equal to 5 ng/mL.
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Antiandrogen withdrawal.
There is evidence that at least 20% of AIPC patients will have clinical and PSA responses by stopping their antiandrogen treatment.3 Therefore, to standardize results, all patients need to demonstrate continued elevation of their PSA 4 to 6 weeks after the cessation of their antiandrogen treatment. The length of time is dependent on the half-life of the agent used. Four weeks is sufficient after flutamide withdrawal, and 6 weeks is required for other agents commercially available at this time.
Testosterone levels/suppression.
To standardize this population as much as possible, all patients without surgical castration should have a serum testosterone level less than 50 ng/dL. There is no need to document a serum testosterone in patients having a prior surgical castration. In addition, patients should continue primary androgen suppression if they have not undergone surgical castration. The data for continuing androgen suppression are not definitive, but again, the intention is to make the patient populations from each trial as comparable as possible.
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REPORTING TRIAL OUTCOMES
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Posttherapy PSA Changes
The purpose of determining the number of patients whose PSA decreases in a phase II trial of AIPC is to guide the selection of agents for further testing and phase III trials. There have been attempts to determine if a posttherapy decline in PSA is of prognostic significance.14-17,19 Many, but not all investigators have observed an association in uncontrolled trials between a decline in PSA levels of 50% or greater and survival.11 There is also considerable controversy about the timing of the determination of the PSA level and the determination of the length of the response. The goal of the criteria herein proposed is quite focused to not use decline in PSA as a surrogate marker for survival but, instead, to use it as an outcome measure to guide the development of further trials, generally randomized. Thus, it is acceptable that these criteria are necessarily arbitrary. We propose that investigators should report, at minimum, a PSA decline of at least 50%, which must be confirmed by a second PSA value 4 or more weeks later. The reference PSA for these declines should be a PSA measured within 2 weeks before starting therapy. Patients may not demonstrate clinical or radiographic evidence of disease progression during this time period. Some investigators may want to report additional measures of PSA changes (ie, 75% decline and 90% decline).
For the purpose of defining duration of biochemical decline in PSA, we suggest defining two points on a time course, time to 50% increase from PSA nadir (PSA response duration) and time to first consistent PSA increase (ie, time to inflection or time to positive slope; see Fig 2). The PSA response duration should commence on the date of the first 50% decline in PSA. The response duration ends when the PSA value increases by 50% above the nadir, provided that the increase is at least 5 ng/mL (or back to the baseline). All PSA responses and progressions should be confirmed by a second determination.
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Fig 2. The duration of both PSA-based reporting end points are measured from the first time point at which the PSA has declined by at least 50% (which must eventually be confirmed by a second value). The duration of PSA response is the time until PSA has increased back to 50% of the original on-study value. However, in many cases, it will be possible (in retrospect) to identify an inflection point, the point at which PSA began what became a continuous increase. Some investigators feel that this may be considered the point at which disease control could be assumed to be lost. Thus, the duration of PSA control may be also be reported. Others prefer the time to PSA progression, which is defined as the time at which therapy started and ends when the PSA increases by 50% above the nadir.
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The time from initial 50% decline until the time at which the PSA begins to consistently increase (the inflection point) is also of interest to investigators. For an individual patient, this inflection point would be defined retrospectively. We emphasize that clear radiographic or clinical evidence of disease progression would constitute evidence of progression regardless of changes in PSA.
Objective Response
Patients with measurable soft tissue disease may also meet traditional guidelines for tumor response. We believe that this should also be noted and included in any description of a clinical trial.
PSA Normalization
We strongly discourage the term "PSA complete response." There is no compelling evidence that patients whose PSA has normalized have a different long-term outcome than patients whose PSAs have declined by 50%. However, investigators may wish to report the number of patients achieving a PSA of less than 0.2 ng/mL.
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DEFINING PROGRESSIVE DISEASE
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Progressive Measurable Disease
Progressive measurable disease (changes in size of lymph nodes or parenchymal masses on physical examination or x-rays) is evidence of disease progression, regardless of changes in PSA, bone scan, or performance status.
Bone Scan Progression
Most investigators believe that a worsening bone scan is adequate evidence of progressive disease, regardless of changes in PSA. If there is strong evidence that a bone scan change is not indicative of progressive disease, then this should be noted and the patient continued on trial. Changes in the intensity or the size of a lesion may be difficult to interpret. Thus, we suggest that, if there is no evidence of flare, one or more new lesions are required to identify disease progression.25
PSA Progression
An increasing PSA may be the only marker of presumed progressive disease. In patients whose PSA has not decreased, progressive disease is a 25% increase over the baseline (on-study) and an increase in the absolute-value PSA level by at least 5 ng/mL, which is confirmed by a second value. In patients whose PSA has decreased but has not reached response criteria, progressive disease would be considered to have occurred when PSA increases 25% over the nadir, provided that the increase is a minimum of 5 ng/mL and is confirmed.
There are some trials in which investigators may wish to administer at least two cycles of therapy before removing patients from the study because of PSA progression. This is especially true for cytostatic agents that may require a period of time before treatment effect.
Time to PSA Progression
In the absence of evidence of clinical progression, the time to PSA progression is an appropriate outcome to report (especially for noncytotoxic agents). PSA progression may occur before clinical progression. The start of the time to PSA progression is the day treatment is initiated (time to progression as shown in Fig 2). If at least a 50% decline in PSA has been achieved, the end date is the time the PSA has increased 50% above the nadir at a minimum of 5 ng/mL (this is the same as the parameter for PSA response). For patients without a PSA decrease of this magnitude (or no decrease in PSA), the end point for progression will be calculated at the time a 25% increase in PSA has been achieved (see above). All end dates require a confirmatory PSA.
Stable Disease
The category of "stable disease" is controversial. There is no need to define or report stable disease as a category because the same information is contained in a more robust way within the definitions of time to PSA progression. The term stable disease may be used in the clinical situation as an interim classification of patients on an ongoing trial; however, this term should not be used when reporting an analysis of the data.
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DESIGN, ANALYSIS, AND REPORTING
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In general, multi-institutional phase II trials are preferred and encouraged because they tend to be less prone to extremes of patient selection bias and also serve better to test the "real world" feasibility of the therapy (facilitating the transition to phase III trials). For all phase II trials, primary analysis and reporting should be done in a fashion consistent with an intent-to-treat approach, treated patients should not be excluded from the analysis for disease progression or toxicity before an arbitrary time point, such as one or two cycles of therapy. The only exclusions should be patients who never started therapy or who died of an unrelated cause before initial evaluation. However, it is acknowledged that some investigators feel that adequate trials of cytostatic agents may require considerable periods of exposure before treatment effects may be observed. In such cases, the treatment protocol should include a prospective definition of an adequate trial, and a secondary analysis may be reported that is based on a denominator of adequately treated patients.
For all phase II trials, there should be a prospective identified, explicit, response rate of interest (or a time to PSA progression of interest, or both) and a (one- or two-stage) statistical design that explains the alpha and beta errors of the design. If the study includes different cohorts of patients (PSA only, PSA plus assessable disease or symptoms, or PSA plus measurable disease), it may be appropriate to have separate outcome parameters for these cohorts. Some patients will have AIPC yet have no evidence of disease on physical exam, bone scan, or computed tomography scan. These patients, when included in these trials, should be distinguished separately in the report from patients who have measurable or assessable evidence of disease. It is also recognized that prior treatment for patients with AIPC may influence subsequent response. For that reason, in the reporting of data, patients should be categorized by the number and type of hormonal and nonhormonal treatments previously administered.
If time to PSA progression will be a planned primary end point, the time of interest should be chosen to be sufficiently long, so as to be of likely clinical importance, and the intervals for PSA testing should be appropriate to the time frame. We recommend that PSA be monitored at a minimum of once a month.
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DISCUSSION
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A serum PSA is much simpler to obtain than traditional measurements of treatment outcome and can also be obtained more frequently. In addition, patients often become quite focused on their PSA value and its sense of seemingly mathematical objectivity, and they desire to have it tested frequently. Trials have used weekly, biweekly, and monthly measurements of PSA to assess response. The time for which the decline must be maintained to be considered a relevant end point and the number of values required have also varied.
Surrogate end points have been defined as response variables that can substitute for a true end point for the purpose of comparing specific interventions or treatments in a clinical trial. It is generally agreed that PSA changes alone do not currently meet the criteria for surrogacy. But changes in PSA can still be of use as an aid in determining which agents should be tested in phase III trials using more traditional end points.
A standardized set of eligibility and response criteria is needed as new agents undergo clinical testing. The definitions described in this paper have not been validated; nonetheless, the guidelines outlined in this article attempt to allow clinical investigators who are evaluating new regimens in AIPC to speak the same language. There is not necessarily a correct set of guidelines, but we believe our definitions are reasonable to incorporate into most trials for patients with AIPC. Obviously, there may be times when these criteria may not seem to fit the clinical question posed. In that situation, the investigators may modify these criteria, clearly document the reason why they have done so, and clarify how their reporting differs from that used in this document. It is recognized that new validation data may come forward that advances the field, rendering these criteria obsolete.
Response duration and the time to PSA progression may also be important clinical end points. A short dramatic decrease in PSA may not be as important as a sustained decrease, even if it is not of the same magnitude. The date of the confirmatory PSA values should have no impact on the response duration and time to disease progression. Clearly, there may not be any clinical or radiographic evidence of progressive disease in responding patients.
We believe that these are practical guidelines for using PSA as a measurement of outcome. The use of common standards is important as we determine which agents should progress to randomized trials that will use survival as an end point. These guidelines may need to be updated as more is learned about the use of PSA in this population.
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METHODS FOR CONFERENCE
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This conference was organized by investigators from the Medicine Branch [and Cancer Treatment Evaluation program] of the National Cancer Institute, Bethesda, MD, and paid for through the Office of Special Populations, National Cancer Institute, Bethesda, MD, and the Office of Research on Minority Health, National Institutes of Health, Bethesda, MD. The objective was to standardize eligibility and response criteria for phase II clinical trials of patients with androgen-independent prostate cancer. The participants were recognized as expert clinical investigators in the field of metastatic prostate cancer and included a broad representation from the different cooperative groups. The conference was held over 2 days (March 10-11, 1999) in McLean, VA.
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ACKNOWLEDGMENTS
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ACKNOWLEDGMENT
We thank Hank Porterfield of U.S. TOO, Hinsdale, IL; John Willie of National Prostate Cancer Coalition, Washington, DC; Howard Soule, PhD, the Association for the Cure of Cancer of the Prostate (CaP CURE), Santa Monica, CA; Barry Kramer, MD, National Cancer Institute, Bethesda, MD; and Steve Hirschfeld, MD, Food and Drug Administration, Rockville, MD for assisting with the development of these guidelines. The following investigators were invited but unable to participate: Philip Kantoff, MD; William K. Kelly, MD; David Smith, MD; Ken Pienta, MD; Nick Vogelzang, MD; Ian Tannock, MD; Otis Brawley, MD; and Chris Logothetis, MD.
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Submitted April 19, 1999;
accepted August 3, 1999.
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TOP
ABSTRACT
INTRODUCTION
