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Phase II oral estramustine and oral etoposide in
hormone-refractory adenocarcinoma of the prostate.
Proc Am Soc Clin Oncol 17:329A, 1998.
No abstract.
Phase II evaluation of oral estramustine and oral
etoposide in hormone-refractory adenocarcinoma of the
prostate.
Pienta KJ, Redman B, Hussain M, Cummings G, Esper PS, Appel
C, Flaherty LE
Meyer L. Prentis Comprehensive Cancer Center of Metropolitan
Detroit, MI.
J Clin Oncol 1994 Oct;12(10):2005-12
PURPOSE: Estramustine and etoposide (VP-16) have been
demonstrated to inhibit the growth of prostate cancer cells in
experimental models. This led us to evaluate the effectiveness
of this combination in the treatment of patients with
metastatic prostate carcinoma refractory to hormone
therapy.
PATIENTS AND METHODS: Estramustine 15 mg/kg/d and VP-16 50
mg/m2/d, were administered orally in divided doses for 21
days. Patients were then taken off therapy for 7 days and the
cycle then repeated. Therapy continued until evidence of
disease progression.
RESULTS: Forty-two patients have been enrolled onto this
trial with a minimum of 40 weeks follow-up. Of 18 patients
with measurable soft tissue disease, three demonstrated a
complete response (CR) and six a partial response (PR) for
longer than 2 months. Of these 18 patients, pretreatment
prostate-specific antigen (PSA) levels decreased by at least
75% in five men (28%) and by at least 50% in nine (50%). The
median survival duration has not been reached in those
patients who demonstrated a response either by soft tissue or
PSA criteria. Of 24 patients with disease limited to bone, six
(25%) demonstrated improvement and nine (38%) demonstrated
stability in their bone scans. Five men (21%) demonstrated a
decrease of at least 75% in pretreatment PSA levels and 14
(58%) demonstrated at least a 50% decrease; the median
survival duration has not been reached in these patients.
Pretreatment performance status is an important predictor of
survival.
CONCLUSION: We conclude that the combination of
estramustine and VP-16 is an active oral regimen in
hormone-refractory prostate cancer.
Platinum-based chemotherapy for patients with
poorly differentiated hormone-refractory prostate cancers
(HRPC): response and pathologic correlations.
Proc Amer Soc Clin Oncol 14:232, 1995.
No abstract.
Estramustine and vinblastine: use of prostate
specific antigen as a clinical trial end point for hormone
refractory prostatic cancer.
Seidman AD, Scher HI, Petrylak D, Dershaw DD, Curley T
Department of Medicine, Memorial Sloan-Kettering Cancer
Center, New York, New York 10021.
J Urol 1992 Mar;147(3 Pt 2):931-4
The combination of estramustine phosphate and vinblastine
sulfate, 2 agents with separate and unique antimicrotubular
effects, has demonstrated additive cytotoxicity against the
DU145 human prostate derived cell line in vitro. We evaluated
this combination in 25 patients with progressive hormone
refractory prostate cancer. Of 24 patients with an elevated
prostate specific antigen (PSA) level at the start of
treatment 13 (54%, 95% confidence limits 34 to 74%) had a
greater than 50% decrease in PSA levels on at least 3
consecutive biweekly determinations. The median decrease in
PSA in responding patients was 64% (mean 71.7%) and the median
duration of response was 7 months. In 5 patients with
bidimensionally measurable disease 2 partial responses were
observed. Treatment was well tolerated, with mild and
manageable toxicity. This is a well tolerated outpatient
treatment regimen for patients with hormone-refractory
prostatic cancer which deserves further investigation.
Weekly paclitaxel by 3-hour infusion plus oral
estramustine (EMP) in metastatic hormone refractory prostate
cancer(HRPC).
Proc Am Soc Clin Oncol 18:340A, 1999.
No abstract.
Paclitaxel (T), estramustine (E) and carboplatin(C)
in patients (pts) with advanced prostate cancer (PC).
J Urol 161:177A, 1999.
No abstract.
Activity of docetaxel (D) + estramustine (E) after
dexamethasone (Dex) treatment in patients (pts) with androgen
insensitive prostate cancer (AIP).
Proc Am Soc Clin Oncol 17:343A, 1998.
No abstract.
Phase II trial of 96-hour paclitaxel plus oral
estramustine phosphate in metastatic hormone-refractory
prostate cancer.
Hudes GR, Nathan F, Khater C, Haas N, Cornfield M, Giantonio
B, Greenberg R, Gomella L, Litwin S, Ross E, Roethke S,
McAleer C
Department of Medical Oncology, Fox Chase Cancer Center,
Philadelphia, PA, USA.
g_hudes@fccc.edu
J Clin Oncol 1997 Sep;15(9):3156-63
PURPOSE: To evaluate the antitumor activity of 96-hour
paclitaxel and daily oral estramustine phosphate (EMP) in
patients with metastatic hormone-refractory prostate cancer
(HRPC).
PATIENTS AND METHODS: Thirty-four patients with
adenocarcinoma of the prostate that progressed after one or
more hormonal therapies and a trial of antiandrogen withdrawal
were enrolled onto this phase II trial. Patients received
paclitaxel 120 mg/m2 by 96-hour intravenous (i.v.) infusion on
days 1 through 4 of each 21-day cycle, together with daily
oral EMP 600 mg/m2/d, continuously.
RESULTS: Four of nine patients with measurable disease had
objective responses (one complete response [CR] and three
partial responses [PRs]) in liver (two patients) or nodes (two
patients) of 2, 6, 8, and 20 months' duration. Of 25
assessable patients with metastases limited to bone, 14 had a
> or = 50% decline in pretreatment prostate-specific
antigen (PSA) level sustained for at least 6 weeks and seven
had a > or = 80% decline. Overall, 17 of 32 patients
(53.1%) with elevated pretreatment PSA levels had a > or =
50% decline of PSA and nine (28.1%) had a > or = 80%
decrease. The main toxicities (> or = grade 2) were nausea,
fluid retention, and fatigue, which occurred in 33%, 33%, and
24.2% of patients. Median time to progression, based on
increasing PSA level and other clinical criteria, was 22.5
weeks. The estimated median overall survival time is 69
weeks.
CONCLUSION: The combination of EMP and 96-hour paclitaxel
is an active regimen for patients with HRPC. These results
further support the therapeutic strategy of combining agents
that impair microtubule function by complementary
mechanisms.
Phase I/II trial of estramustine (E) with taxotere
(T) or vinorelbine (V) in patients (pts) with metastatic
hormone-refractory prostate cancer (HRPC).
Proc Am Soc Clin Oncol 17:338a, 1998.
No abstract.
Phase I/II trial of estramustine (E) and taxotere
(T) in patients with metastatic hormone-refractory prostate
cancer (HRPC).
Proc Am Soc Clin Oncol 18:348A, 1999.
No abstract.
Phase I trial of docetaxel with estramustine in
androgen-independent prostate cancer.
Petrylak DP, Macarthur RB, O'Connor J, Shelton G, Judge T,
Balog J, Pfaff C, Bagiella E, Heitjan D, Fine R, Zuech N,
Sawczuk I, Benson M, Olsson CA
Department of Medicine, Columbia Presbyterian Medical Center,
New York, NY 10032, USA.
dpp5@columbia.edu
J Clin Oncol 1999 Mar;17(3):958-67
PURPOSE: To evaluate the toxicity, efficacy, and
pharmacokinetics of docetaxel when combined with oral
estramustine and dexamethasone in a phase I study in patients
with progressive metastatic androgen-independent prostate
cancer.
PATIENTS AND METHODS: Thirty-four men were stratified into
minimally pretreated (MPT) and extensively pretreated (EPT)
groups. Estramustine 280 mg PO tid was administered 1 hour
before or 2 hours after meals on days 1 through 5, with
escalated doses of docetaxel from 40 to 80 mg/m2 on day 2.
Treatment was repeated every 21 days.
RESULTS: Thirty-four patients were assessable for toxicity
and 33 for response. In the MPT patients, dose-limiting
myelosuppression was reached at 80 mg/m2, with six patients
experiencing grade 3/4 granulocytopenia. In EPT patients,
escalation above 70 mg/m2 was not attempted. Fourteen MPT
(70%) and six EPT (50%) patients had a > or = 50% decline
in serum PSA on two consecutive measurements taken at least 2
weeks apart. The overall 50% PSA response rate was 63% (95%
confidence interval [CI], 28% to 81%). Of the 18 patients with
bidimensionally measurable disease, five (28%; 95% CI, 11% to
54%) achieved a partial response. At the time of entry onto
the study, 15 patients required narcotic analgesics for bone
pain; after treatment, eight (53%) discontinued their pain
medications. The area under the curve for docetaxel increased
linearly from 40 to 70 mg/m2. At 80 mg/m2, the measured area
under the curve was 8.37 (standard deviation, 0.724), which
was significantly higher than the previously reported
values.
CONCLUSION: The recommended phase II dose of docetaxel
combined with estramustine is 70 mg/m2 in MPT patients and 60
mg/m2 in EPT patients. This combination is active in men with
androgen-independent prostate cancer.
A phase II study of docetaxel, estramustine, and
low dose hydrocortisone in hormone refractory prostate cancer:
preliminary results of CALGB 9780
Proc Am Soc Clin Oncol 18:321a, 1999.
No abstract.
Phase II study of estramustine (E) combined with
docetaxel (D) in patients with androgen-independent prostate
cancer (AIPCa).
Proc Am Soc Clin Oncol 18:355A, 1999.
No abstract.
A phase II trial of docetaxel in patients with
hormone refractory prostate cancer(HRPC): long term
results.
Proc Am Soc Clin Oncol 18:314a, 1999.
No abstract.
A phase II trial of docetaxel (Taxotere) in
hormone-refractory prostate cancer: correlation of antitumor
effect to phosphorylation of Bcl-2.
Friedland D, Cohen J, Miller R Jr, Voloshin M, Gluckman R,
Lembersky B, Zidar B, Keating M, Reilly N, Dimitt B
Oncology-Hematology Association, Allegheny Cancer Center, and
the Triangle Urological Group, Pittsburgh, PA 15212,
USA.
Semin Oncol 1999 Oct;26(5 Suppl 17):19-23
Twenty-one patients with hormone refractory prostate cancer
were enrolled to receive single-agent docetaxel (Taxotere;
Rhone-Poulenc Rorer, Collegeville, PA) 75 mg/m2 intravenously
every 21 days. Six patients consented to biopsies of the
prostate tumor before and following the first cycle of
chemotherapy and 11 patients underwent periodic blood
collection for isolation of the mononuclear cell fraction. The
toxicities of treatment were moderate but included eight
episodes of grade III and two episodes of grade IV
nonhematologic toxicity as well as seven episodes of grade III
and 11 episodes of grade IV hematologic toxicity (primarily
neutropenia, including four episodes of febrile neutropenia).
An objective response of more than 50% reduction in
prostate-specific antigen was observed in seven patients (38%)
and more than half of the patients with symptomatic disease at
the initiation of therapy had improvements on treatment.
Radiographic or scintigraphic evidence of tumor regression was
observed in six patients. Nine patients experienced a
prolonged period of stable disease on treatment (median, six
cycles). Tumor specimens are currently being analyzed for
bcl-2 expression and phosphorylation. The current series
confirms the substantial single-agent activity of docetaxel in
hormone refractory prostate cancer and may help to further
elucidate its mechanism of action at the molecular level.
Hydrocortisone and stilboestrol in combination for
castration-relapsed prostate cancer.
Proc Am Soc Clin Oncol 17:325a, 1998.
No abstract.
5-fluorouracil and low-dose recombinant
interferon-alpha-2a in patients with hormone-refractory
adenocarcinoma of the prostate.
Shinohara N, Demura T, Matsumura K, Toyoda K, Kashiwagi A,
Nagamori S, Ohmuro H, Ohzono S, Koyanagi T
Department of Urology, Hokkaido University School of
Medicine, Japan.
nobuo-s@med.hokudai.ac.jp
Prostate 1998 Apr 1;35(1):56-62
BACKGROUND: The effectiveness of a chemotherapy regimen
including 5-fluorouracil (5-FU) and recombinant
interferon-alpha-2a (rIFN-alpha-2a) was evaluated in
hormone-refractory prostate cancer patients.
METHODS: Patients received a continuous intravenous
infusion of 5-FU at 600 mg/m2/day for 5 days (D1-D5), followed
by a bolus injection of 5-FU on D15 and D22. Patients received
intramuscular injection of rIFN-alpha-2a at 3 million IU on
D1, D3, D5, D15, and D22. This schedule was repeated every 4
weeks.
RESULTS: Between 1993 and 1995, 23 patients with hormone
refractory prostate cancer were enrolled in this study. Two of
five patients with nodal disease exhibited partial responses
according to the NPCP criteria. Fourteen of 17 patients with
bone disease showed stable disease. Of 21 patients assessible
for response, 9 patients had a decrease in the PSA level
greater than 50% of baseline. Bone pain disappeared partially
or completely in 8 of 14 patients with this symptom at entry.
The median overall survival was 18 months. The associate
toxicity was well tolerable.
CONCLUSIONS: Combination chemotherapy of 5-FU and low dose
rIFN-alpha-2a in patients with hormone-refractory prostate
cancer proved feasible, and with acceptable toxicity.
Intermittent androgen deprivation (IAD) with
finasteride (F) during induction and maintenance permits
prolonged time off IAD in localized prostate cancer
(LPC).
J Urol 161:156A, 1999.
No abstract.
The Androgen Deprivation Syndrome: the incidence
and severity in prostate cancer patients receiving hormone
blockade. Accepted for poster presentation at the ASCO meeting
May 19th, 1998, Los Angeles, CA.
Proc Amer Soc Clin Oncol. 17: 316A, 1998.
No abstract.
Dietary phytoestrogens and prostate cancer.
Proc Annu Meet Am Assoc Cancer Res 36:687, 1995.
No abstract.
Hereditary prostate cancer: epidemiologic and
clinical features.
Carter BS, Bova GS, Beaty TH, Steinberg GD, Childs B, Isaacs
WB, Walsh PC
Department of Urology, Johns Hopkins Medical Institutions,
Baltimore, Maryland 21287-2101.
J Urol 1993 Sep;150(3):797-802
No abstract.
Genetic epidemiology of prostate cancer in the Utah
Mormon Genealogy.
Cancer Surv 1:47-69, 1982.
No abstract.
Familial clustering of cancers of the breast and
prostate in a population-based sample of postmenopausal
women.
Proc Annu Meet Am Assoc Cancer Res 35:A1724,
1994.
No abstract.
The anti-oxidant revolution.
Thomas Nelson Publisher. 1994.
No abstract.
Enter the zone.
Regan Books, 1995.
No abstract.
The Anti-aging zone.
Regan Books, 1999.
No abstract.
Inhibition of epidermal growth factor receptor
(EGFr) tyrosine kinase activity by silymarin, a polyphenolic
antioxidant and potent cancer chemopreventive agent.
Proc Annu Meet Am Assoc Cancer Res 38:A1766,
1997.
No abstract.
19-nor-hexafluoride analogs of vitamin D3: A novel
class of potent inhibitors of proliferation and induction of
p27/Kip1 in human breast cancer cell lines.
Proc Annu Meet Am Assoc Cancer Res 38:A579,
1997.
No abstract.
Overexpression of uPA by the MatLyLu rat prostatic
cancer cell line results in enhanced tumor angiogenesis.
Proc Annu Meet Am Assoc Cancer Res 38:A3518,
1997.
No abstract.
Green tea polyphenols inhibit growth of PC
xenograft cwr-22 and decrease ornithine decarboxylase
activity: implications for PC chemoprevention.
J Urol 155: 510A, 1996.
No abstract.
Heterogeneity of prostate cancer in radical
prostatectomy samples.
Urology 43:60-4, 1994.
No abstract.
Oncogene overexpression in human prostate cancer
cell lines.
Proc Annu Meet Am Assoc Cancer Res 34:A2309,
1993.
No abstract.
Adrenal androgens predict for early progression to
flutamide withdrawal in patients with androgen-independent
prostate carcinoma.
Proc Am Soc Clin Oncol 13:237, 1994.
No abstract.
A double-blind assessment of antiandrogen
withdrawal from Casodex (C) or Eulexin (E) therapy while
continuing luteinizing hormone releasing hormone analogue
(LHRH-A) therapy for patients (Pts) with stage D2 prostate
cancer (PCA).
Proc Am Soc Clin Oncol 15:255A, 1996.
No abstract.
Dramatic PSA decline in response to discontinuation
of megestrol acetate in advanced prostate cancer; expansion of
the antiandrogen withdrawal syndrome.
J Urol 153:1956-7, 1995.
No abstract.
Optimal dosing of ketoconazole (Keto) and
hydrocortisone (HC) leads to long responses in hormone
refractory prostate cancer.
Proc Am Soc Clin Oncol 13:229A, 1994.
No abstract.
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