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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