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PubMed1978

In vivo interaction between steroidal alkylating agents and oestrogen receptors in rabbit uteri.

The binding of steroidal alkylating agents to specific tissue component is necessary for the selective distribution of these compounds to their target tissues. The in vivo interaction of Estracyt or NSC-112259 with oestrogen receptors may play an important role in their action mechanism. Both Estracyt and NSC-112259 which were administered in vivo, gradually reduced the binding of [3H] oestradiol to cytoplasmic oestrogen receptor in rabbit uteri. From this, it was suggested that a negligible amount of oestradiol was released from these compounds and that the oestradiol moiety was useful as a carrier for the nitrogen mustard moiety. And it appeared that the synthesis of a new receptor protein was inhibited by the nitrogen mustard moiety, thereby causing a decrease in the cytoplasmic oestrogen receptor level.

Animals↗
PubMed2003

What next after hormonotherapy in cancer prostate?

Treatment of hormone-resistance cancer prostate (HRCP) is undergoing evolution. Chemotherapy is now increasingly being utilized. The steps involved in the hormone management and the role for chemotherapy in the current time are being discussed. Hormonal management is carried out at different stages of hormonal sensitivity by sequential hormonal use. Once hormonal resistance is established, the combination of mitoxantrone and prednisone become a standard chemotherapeutic approach. New agents, such as docetaxel, are being tested in phase-III trials against mitoxantrone plus prednisone. HRCP is now regarded as a chemotherapy-sensitive tumor. The goals of chemotherapy in HRCP are to decrease PSA level and improve quality of life. New agents and combinations are needed to improve survival to meet this end.

Antineoplastic Agents, Hormonal↗
PubMed1995

Goserelin. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in prostate cancer.

Goserelin is a gonadotrophin-releasing hormone (GnRH) analogue which during long term administration reduces circulating levels of gonadotrophins (luteinising hormone and follicle stimulating hormone) and sex hormones. Goserelin is administered subcutaneously as a biodegradable depot formulation incorporating 3.6mg of the drug, which is released continuously over 4 weeks. In men with untreated advanced prostate cancer, monthly goserelin 3.6mg has been confirmed as similar in efficacy to surgical castration and diethylstilbestrol (stilboestrol) 3mg daily taken orally. Goserelin is better tolerated than diethylstilbestrol and appears to have a more favourable effect on quality of life than surgical castration. Treatment of prostate cancer with a combination of goserelin and an antiandrogen remains controversial as a result of inconsistent findings, despite extended data from a large trial which indicated an advantage for the combined regimen over surgical castration with respect to duration of time to progression and survival. Combination therapy also minimises the initial increase in signs and symptoms (disease flare) that occurs in up to 4% of patients at the beginning of treatment with a GnRH analogue. Surgical castration remains the treatment of choice in patients at risk of metastatic compression of the spinal cord or ureteric obstruction. However, goserelin is an effective alternative to surgery, or estrogen therapy, in men with previously untreated advanced prostate cancer. Goserelin seems to be preferred to surgery by the majority of patients given a choice of treatment, and importantly in a palliative care situation where there are no survival advantages for treatment alternatives, it appears to have a more beneficial effect on the quality of life than surgery.

Absorption↗
PubMed2001

Treatment options in hormone-refractory prostate cancer: current and future approaches.

Prostate cancer is the second leading cause of cancer mortality among men in Western countries. The initial treatment of advanced prostate cancer is suppression of testicular androgen production by medical or surgical castration, but nearly all men with metastases will develop disease progression. Patients with hormone refractory prostate cancer (HRPC) have a median survival of approximately 18 months and no therapy has yet demonstrated a definitive survival advantage. However, in the past several years, a number of promising new treatment strategies have emerged. One of the most important new treatment strategies involves secondary hormonal manipulation after the failure of primary androgen deprivation. This approach is predicated on the recognition that HRPC is a heterogeneous disease and some patients may respond to alternative hormonal interventions despite the presence of castrate levels of testosterone. Until recently, cytotoxic chemotherapy was felt to be relatively ineffective in the treatment of HRPC. Combination regimens incorporating new active agents have demonstrated significant activity in this setting, renewing interest in the use of chemotherapy to treat HRPC. Recent advances in the understanding of prostate cancer biology have led to the development of drugs directed against precise molecular alterations in the prostate tumour cell. Biologic agents now in development include those capable of altering signal transduction, blocking angiogenesis, inhibiting cell cycle progression, and stimulating apoptosis. In addition, many types of immune therapies are showing promise. Evaluating these agents, and incorporating them into existing regimens, are major goals of ongoing clinical research in advanced prostate cancer.

Androgen Antagonists↗
PubMed1983

Cisobitan in treatment of prostatic cancer. A prospective controlled multicentre study.

Cisobitan, an organosilicon compound with estrogenic and antigonadotropic properties has been evaluated clinically in comparison with an estrogen preparation. In a multicenter study a total of 140 patients with well and moderately well differentiated prostatic cancer were randomly allocated to treatment with Cisobitan or Estradurin/Etivex, 70 to each group. Of 34 patients with poorly differentiated prostatic cancer 18 were given Cisobitan--and 16 were given Estracyt-treatment. Among the patients with well and moderately well differentiated prostatic cancer there were, disregarding mortality, no major differences in subjective, objective or laboratory response to the two kinds of treatment. The pattern of side effects was similar, but oedema requiring diuretics occurred more often in the estrogen treated group. There was a significant difference in mortality at 12 months between the groups, two in the Cisobitan group and ten in the estrogen treated group. Cancer was the cause of death in two patients in the estrogen treated group. All other patients succumbed in cardiovascular diseases. At 24 months the difference in mortality rate was less pronounced: Another ten patients had died in the Cisobitan treated group and seven among the estrogen treated patients. Cancer was responsible for the deaths in seven of the Cisobitan patients compared to four of the estrogen treated patients. Within three years one more patient in both groups had died. Of the 34 patients with poorly differentiated cancer, twelve were alive at the 24 months' follow up, six in the Cisobitan group and six in the Estracyt group.

Clinical Trials as Topic↗
PubMed1975

Antiprostatic effects of a nitrogen mustard of estriol.

The chemical ester of a nitrogen mustard with estriol was tested for its antiprostatic effects in dogs and rats. The E33-mustard was shown to interfere with the uptake of labeled estriol in the dog prostate and by the ventral prostate of the rat; and to increase the uptake of the radioactivity associated with testosterone in the dog prostate. The weights of the ventral and dorsolateral prostates of the rat were significantly reduced following the administration of E3-mustard for 2 days. The results are interpreted to be very similar to those obtained with the mustard of E (Estracyt) and the effects are probably a combination of the actions of the released estrogen (D) and/or mustard, either adding individually or in concert.

Animals↗
PubMedDate not supplied

Advances in prostate cancer chemotherapy: a new era begins.

Prostate cancer continues to be the most common lethal malignancy diagnosed in American men and the second leading cause of male cancer mortality. Over 60 years ago, Huggins and Hodges discovered androgen deprivation as a first-line therapy for metastatic prostate cancer, which leads to remissions typically lasting 2 to 3 years, but in most men prostate cancer ultimately progresses to an androgen-independent state resulting in death due to widespread metastases. Multiple mechanisms of androgen independence have now been documented, including amplification of the androgen receptor as well as signal transduction pathways that bypass the androgen receptor completely. In 2004, two landmark studies demonstrated a survival advantage in androgen-independent prostate cancer patients utilizing docetaxel chemotherapy, setting a new standard of care for this disease. In addition, treatments with the bisphosphonate zoledronic acid and systemic radioisotopes have also been shown to have palliative benefits in this population. Building on these advances, several new traditional chemotherapeutic agents as well as new targeted therapies are under development.

Antineoplastic Agents, Phytogenic↗
PubMed1980

The chemotherapy of prostatic adenocarcinoma.

A number of chemotherapeutic agents show moderate promise for the palliative treatment of metastatic prostatic carcinoma. Although patterns of metastatic disease make classic response rates difficult to obtain and interpret, doxorubicin, cyclophosphamide, dacarbazine (DTIC), and cisplatin have activity in patients who have failed conventional hormonal treatment. In most studies, a survival advantage is seen for responders to these and other chemotherapeutic agents, but no survival advantage has been seen for the treatment cohorts when compared to groups not receiving chemotherapy. Therefore, estimates of the usefulness of these agents must be considered tentative. Multiple drug therapy has not yet shown definite superiority to single agent treatment. The uses and limitations of acid phosphatase as a tumor marker, as well as particular difficulties in measuring tumor response in the disease, are detailed herein.

Acid Phosphatase↗
PubMed1999

Chemotherapy in advanced prostate cancer.

In the United States, prostate cancer is the most commonly diagnosed cancer and the second leading cause of cancer death in men. Prostate cancer is a rare disease before age 40; however, the prevalence increases quickly to 80% by the age of 80, and with increasing life expectancy, hormone-refractory prostate cancer (HRPC) will soon represent the most common cancer in the male population in the United States and other Western countries. The evolution of early prostate cancer is variable and extends over many years; some tumors progress slowly or not at all, whereas others may progress more rapidly and be fatal after a few years. A widely held view is that chemotherapy has no role in HRPC because no single agent or combination has been shown to prolong survival in a randomized trial. This concept may be obsolete, as preliminary results for a number of approaches, mostly derived from laboratory observations, show that prostate cancers are not as resistant to chemotherapy as traditionally believed. The population of early "geriatric" HRPC patients is rapidly increasing, posing an even greater challenge to oncologists in coping with this difficult-to-manage patient population. In this article, we analyze the most novel chemotherapeutic combinations for the treatment of HRPC in otherwise healthy elderly men.

Antineoplastic Agents↗
PubMedDate not supplied

The study of gemcitabine in combination with other chemotherapeutic agents as an effective treatment for prostate cancer.

BACKGROUND: Gemcitabine has demonstrated clinical activity against several common cancers. Our studies examine the ability of gemcitabine, both alone and in combination with other chemotherapeutic agents, to inhibit the in vitro and in vivo growth of several prostate cancer cell lines. MATERIALS AND METHODS: Cultures of LNCaP, PC-3 or MLL cells were exposed to either gemcitabine or other appropriate agents for specified amounts of time. Cells were lysed and nuclei counted utilizing a Coulter Counter. For in vivo experiments, animals were injected with 1 x 10(5) MLL cells subcutaneously into the right flank. Animals were treated as indicated for 14 days. Tumors were then excised, weighed and measured. RESULTS: In both human (PC-3 and LNCaP) and rat prostate (MLL) cancer cell lines our studies demonstrated gemcitabine had a strong effect in vitro, with an IC50 of approximately 500 nM in the human lines and 10 nM in MLL cells. In vivo, studies using the Dunning prostate cancer model in Copenhagen rats resulted in a dose response inhibition of tumor growth, with an 80% decrease in tumor size in rats treated with gemcitabine at 10 mg/kg. CONCLUSIONS: Our results demonstrated the potent activity of gemcitabine against prostate cancer in the Dunning rat model and suggest the addition of paclitaxel may not aid in this activity.

Animals↗