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Background. In the treatment of advanced-stage ovarian cancer, it is common practice to treat elderly patients in a less aggressive fashion than young patients. This approach is based on the notion that age is associated with poor patient tolerance to aggressive chemotherapy. Relatively little data exist to support this contention. The most exciting new chemotherapy agent to be developed in the last 10 years is taxol, a diterpeniod derivative of the Northwestern yew Taxus brevifolia. Methods. The ability to administer dose-intensive taxol to adult patients with recurrent ovarian cancer was assessed retrospectively, and the question was asked whether the administered dose intensity of taxol was unfavorably influenced by age. Forty-eight patients with recurrent ovarian carcinoma received taxol at an initial dose of 250 Mg/[m.sup.2] every 3 weeks. Age in this cohort ranged from 26 to 74 years, with a median of 55. Twenty-nine percent (14 of 48) of the patients treated were 61 years of age or greater. Criteria for administration of taxol included a creatinine clearance of > 45 ml/minute, minimal abnormalities in liver function tests, good performance status, and the absence of substantial comorbid disease. Results. Elder y patients in this cohort (age > 60 years) did not differ from younger patients with respect to administered dose intensity, number of cycles of therapy administered, or the occurrence of serious or mild toxicities. Conclusions. Age, in and of itself, should not be a factor in the consideration of dose modifications of taxol. Cancer 1993; 71:594-600.

Prostate cancer is extremely common among older men. In 1991, an estimated 122,000 new cases occurred in the US, and 32,000 men died from this disease. It is estimated that 70 percent of patients with prostate cancer will develop metastatic disease. This spread of prostate cancer to other organs, often bones, may be temporarily controlled, but, as is the case for many cancers, metastatic disease is rarely cured. Prostate cancer is sensitive to stimulation by male hormones, and therapy for metastatic prostate cancer is directed at removing this source of stimulation. This is accomplished by surgically removing the source of male hormones or by chemically interfering with the normal production of male hormones. Temporary tumor control may be achieved in 80 to 85 percent of cases, but overall survival is less than three years after treatment. A pilot study was conducted to evaluate the combination of hormonal treatment with standard chemotherapy. Fifteen patients were treated with leuprolide and flutamide, drugs that block the synthesis of male hormones (androgens) and interfere with their effects. Prior to the standard chemotherapy, the patients were primed with androgens. This priming stimulates the cancer cells which had been suppressed by the antiandrogen treatment; the idea is to catch them with the cytotoxic chemotherapeutic drugs just at they are starting to multiply again. Three patients achieved a complete response, that is, a disappearance of the symptoms of cancer, as a result of this treatment. Eight patients experienced a partial response, which is generally defined as a reduction in apparent tumor mass of at least 50 percent. The remaining four patients experienced stabilization of their cancer. The median time to disease progression among these patients was 31 months, and nine of the 15 patients are still alive after a median follow-up time of 42 months. The results of the present study were excellent and suggest that a larger trial of this combination of hormonal and chemotherapy is in order. (Consumer Summary produced by Reliance Medical Information, Inc.)

Titers of circulating interferon (IFN) and the activity of 2′–5′ oligoadenylate (2–5A) synthetase, an enzyme specifically induced by IFN, were measured in 28 homosexual men with acquired immunodeficiency syndrome (AIDS) who received one- to six-month courses of antineoplastic therapy with IFN-α and in homosexual and heterosexual controls. Fifteen of the patients and two of seven healthy homosexual men had high endogenous levels of 2–5A synthetase. IFN therapy induced further increases in this enzyme in only 10 of the 28 patients with AIDS. Furthermore, peripheral blood cells from all but one of the patients with AIDS and homosexual controls tested were markedly deficient in their ability to respond to IFN in vitro, as measured by increased levels of 2–5A synthetase. We did not find a statistical correlation between cytomegalovirus viremia and pretherapy endogenous circulating IFN, nor any apparent correlation between disseminated infection with cytomegalovirus and either basal levels of 2–5A synthetase or changes in enzyme level during therapy. Pretherapy circulating IFN was significantly correlated with progressive Kaposi's sarcoma during therapy, but rises in levels of 2–5A synthetase were not sufficient to predict a good clinical response.