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Spontaneous regression of advanced breast cancer is a rare phenomenon. Efforts have been made in order to explain it by means of immunological mechanisms. Corticosteroids have demonstrated important efficacy in the treatment of breast cancer. We present a patient with stage IV breast cancer in whom large tumour masses dramatically regressed during treatment with dexamethasone alone. In this patient, histological and hormonal findings, with results of analyses on surface and intracellular blood cells markers demonstrated significant redistribution of lymphocytes and accumulation of natural killer cells in tumour masses. It seems that dexamethasone has acted through the hypophyse against cancer.

Between February 1985 and October 1989, 26 patients previously treated for metastatic breast cancer received oral tegafur, at a median daily dose of 1200 mg. Of these, 21 were evaluable for response. The overall response rate was 29%; six (two in lungs, two in skin and two in lymph nodes) of 44 evaluable lesions (14%) responded to therapy. Haematological toxicity was mild, and no other dose-limiting toxicity was seen. The data indicate some activity in heavily pretreated metastatic breast cancer even after previous 5-FU therapy.

59 patients who had earlier developed an infection following antineoplastic chemotherapy were randomised to receive either granulocyte colony-stimulating factor (G-CSF) alone or G-CSF+quinolone as prophylaxis during subsequent identical chemotherapy courses. 30 patients received 48 courses of G+CSF, while 29 patients received 44 courses of G-CSF+ofloxacin or ciprofloxacin. The overall infection rate was 23%. Patients with WHO grade IV leukopenia at the onset of prophylactic treatment developed infection in 61% of cases when on G-CSF, but only in 22% when on G-CSF+quinolone (P = 0.002). Patients with initial leukopenia of grade WHO III-I had only a 11% infection rate showing no significant difference between the treatment groups. The median duration of leukopenia < 1 x 10(9)/l was 4 days for patients receiving G-CSF alone and 3.5 days for those receiving additional quinolone. Patients developing infection had grade IV leukopenia for a median of 5 days. Both prophylactic treatments were well tolerated. We conclude that when prophylactic G-CSF is initiated at WHO grade IV leukopenia, addition of an oral quinolone reduces the risk of infection.