Interleukin-10 (IL-10) has been shown in vitro to inhibit survival and spontaneous DNA synthesis in B-cell chronic lymphocytic leukaemia (B-CELL) cells by induction of programmed cell death. We have analysed the presence of mRNA transcripts for IL-10 in purified B-CLL cells from 35 patients by RT-PCR. Transcripts for IL-10 were detected in 11/20 patients with non-progressive disease. In cell preparations from patients with progressive B-CLL IL-10 mRNA were detected in only 2/15 samples (P < or = 0.01). The Epstein-Barr virus status of the cells did not account for the difference in IL-10 mRNA expression observed between the two groups of patients. Thus, IL-10 mRNA expression in leukaemic cells from patients with B-CLL was strongly associated with non-progressive disease. This finding may support other observations suggesting that IL-10 might be a candidate for immune therapy of progressive B-CLL.

In the present retrospective study we found limited sensitivity of NP-59 scintigraphy. However, when a lateralized scintigraphic uptake is achieved it has a high accuracy. Scintigraphy may be used as an adjunct in cases where adrenal venous sampling is inconclusive.

Surface la-positive cells were found to vary from 0 to 100% in initial blood specimens from 37 adults with acute myelogenous leukemia (AML). When myeloblasts from 19 patients were tested against panels of lymphocytes from 5 to 19 normal donors, mean stimulation indices ranged from 1 to 60. Some leukemic myeloblasts strongly stimulated most allogenic responder lymphocytes whereas others produced almost no stimulation. The addition of antibody against human la to 28 mixed leukocyte reaction (MLR) combinations resulted in significant inhibition (p < 0.001) of ³H-thymidine incorporation. Testing of myeloblastic la may have clinical relevance because patients with > 50% la-positive myeloblasts had a significantly longer survival than patients with fewer la-positive myeloblasts (p < 0.04).

Fifty-six patients with acute, non-lymphatic leukemia in the initial phase were studied. The poor prognostic signs were excessive in vitro growth, many HLA-DR-positive cells, or a low ratio of leukemic cell antigenicity to HLA-DR positivity and age. The cells from older patients formed more clusters (P less than 0.05), and they had less capacity to stimulate normal allogeneic lymphocytes (P less than 0.05) than those from younger patients. Cells forming many clusters also were more often (P less than 0.01) HLA-DR-positive than those forming few clusters. It is suggested that the prognosis in old patients with acute leukemia is poor in part because their leukemic cells have characteristics different from those of young patients.

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