Stem cell factor (SCF) acts in concert with lineage-specific growth factors to stimulate the growth of hematopoietic colonies. To determine if neoplastic human hematopoietic cells would also respond to SCF, we cultured marrow mononuclear cells from 20 patients with newly diagnosed acute myelogenous leukemia (AML) and two normal donors with SCF, interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), or combinations of growth factors in semisolid medium, and assessed colony growth. SCF receptors (c-kit receptors) were quantitated by equilibrium binding studies with 125I-SCF, and binding parameters were estimated using the ligand program. The cellular distribution of c-kit receptors was determined by autoradiography. Our results show that SCF alone or in combination with IL-3 or GM-CSF increased both the number and size of colonies in 10 of the patients. Receptors for SCF were identified on the blasts from all 20 AML patients. The number of receptors ranged from 600 to 29,000 per cell. In the majority of patients, both high- and low-affinity binding sites were identified. Neither the number of receptors per cell nor the finding of one or two classes of receptors correlated with growth response to SCF. Autoradiographic analysis of 125I-SCF binding to normal marrow mononuclear cells revealed grains associated with blasts and megakaryocytes. Grain counts on blasts from 10 AML patients and on normal marrow blasts suggested that high-affinity c-kit receptor expression on AML blasts is lower than or similar to that of normal blasts. These results identify c-kit receptors on human AML blasts, and indicate that SCF acts synergistically with IL-3 or GM-CSF to stimulate colony growth from the marrow cells of a portion of patients with AML.
Chickenpox (varicella), a common and usually mild infection of childhood, is frequently more serious in adults. The principal complication of adult varicella is pneumonia which may be fatal in a fifth of cases.' We describe two patients with rapidly fulminating varicella pneumonia who responded to vidarabine therapy. Case reports CASE ONE A 34-year-old teacher, previously in good health, was admitted with rapidly progressive shortness of breath complicating varicella. He first became unwell four days before admission with fever, sweats, and anorexia. The varicella eruption appeared the next day and spread rapidly to cover his body and face. Two days before admission he developed severe, dull central chest pain, a dry cough, and increasing dyspnoea. His two daughters, aged 3 and 5 years, had had varicella, six and three weeks previously. On examination he looked ill and was covered with the lesions of haemorrhagic varicella. His temperature was 39 2°C, pulse 110 beats/minute, blood pressure normal, respiratory rate 30/minute, and he was
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