Thirty-one adults with Wilms tumor were reported to the National Wilms Tumor Study from 1968 to 1979. Treatment and survival data for these patients were analyzed and compared to similar information derived from children enrolled in the first National Wilms Tumor Study. The ages of the 31 adults ranged from 17 to 63 years (mean 29 years). All but 3 patients had surgical resection or excision of tumor, 7 did not receive postoperative irradiation and all but 1 had chemotherapy. Actinomycin D and vincristine were the drugs used most commonly, 26 of the 31 patients receiving both agents. Advanced disease at diagnosis (6 stage III and 9 stage IV versus 9 stage I and 5 stage II--in 2 cases stage was not known) was found more often than in children in whom stages III and IV disease made up 27 per cent of the first National Wilms Tumor Study population. The 3-year actuarial survival rate for the 31 adults was 24 per cent: 48 per cent for stages I and II disease and 11 per cent for Stage IV disease. Comparable data for children in the first National Wilms Tumor Study, adjusted for stage, were 74, 87 and 53 per cent, respectively. It is concluded that adults with Wilms tumor treated as were these have a worse prognosis than children managed according to the first National Wilms Tumor Study regimen. However, those adults in this series who were treated aggressively, that is surgical excision, postoperative irradiation and multi-agent chemotherapy, appeared to have fared better than adults treated in the pre-chemotherapy era. It is concluded that aggressive therapy should be given to all adults with Wilms tumor irrespective of stage.

The lipid composition has been characterized in erythrocytes obtained from the cord blood of fullterm normal infants. There is an increase in total lipid, lipid phosphorous and cholesterol per cell (total lipid = 6.45 X 10" 10 mg; Lipid P = 1.54 X 10" 11 mg; cholesterol = 1.79 X 10" 10 mg) when compared with adult controls (total lipid = 5.07 X 10" 10 mg; Lipid P = 1.22 X 10" 11 mg; cholesterol = 1.33 X 10~1 0 mg). Despite the increased lipid content, the percentages of total lipid comprised by lipid phosphorous and cholesterol are similar to those found in the adult (P = 2.40 % of total lipid in infants, 2.41 % in adults: cholesterol = 27.1 % of total lipid in infants, 26.0 % in adults). Phospholipid fractionation shows minor variations between the two groups. Cord blood erythrocyte phospholipid has 1.0% lysolecithin, 26.0% sphingomyelin, 27.7% phosphatidylcholine, 15.2% combined phosphatidylserine and phosphatidylinositol, and 29.1 % phosphatidylethanolamine. Adult erythrocyte phospholipid has 1.2% lysolecithin, 24.1% sphingomyelin, 29.5% phosphatidylcholine, 13.1% combined phosphatidylserine and phosphatidylinositol and 31.2% phosphatidylethanolamine. Phospholipid fatty acid patterns in cord blood erythrocytes show an increased percentage of palmitic acid (cord = 21.3%, adult = 17.0%), stearic acid (cord = 16.3%, adult = 15.3%) arachidonic acid (cord = 19.6%, adult = 17.4%) and combined 22 and 24 carbon fatty acids (cord = 17.6%, adult = 16.3%) associated with decreased percentages of oleic acid (cord = 11.9%, adult = 14.6%) and linoleic acid (cord = 3.4%, adult = 10.9%). SpeculationThe erythrocyte lipids of the newborn show deviations from the adult pattern which may have adaptive value for intrauterine life. These same adaptations may render the cell more vulnerable to oxidative damage in postnatal life. Introductionproportion of phosphatidylcholine and phosphatidylethanolamine and the presence of phosphatidylserine The lipid composition of erythrocytes has recently be-imprint a pattern of erythrocyte lipid in the adult come a matter of great interest. Studies have shown clearly different from that of the plasma-environment, that the red cell lipid is composed almost entirely of Adult plasma has two-thirds of the cholesterol in the free cholesterol and phospholipid [32,40]. The minute esterified form, a proportion of phosphatidylcholine amounts of cholesterol esters, the roughly equivalent ten times that of phosphatidylethanolamine and lacks

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Marrow and peripheral blood cells from nine children with juvenile chronic granulocytic leukemia (JCGL) demonstrated intense (94±16% maximum) spontaneous granulocyte/macrophage colony growth but cells from five children with the adult variety of CGL did not. This unusual pattern of colony growth depended upon a stimulatory protein(s) produced by mononuclear phagocytes. No GM-CSA activity was found in any chromatofocused fraction of JCGL monocyte-conditioned media but an activity that induced GM-CSA in umbilical vein endothelial cells was detected at pI 6.9-7.2. Moreover, the CSA-inducing monokine was neutralized by an anti-IL-i antibody in vitro and, in the one case so tested, the same antibody also inhibited "spontaneous" colony growth. Therefore granulocyte/macrophage colony growth in JCGL is characteristically abnormal and distinguishes JCGL from the adult form of the disease. This abnormality depends upon the production, by mononuclear phagocytes, of IL-1 which, in turn, stimulates the release of high levels of colony stimulating activity by other cells. The high proliferative activity of CFU-GM we found in JCGL patients, and the high levels of GM-CSA found in their serum are compatible with the view that the in vitro abnormality reflects a similar abnormality in vivo.