To determine the pathologic factors useful in predicting prognosis in patients with stage A prostatic cancer we studied 117 patients followed for 2 to 15 years. Since no patient was treated until progression of disease occurred we were able to correlate pathologic findings with the natural history of the disease in an untreated population of patients. In 14 patients (12 per cent) extensive local (2) or metastatic (12) disease developed. Because 12 of the 14 patients had progression of the disease within 4 years we thought than an analysis of all patients followed for 4 years would be useful. Extent and grade of disease were the 2 factors that most accurately predicted progression. No patient with a low grade lesion (Hopkins grade 1 or Gleason total score 2 to 4) had progression and only 2 per cent of patients with less than 5 per cent cancer had progression. These patients were classified as stage A1 and 60 per cent of all patients were in this category. We believe that these patients require no further therapy. Of the patients with more than 5 per cent cancer 32 per cent had progression and 17 per cent of the patients with either Hopkins grade 2 to 3 disease or Gleason total score more than 4 had progression. These patients were classified as stage A2 and their optimal management remains to be determined.

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A 7000 g cystic tumor replacing the body and tail of the pancreas was resected in a 64-year-old man. Numerous peritoneal implants confirmed its malignant nature. Light microscopy of both the primary tumor and the implants revealed distinctive cytoplasmic eosinophilia and apical granules. Ultrastructural examination demonstrated numerous zymogen granules and abundant, rough endoplasmic reticulum, which confirmed that the tumor was composed of acinar cells. No mucinous or serous differentiation was detected. We have not found report of a similar tumor.

The second reported papillary prostatic urethral carcinoma displaying an unusual clear-cell or so-called mesonephroid histologic appearance is described. Neoplasms arising from the utricular region have generated considerable discussion of their histogenesis and hormone-responsiveness. A review of the literature as well as consideration of this case suggests that the lesion's clear-cell appearance should not be used as evidence for müllerian derivation from the utricle. The authors favor a periurethral gland origin for this particular tumor.

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We have recently observed 3 children with AML treated with daunorubicin (DNR), ara-c and thioguanine (TG) who during remission developed marked hepatomegaly (H) in the absence of jaundice or significant tranaaminaaemia. Liver scans revealed diffuse non-homogeneous reduction in uptake suggesting leukemic infiltration. Liver biopsies showed no significant infiltration, but instead thickening of the walls of the central veins, and intense centrilobular congestion and hemorrhage, a pattern resembling VOD caused by plant alkaloid poisoning. One child had a large R. pleural effusion requiring chest drainage for 1 month. All 3 children have been since maintained only on TG. H and abnormal liver scans have improved but remain abnormal 8-10 months later. One child in relapse was re-treated with all 3 druga and developed an exacerbation of the liver disease and pleural effusion. The erythrocytes of the newborn infant posseas a variety of metabolic characteriatics that serve to distinguish them from the red cells of n o r m 1 adults. In an attempt to define the functional significance of w r a of t h e m differencea the red cell. of nnrborn infanta were etudied at reduced oxyeen tenaions rather than in room air. in order to m r e closely mimic the intrauterine wvironrant. Red cells from 10 adults and 10 infants were incubated for 3 hours in room air, 5X 02. 2X 02, and in nitrogen, and measureuntm of glycolysim, glycolytic interudiates, and re8ponae to mnadione (7.5 ug/ml) were performed. Glucose conmumption and pymvate and lactate production roae in a similar fashion in both group#. In the adult. the incream in glucoae conrumption cns araociated with an increme in the levels of trio-phosphataa and 2.3-DPG. A 16 year old girl developed hypercalcemia (14.4 mgmfdl) at the time of exacerbation of acute lymphoblastic leukemia which required intensive therapy, including mithramycin, to reduce calcium levels. Parathormone (PTH) was inappropriately elevated to 82 p1Eqlml with a calcium level of 13.7 mgmldl.To determine if ectopic PTH production by leukemic cella was occurring in thia patient, bone marrow (952 lymphoblasta) was cultured in vitro in a liquid culture aystem containing 15% fetal calf serum. No measurable PTH was present at 0 time or at 20 hours, however, 247p1Eq/ml PTH was measured at 68 hours. PTH levels increased in the culture aystem with levels of 349 p1Eqlml at 10 days and 533 plEqlml at 13 da3a. PTH was undetectable when no viable cella remained in culture at 17 days. PTH production was similar when the cells were cultured in media with calcium levels ranging from 2.7 -5.9 mgmldl. This is the initial demonstration of autonomous PTH production in culture of lymphoblastic leukemia cells, and is another example of a non-endocrine cell produring a biologically active polypeptide hormone. Autonomous production of PTH should be considered in the etiology of hypercalcemia in acute lymphoblastic leukemia.

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