Evaluation of plasma hCG measurement in the diagnosis of nontrophoblastic neoplasms and assessment of the value of concomitant measurement of plasma hCG and CEA in patients with bronchogenic carcinoma and neoplasms of the digestive tract were undertaken. Only one of 70 normal control subjects had positive plasma hCG (3.5 ng/ml), whereas 54 of 320 patients with nontrophoblastic neoplasms had measurable plasma hCG (1.9 to 160 ng/ml). Forty of these patients had less than 5.1 ng/ml, 10 had 5.1 to 10 ng/ml, and only three had high levels of 96,110, and 160 ng/ml. Elevated plasma CEA levels of 3.6 to 140 ng/ml were found in 38 of the 70 patients with bronchogenic carcinoma and 30 of the 72 patients with neoplasms of the digestive tract in this series. Concomitant positive hCG was found in only six of the 68 patients who had elevated CEA levels, and positive hCG was found in eight of 74 patients who had normal plasma CEA. The low frequency and the modest elevation of plasma hCG, despite frequent advanced disease, indicate plasma hCG has limited value as a biologic marker fQr diagnosis and assessment of nontrophoblastic neoplasms.

Patients with acute nonlymphocytic leukemia were given remission induction therapy consisting of cytosine arabinoside and an anthracycline. Those patients who experienced complete remission received two courses of consolidation therapy and were randomized to receive maintenance therapy consisting of either daily chemotherapy with reinforcements every 3 mo or reinforcement therapy only every 6 wk. The overall complete remission rate was 66%, with 80% complete remission for previously untreated patients less than 60 yr of age who did not have a prior history of malignancy. Remission durations were the same for patients treated with both maintenance regimens. The major determinant for successful remission induction therapy was patient age, with older patients frequently succumbing to intercurrent infection. Documented leukemic cell resistance to the therapy employed was only rarely encountered. Once remission was achieved, age was no longer a determinant of patient survival, since duration of remission was independent of age. Remission durations were directly related to leukemic cell retention of cytosine arabinoside triphosphate. Hence therapy for acute nonlymphocytic leukemia can be divided into two separate areas: remission induction and remission maintenance.

In 5 patients treated with L-asparaginase, plasma insulin response to intravenous glucose injection was measured by radioimmunoassay. Two of the patients developed a diabetic state (2 and 4 days) after a single dose of L-asparaginase, while a third patient developed diabetes 2 days after the fourth dose of L-asparaginase. Plasma insulin was not detectable by radioimmunoassay during the diabetic state in each of them. The normal pattern of insulin response returned completely in one of the 3 patients within 23 days, whereas suboptimal response persisted for 2 weeks and 9 months in the remaining 2 patients. The two remaining patients were studied prior to and 6 days after a single dose of L-asparaginase; neither developed a diabetic state.

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Seventeen patients with advanced neoplastic diseases were fed a formula diet deficient in vitamin B6 for 10 to 80 days. In addition, nine of the patients received the B6 antagonist, 4‐deoxypyridoxine (4‐DOP), for periods ranging from 6 to 46 days. No definite antitumor effect could be observed in any of the patients studied despite ample biochemical and clinical evidence of vitamin B6 depletion. The study confirmed previous reported experiences in man and many other animal species that 4‐DOP accentuates some of the manifestations of vitamin‐B6 deficiency, particularly neurologic and dermatologic side effects. The lymphopenic effect of 4‐DOP was demonstrated only in patients with normal bone marrow. In three of four patients with lymphoproliferative disease the peripheral lymphocyte count rose coincidentally with 4‐DOP administration while in the fourth the rise developed immediately after discontinuation of 4‐DOP and at the peak of toxicity. The study showed evidence of progressive tissue depletion when the patient was fed the deficient diet alone. Addition of 4‐DOP to the deficient diet led to the transient reappearance of measurable pyridoxal phosphate in leukocytes and pyridoxic acid in the urine. This and the slight increase in reticulocyte counts during administration of 4‐DOP raise the possibility that vitamin B6 was mobilized from certain tissue depots by the 4‐DOP and was thus available for oxidation to pyridoxic acid and for use by the less depressed of the enzymes dependent upon vitamin B6.