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The in vitro effect of a calf thymus extract, thymostimulin (TP--1), on the E-rosette-forming capacity and on the PHA blastogenic response of peripheral blood lymphocytes was evaluated in 20 patients with untreated Hodgkin's disease. The mean percentage of lymphocytes forming E rosettes increased in patients from 44.2% to 57.5% (P less than 0.005). The mean PHA stimulation index rose with all three concentrations tested, but returned to the normal range only with the highest PHA concentration (60 mu/ml). An increase in the immune parameters was greatest in those patients who presented with decreased E-rosetting cells of total lymphocyte counts or whose disease was Stage III or IV or of mixed cellular histology.

A case is reported of undifferentiated metastatic lung carcinoma in which both a supraclavicular lymph node and bone marrow were infiltrated by anaplastic tumor cells which had engulfed erythrocytes and nucleated elements. The possibility of a histiocytic origin for the phagocytizing neoplastic cells was excluded by ultrastructural, cytochemical, and immunoperoxidase studies. This investigation shows that epithelial tumor cells may, at times develop phagocytizing activity, a phenomenon observed in certain experimentally induced tumors. The mechanism responsible for this phenomenon is not clear.

A patient with leukemic reticuloendotheliosis ("hairy cell" leukemia) with sideroblastic anemia and an epinephrine-induced platelet-aggregation abnormality is presented. Immunologic membrane marker studies supported a B-lymphocyte origin of the hairy cells. It is hypothesized that a defect in the pluripotent marrow stem cell may be responsible for the hairy cell leukemia and for the intrinsic abnormalities in erythrocytes and platelets.

T-cell phenotypes, as defined by murine monoclonal antibodies, (OKT3, OKT4, OKT8, OKIa1), and phytohemagglutinin (PHA) reactivity, were evaluated in E-rosette forming cells (T-cells) from 10 untreated chronic myelocytic leukemia patients. The proportion of T4+ cells was lower in patients than in controls (41.6 versus 61.7%, P less than 0.02); whereas the proportion of T8+ cells was similar in patients and controls. The decrease in T4+ cells in CML resulted in a decrease in circulating T4+/T8+ ratio (P less than 0.02). The Ia1+ T-cells were increased in most CML (8 of 9) patients, while control subjects never displayed Ia1+ T-lymphocytes (P less than 0.01). The PHA reactivity of E-rosette forming lymphocytes was significantly impaired in CML patients with respect to controls (P less than 0.02). The presence of Ia antigen on T-cells was positively correlated with the T8+ cell phenotype (P less than 0.001) and inversely correlated with the T4+ (helper) cell phenotype (P less than 0.05). Furthermore, there was a trend towards an inverse correlation between the PHA response and the level of Ia1+ or T8+ cells, there is no correlation between PHA reactivity and T4+ phenotype. The results suggest that the T-lymphocyte population from untreated CML patients is intrinsically abnormal.