Effects of superelongation disease, caused by the fungus Elsinoe Brasiliensis Zeigler and Lozano, on cassava (Manihot esculenta Crantz) clones (different genotypes) were studied in fields under high natural disease infection to assess value of genetic resistance and efficiency of field selection. The disease caused 20 to 70% yield reduction on susceptible clones relative to resistant clones depending on planting time and presence of cassava bacterial blight. Susceptible clones could not produce good planting stakes for next plantings. On resistant clones, the disease spread slowly while on susceptible ones it spread rapidly causing abnormal stem elongation and leaf death. Resistance was a quantitative trait controlled largely by additive genetic factors and not negatively correlated with yielding ability per se. Cultivar order of resistance was stable over 8 years of observation. Use of resistant parents in hybridizations combined with simple phenotypic field selection under high natural disease pressure should effectively improve resistance of cassava cultivars.

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Summary.-Lipids extracted from leucocyte pellets with chloroform-methanol were applied to a DEAE-Sephadex column and the gangliosides were eluted with 02M sodium acetate in methanol. The eluate was desalted by Sephadex G-50 column chromatography. The purified ganglioside was spotted on the high-performance thin-layer plate. The plate was developed and sprayed with resorcinol reagents and heated.Seventeen bands of gangliosides were demonstrated in normal human leucocytes. The composition of these gangliosides was different in the various kinds of leucocytes. Amounts of GM3 ganglioside were apparently greater in normal lymphocytes and leukaemic cells than in granulocytes. Among the acute-leukaemic cells, some kinds of complex gangliosides were much more abundant in myelogenous cells than in lymphocytic cells. These changes in ganglioside composition are suggested as new biochemical markers for leukaemic cells.

A monoclonal antibody, KM10 (IgG1) was produced by fusing spleen cells from a human gastric cancer cell (MKN45)‐primed BALB/c mouse with the murine myeloma cell line X63‐Ag8‐653. The antibody reacted strongly with the plasma membrane of human gastrointestinal carcinoma. Sections of the malignant and benign tissues were tested with immunoperoxidase. All of 10 (100%) large intestinal cancers, 26 of 31 (84%) gastric cancers, 5 of 7 (71%) pancreatic cancers and all of 3 (100%) ampullary cancers reacted positively. Moderate or weak reactivity was observed with normal human tissues, hepatoma and carcinomas of mammary, thyroid and adrenal glands. According to a study of the distribution of 125I‐labeled KM10 in nude mice bearing human gastric cancer, KM10 selectively localized in tumor tissue rather than normal tissue. Whole body autoradiography also supported such a selective distribution. Destruction of antigenic properties by pronase digestion demonstrated its protein nature and by Western blot analysis, it was identified as a protein with an Mr of 180–200 kd. KM10‐adriamycin (ADM) conjugate was prepared via an oxidized dextran bridge and this immunoconjugate retained the binding activity against human gastric cancer. MKN45 cells were inoculated subcutaneously into athymic mice and intravenous treatment was begun when the tumor became measurable. A dose‐dependent antitnmor activity was observed in vivo with KM10‐ADM conjugate, while this conjugate was less toxic than free ADM.