HEMANGIOMA OF THE SPLEEN.
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Beta1-4 N-acetylglucosaminyltransferase III (GnT-III) synthesizes bisecting N-acetylglucosamine structures on asparagine-linked oligosaccharides. Using B16-hm mouse melanoma cells stably expressing GnT-III activity as positive transfectants, the effect of bisecting N-acetylglucosamine on the function of CD44 was analyzed in association with adhesion to hyaluronate and tumor spread in mice. Transfection of GnT-III caused increased affinity of immunoprecipitated CD44 to erythro-agglutinating phytohemagglutinin, that preferentially recognizes bisecting N-acetylglucosamine, without affecting the surface CD44 amount, indicating an increase in bisecting N-acetylglucosamine residues on CD44 in positive transfectants. CD44-mediated adhesion to immobilized hyaluronate and the binding of fluorescence-labeled hyaluronate to the cell surface were increased in positive transfectants. The enhanced adhesion in positive transfectants was suppressed by the treatment with beta-N-acetylhexosaminidase, indicating that N-acetylglucosamine residues were responsible for the enhanced adhesion. Positive transfectants showed promoted CD44-mediated tumor growth and metastatic development in the spleen after subcutaneous inoculation into mice. These results indicate that glycosylation of CD44 due to GnT-III causes enhanced adhesion to hyaluronate, local tumor growth and metastatic growth in spleen, suggesting that the CD44-mediated adhesion and tumor spread can be modified through introduction of a glycosyltransferase gene.
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Hepatic artery ligation is useful as a palliation of irressectable hepatic tumors, but does not always produce a satisfactory result. Hepatic tumor with high vascularity is expected to respond more favorably. In this context, primary liver cell carcinoma and carcinoid tumor or leiomyosarcoma of the liver have been satistfactorily treated by hepatic artery ligation. A case is presented of hemangiosarcoma of theliver and spleen treated effectively by hepatic artery ligation, splenectomy, and postoperative intraportal infusion of 5-fluorouracil, as indicated by the regression of hepatic tumors on postoperative scanning and arteriograpms.
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The clinical course of a woman with metastatic reticulum cell sarcoma and intractable lactic acidosis is described. Although her illness was dominated by a myelopathy, she developed severe lactic acidosis which could not be related to decreased tissue oxygen delivery. Necropsy showed extensive hepatic replacement with tumor and widespread disease. This and other possible pathogenetic factors causing lactic acidosis are discussed.
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We studied the effect of tumor size on monoclonal antibody (mAb) in a murine hepatic model. Intrasplenic injection of HT-29 LMM metastatic human colon cancer cell line reproducibility results in hepatic metastases formation in congenitally athymic mice. HT-29-15, a murine mAb of the IgG1 class reactive with the HT-29 LMM cell line, and BL-3, an isotype-matched control mAb, were labeled with iodine 125. Labeled mAbs were injected intravenously into mice with hepatic metastases. Animals were sacrificed on day 5, and tumor and normal tissue weighed and counted. Specific mAb uptake (percent injected dose per gram, %ID/g) by hepatic metastases (5.16 +/- 3.96) was significantly greater than nonspecific uptake (1.41 +/- 0.42) (P less than 0.001). %ID/g of tumor was dependent upon the mAb used, and was independent of tumor weight; consequently, a linear correlation between tumor weight and total uptake (%ID) for specific mAb (r = 0.88, P less than 0.0001) and nonspecific mAb (r = 0.99, P less than 0.0001) administration was demonstrated. We have shown both specific and nonspecific mAb uptake per gram of tumor to be a constant for the given mAb/tumor system and with uptake of mAb to be linearly related to tumor weight.
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The relationship between cellular differentiation and carcinoembryonic antigen (CEA) production by human colorectal tumor cells and their ability to form hepatic metastases was studied. Eight human colon cancer cell lines were injected into athymic mice using different routes of administration to characterize their metastatic potential. The four poorly differentiated, non or low CEA producing cell lines were poorly metastatic to the liver after intrasplenic injection. After intraperitoneal implantation the same cell lines were highly tumorigenic, and subsequently metastatic to the liver. In contrast, the four moderate to well-differentiated cell lines that produced moderate to high levels of CEA were highly metastatic to the liver following intrasplenic injection. After intraperitoneal implantation they were less tumorigenic, and metastatic to the liver. We conclude that in this system poorly differentiated non or low CEA producing colorectal cell lines have a lower metastatic capacity compared to the well-differentiated high CEA producing colorectal cell lines. These data correlate directly with the pattern of metastatic spread and clinical course observed in patients with these tumors, suggesting that degree of differentiation and level of CEA production may play a role in development of site-specific metastases.
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Our experiences with organ saving procedures of the spleen in childhood are presented. In 9 out of 12 children (75%) with traumatic rupture we preserved the organ partially or completely. In 4 patients a partial splenectomy was performed, in three cases of splenorrhaphy was done, and once the organ was repaired with fibrin adhesive. One child was treated conservatively. Another patient underwent splenectomy followed by autotransplantation. Two out of twelve died intra- or postoperatively from severe concomitant injuries. Out of 11 patients with Hodgkin's disease we performed partial splenectomy in five. Only in macroscopically involved cases the organ was removed. In one patient a huge epidermoid cyst of the spleen was enucleated. In another child with a big twisted wandering spleen a splenopexy after partial resection was carried out. In children the spleen should be preserved if ever possible.
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