Metastatic pattern of CC531 colon carcinoma cells in the abdominal cavity: an experimental model of peritoneal carcinomatosis in rats.

BACKGROUND: Peritoneal spread of tumour cells is a major source of morbidity and mortality in patients with colorectal cancer. In order to develop strategies to prevent intraperitoneal dissemination and to treat peritoneal carcinomatosis, the spread of tumour cells in the peritoneal cavity was studied. METHODS: Two million CC531 colon carcinoma cells were administered intraperitoneally in five groups of eight rats. The rats were killed after 1, 2, 4 and 8 hours and 3, 7, 14 and 21 days. After inspection of the abdominal cavity, samples of blood and ascites were taken. Liver, spleen, omentum, mesentery, diaphragm, parathymic lymph nodes and lungs were removed for histology and immunohistochemistry. RESULTS: No abnormalities were seen in the abdominal cavity until day 3. Subsequently the peritoneum and omentum became thickened and after 21 days all rats had haemorrhagic ascites and peritoneal carcinomatosis. The abdominal fluid contained tumour cells at all stages. The number of tumour cells decreased in the first 8 hours, and increased thereafter. At microscopy the peritoneum was completely covered by tumour cells after 3 days. Tumour cells concentrated in the milky spots (MS) of the omentum within 4 hours. The size of the MS increased as a result of an increase in number of tumour cells and macrophages. After 7--21 days the MS were completely replaced by tumour cells and new MS were formed. In the diaphragm tumour cells invaded the lymphatic lacunae after 8 h, and obliterated these after 3--7 days. Also invasion of the muscle fibres was seen after 3 days. Microscopically no tumour cells were found in blood, liver, spleen, parathymic nodes and lung. CONCLUSION: After intraperitoneal administration of CC531 colon carcinoma cells, tumour cells spread throughout the abdominal cavity, and concentrate in the milky spots of the greater omentum, the paracolic gutters, the subhepatic and subphrenic spaces and in the lymphatic lacunae of the diaphragm.

Analysis of pleural fluid in idiopathic spontaneous pneumothorax; correlation of eosinophil percentage with the duration of air in the pleural space.

Pleural fluid analysis was performed in patients with idiopathic spontaneous pneumothorax. The objective of the study was to define the cell differentiation, and part of the cytokine profile, in relation to the duration of pneumothorax. In the 23 consecutive patients (19 men, mean age 34.2 years, 17 smokers), pleural fluid was obtained immediately after chest tube drainage (n = 6), or during thoracoscopy (n = 17). Cytospins were carried out, and supernatant analysis of the different cytokines was performed using sandwich ELISA. All concentrations were corrected for dilution. The duration of the pneumothorax was correlated with the rise in eosinophil percentage (r = 0.81, P < 0.00001) in pleural fluid. RANTES, platelet-activating factor (PAF), and monocyte chemotactic protein-1 (MCP-1) were detectable but no relationship with eosinophils or duration of the pneumothorax was found. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interluekin-8 (IL-8) were not detectable. Interleukin-5 (IL-5) concentration correlated with the eosinophil concentration (r = 0.84, P = 0.037) and the eosinophil percentage (r = 0.68, P = 0.005) in the pleural fluid. Idiopathic spontaneous pneumothorax causes a time-related rise in the eosinophil percentage in the pleural space, which correlates with the level of IL-5.

Differentiation induction of HL60 cells in a long-term bone marrow culture of acute myeloid leukemia.

Bone marrow stromal cells are critical for the proliferation and differentiation of hemopoietic stem cells. The hemopoietic microenvironment is reproduced in long term bone marrow culture (LTBMC). Normal LTBMC versus leukemic LTBMC and their stroma conditioned medium were compared with respect to their proliferative and differentiation-inducing capacities. Myeloid leukemic cells (HL60) were layered onto LTBMCs derived from normal volunteers and patients with AML. Differentiation was measured with a comprehensive panel of maturation parameters, i.e. morphology, cytochemistry, quantitative enzyme determination, NBT test and immunophenotyping. Inhibition of proliferation occurred in all cocultures. Clear maturation in monocytic direction was obvious in one culture of HL60 cells layered onto a leukemic stroma. As stroma-derived conditioned medium has no effect, a cellular interaction seems involved. These observations support not only the concept that normal stroma influences leukemic cell growth but also that leukemic stroma can modulate cell growth and maturation.