BACKGROUND.It has been reported previously that the combined loss of chromosomal arms 1p and 19q is a significant predictor of outcome for patients with anaplastic oligodendroglial (AO) tumors and that such chromosomal loss correlates with classic histology in AO. The authors sought to determine whether histology was an equivalent or superior predictor of outcome compared with 1p/19q status in 131 patients with AO tumors. METHODS.The status of 1p and 19q was determined using real-time, quantitative polymerase chain reaction analysis and/or fluorescence in situ hybridization.Clinical features (response to adjuvant therapy and tumor location) and molecular genetic abnormalities (9p and 10q deletions, overexpression of p53 and epidermal growth factor receptor) were determined on available specimens. Histologic assessments for classic oligodendroglial features were performed by five neuropathologists. RESULTS.Classic histology was associated closely with 1p/19q loss, as reported previously. Patients who had tumors that were considered classic by at least four of the five neuropathologists showed significantly increased progression-free and overall survival compared with the patients who had less classic tumors. The authors also tested the correlation between 1p/19q status and outcome in subsets of patients stratified according to classic tumor features. The association of 1p/19q status with survival was related closely to the presence of classic histology. Loss of 1p/19q was predictive of improved outcome only among patients who had tumors with classic histologic features. CONCLUSIONS.The current results suggested that, in addition to 1p/19q status, histologic features contribute information to the prediction of outcome in patients with AO. Loss of 1p and 19q appeared to be a prognostic marker only in the subset of patients who had AO tumors with classic histologic features. Cancer 2005;104: 1468 -77.

Interleukin (IL)-6 reportedly has negative inotropic and hypertrophic effects on the heart. Here, we describe endotoxin-induced IL-6 in the heart that has not previously been well characterized. An intraperitoneal injection of a bacterial lipopolysaccharide into C57BL/6 mice induced IL-6 mRNA in the heart more strongly than in any other tissue examined. Induction of mRNA for two proinflammatory cytokines, IL-1beta and tumor necrosis factor (TNF)-alpha, occurred rapidly before the induction of IL-6 mRNA and protein. Although stimulation of isolated rat neonatal myocardial cells with IL-1beta or TNF-alpha induced IL-6 mRNA in vitro, nonmyocardial heart cells produced higher levels of IL-6 mRNA upon stimulation with IL-1beta. In situ hybridization and immunohistochemical analyses localized the IL-6 expression primarily in nonmyocardial cells in vivo. Endotoxin-induced expression of cardiac IL-1beta, TNF-alpha, and intercellular adhesion molecule 1 was augmented in IL-6-deficient mice compared with control mice. Thus cardiac IL-6, expressed mainly by nonmyocardial cells via IL-1beta action during endotoxemia, is likely to suppress expression of proinflammatory mediators and to regulate itself via a negative feedback mechanism.

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In most tissues increases in ornithine decarboxylase (ODC) are associated with growth. Refeeding fasted rats. a potent stimulus for mucosal growth, strongly increases ODC in both small and large intestinal mucosa. In the small bowel, almost all of this increase occurs in the mature villus cells rather than the proliferative crypt cells. Nevertheless, inhibition of ODC with difluoromethylornithine blocks the growth response. Using a highly specific, polyclonal antiserum to ODC, we have determined that in the fasted rat ODC is localized almost exclusively to the villus cells. Using antiserum dilution techniques, we have shown that, within 2 h, refeeding increases the amount of immunoreactive ODC in both villus and crypt cells. Furthermore, the trophic hormone gastrin also increases ODC, but only in the crypt cells. Epidermal growth factor increased ODC to a greater extent than gastrin, but stimulation was more general, including both crypt and villus cells. Perfusing an isolated segment of small bowel in situ with glycine for 2 h also increased immunoreactive ODC but only in the villus cells. Thus in the small intestine the effect of refeeding on ODC activity appears to be mediated by different types of stimuli: luminal nutrients increase enzyme levels in the absorbing villus cells, while trophic peptides stimulate ODC synthesis in the proliferative crypt cells.

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