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Although CD133 has been shown to be a marker for cancer stem cells in various tumours, its expression in pancreatic cancer has not yet been clinically reported. In this study, we investigated the relationship between CD133 expression and clinicopathological factors in pancreatic cancer. Pancreatic head carcinoma specimens from 80 patients who underwent surgical resection were immunohistochemically assessed for CD133, vascular endothelial growth factor (VEGF)-C, CXCR4, CD34, Ki-67, and cytokeratin (CK) expressions. Sixty percentage (48/80) of specimens were CD133-positive, with less than 15% cells per specimen expressing the marker. CD133-positive cells were found at the peripheral site of adenocarcinoma glandular structures and were negative for CK. There was a significant correlation between CD133 expression and clinicopathological factors, including histological type, lymphatic invasion, and lymph node metastasis (P ¼ 0.0215, 0.0023, and 0.0024, respectively). Vascular endothelial growth factor-C expression was also significantly correlated with CD133 expression (P ¼ 0.0002). Consequently, the 5-year survival rate of CD133-positive patients was significantly lower than that of CD133-negative patients (P ¼ 0.0002) and multivariate analysis revealed that CD133 expression was an independent prognostic factor (P ¼ 0.0103). These results suggest that CD133 expression in pancreatic cancer was significantly associated with lymphatic metastasis, VEGF-C expression, and prognosis.

We have previously reported frequent allelic loss in chromosome bands 16q24.1-q24.2 in human lung cancer. Since the H-cadherin (CDH13) gene has been isolated and mapped to this common region of allelic loss, we have investigated this gene in human lung cancer. The reverse transcription/polymerase chain reaction technique has revealed the loss of expression in four (57%) of seven lung cancer cell lines. To study the CDH13 gene further, we have analyzed deletions, genetic alterations, and methylation status at the 5' region of this gene. Three (75%) of four cell lines that have lost expression show a deletion of the CDH13 locus accompanied by hypermethylation of the remaining allele. Moreover, hypermethylation has been observed in nine (45%) of 20 primary lung cancers. These results suggest that a combination of deletion and hypermethylation causes inactivation of the CDH13 gene in a considerable number of human lung cancers.

Intravenous DEX at a dose of 0.3 μg kg⁻¹ after induction of anesthesia reduced sevoflurane-associated EA and postoperative pain in pediatric ambulatory surgery, with no increase in the incidence of adverse events and with no change in parents' satisfaction level.