Several cellular and extracellular markers that distinguish the phases of the hemangioma life cycle have been described previously. However, details of the phenotypic changes of; the various cellular elements during hemangioma development have not been fully reported, and the extracellular matrix composition, especially in the vicinity of the proliferating endothelial cells, is poorly described. This study examined the expression of cellular and extracellular molecules and cytokines in the proliferative, involuting, and involuted phases of hemangioma. Paraffin-embedded hemangioma specimens, four from each phase, were examined histochemically and immunohistochemically. Throughout the three phases, vascular endothelial cells stained positive for CD31 and von Willebrand factor, although in the involuted phase, not all vessels in the tissue expressed these endothelial markers. Proliferating cell nuclear antigen was expressed by the majority of endothelial cells and pericytes in the proliferative and early involuting phases, but its expression was negligible in the involuted phase. In addition to finding that the total number of mast cells was highest in the involuting phase, the authors observed that the proportion of chymase-positive mast cells decreased with the progression of hemangioma and that virtually all mast cells expressed the biogenic amine phenotype throughout the hemangioma life cycle. The localization of vascular endothelial growth factor predominantly to the pericytes and endothelial cells during the proliferative phase and of basic fibroblast growth factor to the endothelial cells in both the proliferative and early involuting phases is consistent with previous reports, although the latter growth factorwas also observed in mast cells. Type IV collagen and the beta chain of laminin and perlecan were detected in the basement membranes in all phases. Interestingly, collagen types I, III, and V were present in basal membranes throughout the phases and with increasing density in the stromal areas with involution, although type I collagen was less prominent during the proliferative phase. Short-chain collagen type VIII was localized extracellularly throughout the development of hemangioma but, during the early proliferative phase, it was also detected within mast cells. The expression of specific cytokines and cellular and extracellular markers may help distinguish the different clinical phases of the hemangioima life cycle. These results provide further insight into the biology of hemangioma.

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As a group, renal epithelial malignancies are frequently encountered in clinical practice. It is now appreciated that rather than being a single tumor type, they consist of a variety of morphotypes that show differing clinical behavior (1-3). The most frequently encountered subtype is conventional (clear cell) renal cell carcinoma (cRCC), representing 70% of all adult malignant primary renal tumors, whereas papillary renal cell carcinoma (pRCC) account for 10 -15%, and chromophobe renal cell carcinoma (chRCC), for approximately 5%. The remainder is made up of collecting-duct carcinomas and unclassifiable tumors (2-5).

Killer immunoglobulin-like receptors (KIRs) regulate the activity of NK and T cells through interaction with specific HLA class I molecules on target cells. To date, 16 KIR genes and pseudogenes have been identified. Diversity in KIR gene content and KIR allelic and haplotype polymorphism has been observed between different ethnic groups. Here, we present data on the KIR gene distribution in Pacific Islands populations. Sixteen KIR genes were observed in Pacific Islands populations from the Cook Islands, Samoa, Tokelau, and Tonga. The majority of KIR genes were present at similar frequencies between the four populations with KIR2DL4, KIR3DL2, and KIR3DP1 genes observed in all individuals. Commonly observed KIR genes in Pacific Islands populations (pooled frequencies) were KIR2DL1 (0.77), KIR2DL3 (0.77), KIR3DL1 (0.65), KIR3DL3 (0.93), KIR2DS4/1D (0.78), and KIR2DP1 (0.82), compared to the less-frequently observed KIR2DL2 (0.27), KIR2DL5 (0.30), KIR2DS1 (0.19), KIR2DS2 (0.27), KIR2DS3 (0.16), KIR2DS5 (0.17), and KIR3DS1 (0.18) genes. Differences in KIR gene frequency distributions were observed between the Pacific Islands populations and when compared to other populations. Sixty-nine different genotypes were identified, with five genotypes accounting for more then 50% of all genotypes observed. The number of genotypes observed in each population was similar in the Cook Islands, Samoan, and Tokelauan populations (19, 18, and 19, respectively), but 26 different genotypes were observed in Tongans. The putative haplotype A was predominantly observed over haplotype B in all Pacific Islands populations. Significant linkage disequilibrium was observed for a number of KIR gene pairs.