All tumors showed well-defined and mostly lobulated margins. The well-differentiated liposarcomas were composed mainly of fat with septations or nodules, were hyperintense on T2-weighted images, and demonstrated faint enhancement or no enhancement following intravenous contrast. Myxoid liposarcomas were homogeneous or mildly heterogeneous and a pseudocapsule was present in one case. Pleomorphic types showed a markedly heterogeneous internal structure. Both myxoid and pleomorphic lesions-showed moderate or marked heterogeneous enhancement after contrast administration. Well-differentiated liposarcomas may be differentiated from other types of the tumor by their largely lipomatous appearance. The malignancy grade increases in parallel with tumor heterogeneity and contrast enhancement.
The role of p53 mutation has been shown in different human malignancies, including various skin cancers. In this study, we examined p53 protein expression in 25 eccrine poromas and 11 porocarcinomas by immunohistochemistry. P53 expression was observed in 88% (22 of 25) of eccrine poromas and 73% (8 of 11) of porocarcinomas. In eccrine poromas, percentage of cells reactive for p53 was less than 5% (low expresser) in 6 cases, 5 to 50% (moderate expresser) in 14 and greater than 50% (high expresser) in 2 cases. In terms of intensity, 13 cases showed weak staining, 8 moderate, and 1 case showed strong reactivity. On the other hand, 2 cases of porocarcinoma were low expresser, 2 were moderate and 4 were high expresser. All of the high expressers had also strong staining. This study has demonstrated that eccrine poromas showed significant p53 expression as much as porocarcinomas and, therefore, p53 positivity cannot be accepted as a valuable parameter for malignancy. P53 gene may involve in the carcinogenetic pathway of porocarcinoma but it is likely that other oncogenes may also have a role.
hCAP-18/LL-37 has an important role in innate response during periodontal inflammation. Local deficiency in hCAP-18/LL-37 might be a confounding effect in the pathogenesis of generalized aggressive periodontitis.
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