Clinical and histological patterns of dermatofibroma without gross skin surface change: A comparative study with conventional dermatofibroma.

Backg round: Dermatofibroma sometimes clinically presents as a nodular lesion without gross skin surface change. Clinicopathologic features of this variant of dermatofi broma have not been evaluated. Aims: To assess clinicopathologic features of dermatofi broma presenting as a subcutaneous nodule. Methods: This study reviewed the clinical and histological features of 42 cases of subcutaneous dermatofibromas and compared them with 95 cases of conventional dermatofi broma. Results: Dermatofi broma without gross skin surface change was associated with a shorter pre-diagnosis duration than conventional dermatofi broma. Increase in size during the pre-diagnosis period was signifi cantly more frequent in the conventional type. In addition, these dermatofi bromas were more likely than the conventional type to occur in the head and neck region. Although tumor depth was deeper than in the conventional type, less than half of the dermatofi bromas without gross skin surface change were found histologically to be “subcutaneous” or “deep-penetrating dermatofi broma”. Subcutaneous extension was more frequent in these dermatofi bromas while focal stromal hyalinization and hemosiderin deposits were more common in the conventional type. Limitations: This study is a retrospective, single center design. Conclusion: The present study suggests that dermatofi broma without gross skin surface change is a variant type with distinct clinical and histological features that distinguish them from conventional dermatofi broma.

Increased apoptosis in AK-5 tumor cells after transfection with wild type p53 gene.

AK-5 tumor cell death is mediated through necrosis and apoptosis. The apoptotic activity in AK-5 cells has been studied after introduction of wild-type p53 gene. Apoptotic activity both in vitro and in vivo is significantly increased in p53 transfected cells. Similarly there is fragmentation of tumor cell DNA after undergoing apoptosis. These observations suggest an active participation of p53 in inducing apoptosis in AK-5 tumor cells.