Defining the temporal requirements for Myc in the progression and maintenance of skin neoplasia.

The homeostatic integrity of skin epidermis is maintained by a balance between keratinocyte proliferation, on one hand, and terminal differentiation combined with outward migration and shedding, on the other. Perturbation of this balance in favor of proliferation can result in hyperplasia and, potentially, tumorigenesis. We have previously described a reversible transgenic mouse model of epidermal neoplasia in which expression of an acutely regulatable form of Myc, MycERTAM, is targeted to epidermis via the involucrin promoter.

Regulation of EMAP II by hypoxia.

Endothelial-monocyte-activating polypeptide II (EMAP II) is a proinflammatory cytokine and a chemoattractant for monocytes and granulocytes. We have previously shown that EMAP II mRNA is strongly expressed at sites of apoptosis in the mouse embryo and that the mature protein is cleaved from its cellular precursor (proEMAP II/p43) by caspase activation to become released from cells. Here we demonstrate in vivo that EMAP II mRNA expression is strongly increased in tumor necrosis factor alpha (TNF)-treated murine meth A fibrosarcomas and in B16 melanomas, especially in close proximity to areas of tissue necrosis.