A unique presentation of an Epstein-Barr virus-associated natural killer/T-cell lymphoproliferative disorder in a white male adolescent.

Background: Extranasal natural killer (NK)/T-cell lymphoma and aggressive NK-cell leukemia are strongly associated with Epstein-Barr virus (EBV) and most often occur in middle-aged individuals. Overlap between these 2 diagnoses is rare. In addition, pathologic findings for these 2 diagnoses are typically notable for necrosis, apoptosis, angioinvasion, and angiodestruction.

Survivin repression by p53, Rb and E2F2 in normal human melanocytes.

The inhibitor of apoptosis protein survivin is a dual mediator of apoptosis resistance and cell cycle progression and is highly expressed in cancer. We have shown previously that survivin is up-regulated in melanoma compared with normal melanocytes, is required for melanoma cell viability, and that melanocyte expression of survivin predisposes mice to ultraviolet-induced melanoma and metastasis. The mechanism of survivin up-regulation in the course of melanocyte transformation and its repression in normal melanocytes, however, has not been clearly defined.

Replication and expansion of trinucleotide repeats in yeast.

The mechanisms of trinucleotide repeat expansions, underlying more than a dozen hereditary neurological disorders, are yet to be understood. Here we looked at the replication of (CGG)(n) x (CCG)(n) and (CAG)(n) x (CTG)(n) repeats and their propensity to expand in Saccharomyces cerevisiae. Using electrophoretic analysis of replication intermediates, we found that (CGG)(n) x (CCG)(n) repeats significantly attenuate replication fork progression.