Mohammad A. Vasef

Nasopharyngeal Carcinoma, with Emphasis on its Relationship to Epstein-Barr Virus:

Nasopharyngeal carcinoma (NPC) is an epithelial tumor with a distinct geographic distribution and a characteristic histologic appearance. It is rare in Europe and North America, but it is among the most common cancers in southern China. Genetic predisposition, environmental factors, and Epstein-Barr virus (EBV) all have been associated with the pathogenesis of this tumor. There is an increasing body of evidence that among all these factors, EBV appears to be the strongest and most consistently related factor. According to the current sensitive in situ hybridization methods for the detection of EBV-encoded small RNAs (EBER), almost 100% of cases of NPC, irrespective of their histologic subtypes, have demonstrable EBERs in the nuclei of the tumor cells. In this review paper, we discuss the predisposing genetic and environmental factors and the role of EBV in the pathogenesis of this tumor with particular emphasis on the role of EBV.

The t(2;5)-associated p80 NPM/ALK fusion protein in nodal and cutaneous CD30+ lymphoproliferative disorders.

A high percentage of extracutaneous CD30+ anaplastic large cell lymphomas (nodal ALCL) carry a specific chromosomal translocation, t(2;5) (p23;q35), that results in abnormal expression of p80 NPM/ALK chimeric protein (p80). The protein p80 may be detected by immunohistochemistry using polyclonal (anti‐p80) or monoclonal (ALK1) antibody directed against the ALK epitope. Although nodal ALCL, primary cutaneous ALCL, and lymphomatoid papulosis type A (lyp A) have similar histologic and immunohistochemical features, the expression of p80 in these cutaneous lesions has not been extensively studied. We immunostained tissues from 10 nodal ALCL, 8 primary cutaneous ALCL, 24 lyp A, and positive and negative controls using polyclonal rabbit anti‐p80 and the avidin‐biotin‐peroxidase labeling method. Reactivity was determined by comparing staining intensity to positive controls [4 nodal ALCL with t(2;5)] and negative controls (21 non‐ALCL lymphomas). Only cutaneous lesions staining positively with anti‐p80 were further studied with the monoclonal antibody ALK1 and reverse transcription polymerase chain reaction (RT‐PCR) for p80 messenger RNA. All positive controls (4/4), but none of the negative controls (0/21) nor lyp A (0/24), were immunoreactive for anti‐p80. Sixty percent (6/10) of nodal ALCL and a single case (12%) of primary cutaneous ALCL were immunoreactive for anti‐p80. In this exceptional cutaneous lesion, although we did not find NPM/ALK by RT‐PCR, we detected strong expression of ALK using ALK1. We conclude that t(2;5) is rarely involved in the pathogenesis of cutaneous CD30+ lymphoproliferative disorders.