PubMed · 5096643
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P J Fialkow. 1971-11-18. Single or multiple cell origin for tumors?. https://doi.org/10.1056/nejm197111182852111
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Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with the development of both lymphoid and epithelial tumours. As a common virus infection, EBV appears to have evolved to exploit the process of B cell development to persist as a life-long asymptomatic infection. However, the virus can contribute to oncogenesis as evidenced by its frequent detection in certain tumours, namely Burkitt's lymphoma (BL), post-transplant B cell lymphomas, Hodgkin's disease (HD) and nasopharyngeal carcinoma (NPC), and by its unique ability to efficiently transform resting B cells in vitro into permanently growing lymphoblastoid cell lines (LCLs). These transforming effects are associated with the restricted expression of EBV genes such that only a subset of so-called latent virus proteins are expressed in virus infected tumours and in LCLs. Distinct forms of EBV latency are manifest in the different tumours and these appear to be a vestige of the pattern of latent gene expression used by the virus during the establishment of persistent infection within the B cell pool. This review summarises our current knowledge of EBV latent gene function and how this relates to the role of the virus in the aetiology of different tumours.
We report a 12-year-old boy who presented with incomplete right ophthalmoplegia, exophthalmos and headache. Initial CT and MRI revealed a mass in the right cavernous sinus. During tumour work-up, CT identified additional tumour within the mediastinum. Biopsy of the mediastinal lesion identified Burkitt's lymphoma. We report on this case because radiologists and clinicians should be alerted to identify sites of primary Burkitt's lymphoma outside of the central nervous system if clinical symptoms indicate, or imaging shows, CNS lesions. Primary CNS involvement in Burkitt's lymphoma is rare.
Acute lymphoblastic leukemia (ALL) is associated with recurrent chromosomal abnormalities. The cryptic translocation t(12;21)(p13;q22), which leads to the TEL-AML1 fusion gene, is the most common abnormality in childhood B-cell ALL. The aim of this retrospective study was to determine the incidence of TEL-AML1 fusion in childhood and adult B-cell ALL using interphase fluorescence in situ hybridization (I-FISH) and its association with additional changes. FISH, using dual-color extra-signal (ES) DNA probe specific for the TEL and AML1 genes, was performed either on blast cells suspensions stored in liquid nitrogen immediately after Ficoll or on leukemic cells preserved in fixative solution at -20 degrees C after short-term culture. No TEL-AML1 fusion was observed in the 26 ALL adults. The fusion was found among 19.6% of the 57 ALL children, additional changes being identified by conventional cytogenetics in 80% of the cases. A deletion of the untranslocated TEL was observed in 36.3% of the ALL with the TEL-AML1 fusion. The coexpression of myelocytic and B-lymphoid antigens was found in 3 of the 11 of TEL-AML1 fusion positive-ALL. Our results (frequency of TEL-AML1 fusion in children and of the deletion of the untranslocated TEL allele, mean age of the patients and white blood cell count) are within the range observed by others. Structural chromosomal abnormalities other than the t(12;21) are frequent and may play a role in the prognosis of these patients.