Epstein‐Barr virus (EBV) genomes and c‐myc oncogene in oral Burkitt's lymphomas

In addition to Burkitt's lymphomas, tentative evidence suggests the involvement of Epstein‐Barr virus (EBV) in malignant lymphomas of T‐cell origin. The c‐myc proto‐oncogene is strongly associated with the development of lymphoid neoplasias. In the present study, a series of 38 biopsies of oral lymphomas (29 Burkitt's lymphomas, 9 malignant lymphomas of other type) obtained from patients in Tanzania were studied using in situ hybridization (ISH) and polymerase chain reaction (PCR) for detection of EBV DNA and c‐myc oncogene. In ISH applied on formalin‐fixed, paraffin wax‐embedded biopsies, the Bam HI W fragment of EBV DNA was used as the probe. Amplification of c‐myc oncogene was studied by PCR with a primer set from Exon II area. As an internal standard (β‐globin gene was simultaneously amplified. EBV DNA was disclosed by ISH in five Burkitt's lymphomas only. Using the PCR, 20 of the 29 cases (70%) of Burkitt's lymphomas showed amplification for EBV DNA. Of the other EBV‐positive lymphomas, two were of the lymphocytic type (large non‐cleaved cell), one histiocytic and one Burkitt's‐like lymphoma. All EBV‐positive cases found on the agarose gel were positive also with the dot blot, when hybridized with the 32P‐labeled EBV Bam HI W‐fragment probe. All lymphomas showed similar bands on the gel for c‐myc and β‐globin indicating that no amplification of c‐myc was present.