Improved Long-Distance Polymerase Chain Reaction for the Detection of t(8;14)(q24;q32) in Burkitt’s Lymphomas

The t(8;14)(q24;q32), involving MYC gene (8q24) and the immunoglobulin heavy chain (IgH) locus (14q32), represents about 75% of all translocations in Burkitt’s lymphoma (BL). Due to the great variability of the breakpoint region, a standard polymerase chain reaction assay is not sufficient for the detection of this chromosomal translocation. The availability of new and more efficient DNA polymerases that allow the amplification of genomic fragments many kilobase-pairs long, makes it possible to identify the t(8;14) in BL cells by long-distance polymerase chain reaction (LD-PCR). We have established a simplified and efficient LD-PCR for the detection of t(8;14)(q24;q32) that relies on the use of one primer specific for MYC exon II combined, in different reactions, with four primers for the IgH locus: three for the constant regions Cμ, Cγ, and Cα, and one for the joining region (JH). We first studied seven BL cell lines and optimized LD-PCR reaction for analysis of tumor specimens. Five of seven cell lines were positive for the t(8;14), whereas two lines derived from endemic BL were negative, as expected. Of 15 biopsies obtained from pediatric BL and subsequently analyzed, 13 (87%) were positive for the translocation detected by LD-PCR and showed a product ranging in size from 2.0 to 9.5 kb. Cμ region was involved in 6 cases, Cγ and Cα in 2 cases each, and JH in 3 cases. Interestingly, 2 of the tumors positive for JH showed a second, larger PCR product with the Cα- and Cγ-specific primer, respectively. We established that our LD-PCR method could detect 10−3 BL cells within a population of hematopoietic cells lacking the translocation. In conclusion, our LD-PCR method represents a fast, highly sensitive, and specific tool to study sporadic BL and to detect minimal disease and residual disease in patients affected by t(8;14)-positive lymphomas

Hepatocellular carcinoma following chronic delta virus hepatitis in a patient cured of leukemia.

A 20-year-old patient with chronic delta virus hepatitis (CDVH), cured of acute lymphoblastic leukemia (ALL), developed hepatocellular carcinoma (HCC) 14 years after hepatitis B virus (HBV) infection. The association between chronic HBV infection and HCC is well known, but CDVH patients affected by HCC are rarely reported in literature. To our knowledge, the case we describe is the first HCC case reported in literature occurring in a young boy with CDVH. We could expect further similar cases, considering 1) the high prevalence of HDV infection in children affected by ALL in our series, 2) the previous ALL treatment, and 3) a possible natural predisposition to cancer