Lack of BIC and MicroRNA miR-155 expression in primary cases of Burkitt lymphomaKluiver, J., Haralambieva, E., de Jong, D., Blokzijl, T., Jacobs, S., Kroesen, B-J., Poppema, S. & van den Berg, A., Feb-2006, In : GENES CHROMOSOMES & CANCER. 45, 2, p. 147-153 7 p.
Research output: Contribution to journal › Article › Academic › peer-review
We previously demonstrated high expression of primary-microRNA BIC (pri-miR-155) in Hodgkin lymphoma (HL) and lack of expression in most non-Hodgkin lymphoma subtypes including some Burkitt lymphoma (BL) cases. Recently, high expres- sion of BIC was reported in BL in comparison to pediatric leukemia and normal peripheral-blood samples. In this study, we extended our series of BL cases and cell lines to examine expression of BIC using RNA in situ hybridization (ISH) and quantitative RT-PCR (qRT-PCR) and of miR-155 using Northern blotting. Both BIC RNA ISH and qRT-PCR revealed no or low levels of BIC in 25 BL tissue samples [including 7 Epstein-Barr virus (EBV)-positive cases] compared to HL and normal controls. In agreement with these findings, no miR-155 was observed in BL tissues. EBV-negative and EBV latency type I BL cell lines also showed very low BIC and miR-155 expression levels as compared to HL cell lines. Higher levels of BIC and miR-155 were detected in in vitro transformed lymphoblastoid EBV latency type III BL cell lines. An association of latency type III infection and induction of BIC was supported by consistent expression of BIC in 11 and miR-155 in 2 posttransplantation lymphoproliferative disorder (PTLD) cases. In summary, we demonstrated that expression of BIC and miR-155 is not a common finding in BL. Expression of BIC and miR-155 in 3 latency type III EBV-positive BL cell lines and in all primary PTLD cases suggests a pos- sible role for EBV latency type III specific proteins in the induction of BIC expression. (c) 2005 Wiley-Liss, Inc.
|Number of pages||7|
|Journal||GENES CHROMOSOMES & CANCER|
|Publication status||Published - Feb-2006|
- EPSTEIN-BARR-VIRUS, IN-SITU HYBRIDIZATION, C-MYC, TRANSGENIC MICE, NONCODING RNA, CELL-GROWTH, GENE, IDENTIFICATION, ONCOGENESIS, ENCODES