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Hodgkin ' s Disease 374 375

A. Molina, L. Jlao, K. L. Chang,S. T. Traweek, S. J. Formin,NM Jiwa,JA Kummer,A Horstman,W Vos, PhM, Kluin,P van der Valk,JMM Walboomers,CJLM Meijer, F. Al KnatQj, N. Mason

semanticscholar(2005)

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摘要
Molecular and ImmunohistochemicaJ analyses ware performed on frozen and paraffin-embedded tissues from a patient with an unusual lymphoproliferative malignancy characterized by the presence of low grade small cleaved cell lymphoma (LGL) In bone marrow (BM), and composite Hodgkin's disease (HD) and high grade small non-cleaved cell lymphoma (HGU within separate areas of a single lymph node (IN). PCR analysis of DMA extracted from each of these three sites revealed evidence of t(14;18) translocation Involving bcl-2 rearrangement at the major breakpoint region (MBR). DNA sequencing of the two separate PCR-ampliflad products from the LN tissue that contained HD and HGL showed evidence of two different donal bcl-2 rearrangements which share MBR breakpoints at the same nudeotide on chromosome 18 and identical N-insertions but which differ by a deletional mutation. This finding is consistent with the presence of two distinct but related donal populations. Reed-Sternberg cells from the HD component of the LN tissue showed reactivity with antibodies directed against CD30 (Ki1), CD 15 (Leu-M1), bcl-2 protein and EBV latent membrane protein (EBVLMP) but not for CD20 (L26). In contrast, the HGL cells stained with antibodies directed against CD20 and bcl-2 protein and not with CD30, CD 15 or EBV-LMP, findings shared with the LGL cells in BM, and did not exhibit EBV or HD markers. Additionally, p53 expression was detected in the HD and HGL tissues but not in the LGL cells. Our findings suggest that 1) the composite HD and HGL originated from a single clone and 2) the acquisition of EBV infection and p53 expression are associated with the development of HD in this patient. ANALYSIS OF MHC CLASS I EXPRESSION ON REED-STERNBERG CELLS IN RELATION TO THE CYTOTOXIC T-CELL RESPONSE IN EPSTEIN-BARR VIRUS POSITIVE AND NEGATIVE HODGKIN'S DISEASE JJ Oudejans, NM Jiwa, JA Kummer, A Horstman, W Vos, JPA Bank, PhM Kluin*. P van der Valk, JMM Walboomers and CJLM Meijer Depts of Pathology, Free University Hospital Amsterdam and University Hospital Leiden*, The Netherlands
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