HTLV-I associated lymph node and HTLV-I pathogenesis.

成人t细胞白血病/淋巴瘤（Adult T-cell leukemia/lymphoma， ATLL）是一种与人类t细胞白血病病毒I型（HTLVI）相关的人类恶性肿瘤，其组织学通常为多形型，但组织学并不统一。为了明确组织学分型与预后的关系，我们对572例淋巴结t细胞淋巴瘤进行了重新分型。在所有病例中，使用Southern blot分析检测HTLV-I原病毒DNA的克隆整合。572例分为3组；(A)有克隆整合者[247例]，(B)有AThA和无HTLV-I前病毒DNA克隆整合者[66例]，(C)无ILA者[259例]。A组临床预后较B组和c组差。结论确定A组为HTLV-I相关t细胞淋巴瘤（ATLL）。[J] .中华血友病杂志，1998,19 (2):1)ATLL表现为染色体无性系异常，但其核型在数量和结构上都非常复杂。在ATLL中没有特异性的染色体异常。我们利用反相pcr和FISH技术研究了HTLY-I的整合位点。随机积分得到了证实。18例中有15例HTLV-I整合的染色体出现异常，特别是2例单纯染色体异常的病例，HILV-I整合到异常染色体上，而没有整合到正常染色体上。因此，HTLY-I前病毒整合似乎与染色体异常有关。（Cancer Letters, 1998, 32, 203-12）最近发现的诱饵受体3 （DcR3）与Fa结合。并抑制fasl诱导的细胞凋亡，被认为在肿瘤细胞的免疫逃逸系统中发挥作用。采用斑点杂交和原位杂交（ISH）技术对45例患者DcR3基因的扩增和表达进行了分析，其中EBV相关淋巴瘤17例，成人t细胞白血病淋巴瘤（AILL） 7例。ebv相关PAL和NKL在淋巴瘤细胞中表现出DcR3的扩增和表达。AILL中也有DcR3的表达和扩增。活性细胞中无DcR3表达。（癌症通讯，2000,160,89 -97）BUB基因是芽孢酵母有丝分裂检查点的一个组成部分。最近，研究人员在两种结直肠肿瘤细胞系中发现了hBUB1和hBUBR1的突变等位基因。我们通过研究hBUB1和hBUBR1的突变，以及BAX、胰岛素样生长因子和II型转化生长因子复制错误的最小值，来检验检查点基因在ATLL染色体异常中的作用。10例ATLL患者中有4例检测到hBUBR1或hBUBR1的显著突变/缺失。相比之下，8例B细胞淋巴瘤中只有1例显示hBUBR1无义突变。ATLL和B细胞淋巴瘤均无MIN。(癌症通讯，2000,158,141-50

Adult T-cell leukemia/lymphoma (ATLL) is a human malignancy associated with human T-cell leukemia virus type I (HTLVI), and the histology usually indicates a pleomorphic type, but the histology is not uniform. To clarify the relation between the histological classification and prognosis, we reclassified 572 cases with nodal T-cell lymphoma. In all cases, the clonal integration of HTLV-I proviral DNA was examined, using a Southern blot analysis. 572 cases were classified into 3 groups ; (A) the cases with clonal integration [247 cases], (B) cases with AThA, and those without clonal integration of HTLV-I proviral DNA [66 cases}, (C) cases without A ILA [259 cases]. Group A clinically showed a poorer prognosis than groups B and C. In conclusion, group Awas determined to be ATLL (HTLV-I associated T-cell lymphoma). (Br J haematol 1998, 101, 703-11)ATLL demonstrate clonal chromosome abnormalities, but the karyotypes are very complicated in both number and structure. There are no specific ka … More ryotype abnormalities in ATLL. We investigated the integration site of HTLY-I, using inverse-PCR and FISH. The random integration was confirmed. In 15 of the 18 cases, the chromosomes with HTLV-I integration showed abnormalities, and, especially in 2 cases with simple chromosome abnonnalities, HILV-I integrated int the abnormal chromosome, but not into the normal chromosome. The HTLY-I proviral integration thus seems to, be associated with chromosome abnormalities. (Cancer Letters 1998, 132, 203-12)The recently identified decoy receptor 3 (DcR3) binds to Fa.sL and inhibits FasL-induced apoptosis, and is considered to play a role in the immune escape system of neoplastic cells. We analysed the amplification and expression of DcR3, using dot blot and in situ hybridization (ISH), in 45 cases, which included 17 cases with Epstein-Barr virus (EBV) associated lymphorna, 7 cases with adult T-cell leukemia lymphoma (AILL). EBV-associated PAL and NKL exhibited DcR3 amplification and expression in lymphoma cells. AILL also showed DcR3 expression and amplification. The DcR3 expression was not in the reactive cells. (Cancer Letter, 2000, 160, 89-97)The BUB gene is a component of the mitotic checkpoint in budding yeast. Recently, human homologues of the BUB were identified and mutant alleles of hBUB1 and hBUBR1 were detected in two colorectal tumor cell lines. We examined the role of checkpoint gene in the chromosomal abnormalities of ATLL by investigating mutations of hBUB1 and hBUBR1, and MIN of replication errors of BAX, insulin-like growth factor, and transforming growth factor type II. Significant mutations/deletion of hBUB1 or hBUBR1 were detected in 4 of 10 cases with ATLL. In contrast, only one of eight B cell lymphomas showed nonsense mutation of hBUBR1.None of the ATLL and B cell lymphomas showed MIN. (Cancer Letters, 2000, 158, 141-50) Less