MALIGNANT BEHAVIOR AND CELLULAR ANTIGEN EXPRESSION

这个项目是基于我们早先关于 IgH/myc并置在大鼠浆细胞瘤发生中的作用 免疫细胞瘤(RIC)和人Burkitt淋巴瘤(BL)及其受体15的作用 小鼠T细胞白血病的三体。这个领域在很大程度上是由 我们的细胞遗传学发现和衍生的工作假说，在这个基础上做出的 格兰特。现在，许多实验室都在进行这项研究。我们已经选择了 将我们的继续工作集中在几个选定的主题上，在这些主题中，我们的 实验室有特殊的经验、材料和/或开发了新的 工作中的假设。我们目前的目标如下：一、细胞遗传学和 生物学研究1.浆细胞发生。A)描述 小鼠浆细胞瘤(MPC)前体细胞：B)加速培养的研究 A-MuLV在PC发生中的作用；c)遗传水平的研究 测定嵌合小鼠对PC的耐药性。一、二、淋巴肿大。会吗？ 持续表达的v-抑制：a)正常成纤维细胞 衍生的15号染色体包含一个基因，它能中和T细胞的致瘤性。 带有逆转录病毒重排c-myc或pvt-17的白血病细胞正常 不同谱系的细胞携带不同的抑制基因 染色体：B)不同谱系的正常细胞是否携带抑制子 不同染色体上的基因？C)抑制器损失是否涉及 常规F1代和转基因小鼠的淋巴再生？；d)A 非致瘤性Burkitt淋巴瘤(BL)变异体。二、4.关于腐烂的研究 C-myc基因在正常和IgH/myc易位携带细胞中的表达； 大鼠免疫细胞瘤相关IgH/myc易位的继续研究； 二.6.C-myc易位到功能性腹胀的分子研究 双杂合MPC的染色体产生链；II.7关系 C-myc基因扩增与肿瘤进展之间的关系 可调节的小鼠肿瘤系统；持续的结构和功能 B-myc基因的研究--II.9与非配对相关的IgH基因座 前B细胞易位：人IgH/myc易位模型 伯基特淋巴瘤？

This project is based on our earlier findings concerning the role of the IgH/myc juxtaposition in the genesis of murine plasmacytoma (MPG), rat immunocytoma (RIC) and human Burkitt lymphoma (BL) and the role of chr 15 trisomy in murine T-cell leukemia. This field has been largely initiated by our cytogenetic findings and derived working hypotheses, made under this grant. It is now pursued at numerous laboratories. We have chosen to concentrate our continued work on a few selected topics, where our laboratory has special experience, materials and/or has developed new working hypotheses. Our current aims are the following: I. CYTOGENETIC AND BIOLOGICAL STUDIES I.1. Plasmacytogenesis. a) Characterization of the murine plasmacytoma (MPC) precursor cell: b) Studies on the accelerating effect of A-MuLV on PC-genesis; c) Studies on the level of genetically determined PC- resistance in chimeric mice. I.2. Lymphomagenesis. Does consistutively expressed v-suppression: a) Does the normal fibroblast derived chromosome 15 contain a gene that counteracts tumorigenicity of T- leukemia cells with retrovirally rearranged c-myc or pvt-17: b) Do normal cells of different lineages carry suppressor genes on different chromosomes?: b) Do normal cells of different lineages carry suppressor genes on different chromosomes? c) Is suppressor loss involved in lymphoagenesis in conventional F1 and in transgenic mice?; d) Studies on a non-tumorigenic Burkitt lymphoma (BL) revertant. II.4. Studies on the decay of c-myc mRNA in normal and IgH/myc translocation-carrying cells; Ii.5 Continued studies on the rat immunocytoma associated IgH/myc translocation; II.6. Molecular studies of c-myc translocations to the functional heave chain producing chromosome in double heterozygous MPCs; II.7 Relationship between c-myc amplification and tumor progression in an experimentally modulatable mouse tumor system; II.8. Continued structural and functional studies on the B-myc gene; II.9 IgH-locus associated illegitimate translocations in pro-B-cells: a model for the IgH/myc translocation in Burkitt lymphoma?