NEGATIVE CONTROLS ON CELL GROWTH

本次加州大学洛杉矶分校研讨会将解决迅速扩大的机制阵列 负调控细胞生长的基因 这些机制及其 推论包括：（1）在特定染色体上获得纯合性 在肿瘤进展过程中，被认为反映了失活的基因位点 细胞生长的负调节因子，导致茎的释放， 细胞生长 这些基因被称为“抑癌基因和肿瘤抑制基因 基因”。 (2)肿瘤的高风险、可遗传性传播的基因座 敏感性（例如，家族性视网膜母细胞瘤和结肠息肉病）， 很快就会被发现与“抗癌基因”相似或不同。 （三） 正常细胞中抑制肿瘤细胞生长的基因 体细胞杂交后的恶性肿瘤。 这些基因可能部分 与通过核型和RFLP分析发现的那些重叠。 (4)由癌基因转化产生的独特基因。 此类基因 与肿瘤发生表型的逆转有关， 已经显示出拮抗致癌基因的作用。 (5)蜂窝 抑制邻近其他细胞生长的机制， 限制肿瘤发生并维持正常组织结构;在一些实施方案中， 通过建立并列细胞之间的直接联系。 （六） TGF-β、β-干扰素和TNF是已知的生长抑制因子。 TGF-β在 turn包含了越来越多的相关多肽调节因子 脊椎动物和无脊椎动物的分化（例如， 苗勒管抑制因子）。 最后，（7）发展性增长 终末（或终末期）分化诱导的抑制机制。 会议主题包括：人类癌症的遗传学（体细胞改变， 家族性肿瘤）;生长抑制基因;体细胞遗传学; 癌基因逆转基因;负生长的细胞间介导物 控制;负作用扩散因子。

This UCLA Symposium will address the rapidly expanding array of mechanisms that negatively regulate cell growth. These mechanisms and their corollaries include: (1) Homozygosities acquired at specific chromosomal loci during tumor progression which are thought to reflect the inactivation of negative regulators of cell growth, resulting in the unleashing of stem cell growth. These genes are termed "anti-oncogenes and tumor suppressor genes". (2) Loci conferring high risk, heritable transmission of tumor susceptibility (e.g., familial retinoblastoma and polyposis coli) which may soon be revealed as similar to or distinct from "anti-oncogenes". (3) Growth-suppressing genes in normal cells which suppress tumor cell malignancy upon somatic cell hybridization. These genes may be partially overlapping with those discovered through karyotypic and RFLP analyses. (4) Distinct genes created by transformation with oncogenes. Such genes have been associated with reversion from a tumorigenic phenotype and they have been shown to antagonize the action of oncogenes. (5) Cellular mechanisms which inhibit the growth of other cells in close proximity, limiting tumorigenesis and maintaining normal tissue architecture; in some cases through establishing direct connections between apposed cells. (6) TGF-b, b-interferon, and TNF are known growth inhibitory factors. TGF-b in turn subsumes an increasingly large group of related polypeptide regulators of differentiation in developing vertebrates and invertebrates (e.g., Mullerian inhibiting factor). And, finally (7) Developmental growth inhibiting mechanisms induced with terminal (or end-stage) differentiation. Session Topic Include: Genetics of Human Cancer (Somatic Alteration, Familial Tumors); Growth-Suppressing Genes; Somatic Cell Genetics; Oncogene-Reverting Genes; Intercellular Mediators of Negative Growth Control; Negatively Acting Diffusable Factors.