DEVELOPMENT AND PROGRESSION OF HUMAN COLONIC NEOPLASMS

结肠腺瘤在人类有很高的概率产生 癌，而增生性息肉，另一种类型的良性结肠癌， 肿瘤和正常结肠上皮具有相对低的风险。 结肠癌之间生化差异的表征， 腺瘤、增生性息肉和正常上皮可阐明 恶性肿瘤的基本特征。 肥胖的特点是过度 增殖、不完全分化、侵入邻近组织 和远处器官转移（1），但这一过程知之甚少 在分子水平上。 一组称为癌基因的基因已经被 在一些肿瘤病毒和正常和肿瘤病毒的基因组中鉴定出 细胞 癌基因与肿瘤发生有关， 一种或多种致癌基因信息的浓度有时升高， 肿瘤细胞中的核苷酸序列与来自 正常细胞 此外，一些癌基因来自肿瘤细胞，而不是来自 正常细胞，可以转化培养细胞。 虽然很多信息 关于癌基因畸变的研究已经存在，但对一些 它们在人类肿瘤中表达的潜在重要方面。 的 本研究的目的是确定：1）是否原代人 结肠癌一贯表达相同的癌基因; 2）如果原发性 癌症可以与转移性结肠癌，腺瘤， 增生性息肉与正常结肠粘膜癌基因分型 表达; 3）是否可以表达特定的癌基因， 与从正常粘膜到腺瘤或腺瘤到 癌;以及4）如果在同一个体中出现多个结肠肿瘤 一致地表达相同的致癌基因。 这一信息将澄清 癌基因是否只参与生长， 分化改变或它们是否也参与侵袭 和转移。 此外，如果组织学上不同的肿瘤， 同一个人始终表达相同的癌基因，遗传序列 多态性可能是重要的诱导结肠肿瘤。

Colonic adenomas in humans have a high probability of generating carcinomas, while hyperplastic polyps, another type of benign colonic tumor, and normal colonic epithelium have a relatively low risk. Characterization of the biochemical differences between colonic carcinomas, adenomas, hyperplastic polyps and normal epithelium might elucidate the essential features of malignancy. Malignancy is characterized by excessive proliferation, incomplete differentiation, invasion into adjacent tissues and metastases to distant organs (1), but this process is poorly understood at the molecular level. A group of genes termed oncogenes have been identified in the genomes of some tumor viruses and normal and neoplastic cells. Oncogenes have been implicated in tumorigenesis because the concentrations of one or more oncogene messages are sometimes elevated or altered in nucleotide sequence in neoplastic cells compared to those from normal cells. Moreover, some oncogenes from neoplastic cells, but not from normal cells, can transform cultured cells. Although much information about oncogene aberrations already exists, little is known about some potentially important aspects of their expression in human neoplasms. The purpose of this study is to determine: 1) whether or not primary human colonic cancers consistently express the same oncogenes; 2) if primary cancers can be distinguished from metastatic colonic cancers, adenomas, hyperplastic polyps and normal colonic mucosa by their pattern of oncogene expression; 3) whether or not expression of particular oncogenes can be correlated with progression from normal mucosa to adenoma or adenoma to carcinoma; and 4) if multiple colonic tumors arising in the same individual consistently express the same oncogenes. This information would clarify whether oncogenes were involved exclusively in the growth and differentiation alterations or whether they are also involved in invasion and metastasis. Furthermore, if histologically different neoplasms in the same person consistently expressed the same oncogenes, inherited sequence polymorphisms might be important in the induction of colonic neoplasms.