DEVELOPMENT AND PROGRESSION OF HUMAN COLONIC NEOPLASMS

人类结肠腺瘤有很高的发生几率 癌，而增生性息肉，另一种类型的良性结肠 肿瘤和正常结肠上皮的风险相对较低。 结肠癌之间的生化差异的特征， 腺瘤、增生性息肉和正常上皮可能阐明 恶性肿瘤的基本特征。恶性的特征是过度 增殖、分化不完全、侵袭邻近组织 和远处器官的转移(1)，但对这一过程知之甚少 在分子水平上。一组被称为癌基因的基因已经被 在一些肿瘤病毒以及正常和肿瘤的基因组中发现 细胞。癌基因被认为与肿瘤的发生有关，因为 一个或多个癌基因信息的浓度有时会升高或 肿瘤细胞中核苷酸序列的改变 正常细胞。此外，一些癌基因来自肿瘤细胞，但不是来自 正常细胞，可以转化培养的细胞。虽然有很多信息 关于癌基因异常已经存在，对一些还知之甚少 它们在人类肿瘤中表达的潜在重要方面。这个 这项研究的目的是确定：1)原始人 结肠癌始终表达相同的癌基因；2)如果是原发的 癌症可与转移性结肠癌、腺瘤、 从癌基因模式看增生性息肉与正常结肠粘膜 表达；3)特定癌基因是否可以表达 与从正常粘膜到腺瘤或腺瘤的进展相关 癌症；以及4)如果多个结肠癌发生在同一个人身上 持续表达相同的癌基因。这一信息将澄清 癌基因是否只参与了肿瘤的生长和 分化改变或是否也参与了侵袭 和转移。此外，如果组织学上不同的肿瘤 同一人始终表达相同的癌基因，遗传序列 基因多态可能在结肠肿瘤的发生中起重要作用。

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.