The borderland of embryogenesis and carcinogenesis. Major histocompatibility complex-linked genes affecting development and their possible relationship to the development of cancer.
The borderland of embryogenesis and carcinogenesis. Major histocompatibility complex-linked genes affecting development and their possible relationship to the development of cancer.
复制标题
胚胎发生和癌变的边界。
DOI：
10.1016/0304-419x(84)90008-8
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Gill3rd,TJ
中科院分区：
文献类型：
--
作者：
Gill3rd,TJ
生长控制是生物体发育的核心过程，随着生物体变得越来越复杂，控制的水平也变得越来越复杂。随着控制机制数量的增加，出错的可能性也在增加。正常生长受到干扰会导致发育缺陷，其范围从各种先天性异常到胚胎死亡（自然流产），或者导致有序控制的丧失，从而导致癌症（图1）。胚胎发生的旺盛而系统的生长与癌症，特别是低分化类型的无限制生长之间的关系，在癌症研究中很早就被认识到，为恶性生长的机制提供了线索[1,2]。这些长期存在的形态学观察得到了最近关于癌变的生化、超微结构和分子生物学研究的充分支持。这里提出的假设是基于这样的假设，即调节生长的控制过程可以受到越来越大程度的干扰，最大程度的干扰会导致癌症。因此，恶性肿瘤生长中发生的细胞表面特性的变化是由于正常细胞成分的过量产生或生长早期细胞成分特征（癌胎抗原）的重新表达。影响发育的多个基因座分散在哺乳动物基因组中（参见参考文献3和4）。
The control of growth is the central process in the development of living organisms, and the levels of control become more complex as the organism becomes more sophisticated. As the number of control mechanisms increases, the possibility of error also increases. Normal growth can be perturbed to cause developmental defects, which can range from congenital anomalies of various sorts to embryonic death (spontaneous abortion), or to cause the loss of orderly control which leads to cancer (Fig. 1). The relationship between the exuberant but systematic growth of embryogenesis and the unrestrained growth of cancer, particularly the less differentiated type, was recognized quite early in the study of cancer as providing a clue to the mechanisms of malignant growth [1, 2]. These long-standing morphological observations have received ample support from recent biochemical, ultrastructural and molecular biological investigation of carcinogenesis.The hypothesis presented here is based on the assumption that the control processes regulating growth can be perturbed to increasingly greater extents, with the maximal disruption leading to cancer. As a corollary, the changes in the properties of the cell surfaces that occur in malignant growth are due to an overproduction of normal cellular components or to the reexpression of cellular components characteristic of an earlier stage of growth (oncofetal antigens). Multiple loci influencing development are scattered throughout the mammalian genome (reviewed in Refs. 3 and 4),