Torry D S, Cooper G M
Department of Pathology, Harvard Medical School, Boston, MA.
Am J Reprod Immunol. 1991 Apr;25(3):129-32. doi: 10.1111/j.1600-0897.1991.tb01080.x.
Although analogies are often made comparing development to cancer, there is of course a major difference. Normal development requires complex patterns of rigidly controlled cell proliferation and differentiation. In contrast, cancer represents the pathological condition that results when normal cell growth patterns are uncoupled from their regulatory influences. Genetic studies of RNA tumor viruses have provided insights into the relationships and differences of the genes responsible for normal development and cancer. The presence of discrete genes (oncogenes) within the genome of oncogenic retroviruses is responsible for their tumorigenic potential. Molecular genetic studies have found that normal eukaryotic cells possess genes that are quite homologous to the retroviral oncogenes. These normal cellular genes (proto-oncogenes) are involved in the regulation of proliferation and differentiation. However, if mutated, proto-oncogenes have the potential for inducing neoplastic transformation. The conversion of a proto-oncogene to an oncogene is called activation. Proto-oncogenes can become activated by a variety of genetic mechanisms including transduction, insertional mutagenesis, amplification, point mutations, and chromosomal translocations. In each instance the genetic aberration results in a proto-oncogene that is now free of its normal regulatory constraints. Such deregulation of function imparts a distinct growth advantage to the cell.
尽管人们常常将发育过程与癌症进行类比，但两者之间当然存在重大差异。正常发育需要严格控制细胞增殖和分化的复杂模式。相比之下，癌症代表了正常细胞生长模式与其调节影响脱钩时所产生的病理状况。对RNA肿瘤病毒的遗传学研究为负责正常发育和癌症的基因之间的关系及差异提供了见解。致癌逆转录病毒基因组中离散基因（癌基因）的存在决定了它们的致瘤潜力。分子遗传学研究发现，正常真核细胞拥有与逆转录病毒癌基因非常同源的基因。这些正常细胞基因（原癌基因）参与增殖和分化的调节。然而，如果发生突变，原癌基因就有可能诱导肿瘤转化。原癌基因转变为癌基因的过程称为激活。原癌基因可通过多种遗传机制被激活，包括转导、插入诱变、扩增、点突变和染色体易位。在每种情况下，遗传畸变都会导致一个原癌基因摆脱其正常的调节限制。这种功能失调赋予细胞明显的生长优势。
