Sheridan B L, Reis M D
Department of Laboratory Haematology, Sunnybrook Health Science Centre, Ont., Canada.
Tumour Biol. 1990;11 Suppl 1:44-58. doi: 10.1159/000217676.
The clonal malignancies of acute myeloid leukemia and the myelodysplastic syndromes are associated with numerous chromosomal and oncogenic abnormalities. Activation of oncogenes has been demonstrated, although there is little evidence that this alone causes malignant transformation of diploid cells as a consequence. Patterns of abnormalities can be seen as the patient progresses from myelodysplastic syndrome to acute myeloid leukemia, but no unique or invariant findings have been described. Chromosomal changes, with the exception of some translocations, are neither disease nor lineage specific. At this time the data provide good support for the multistep view of carcinogenesis, and there is indirect or circumstantial evidence for the presence of tumor suppressor genes on 5q and 7q. The continued study of these clonal hematological disorders will provide considerable insight into mechanisms of tumorigenesis and possibly may lead to new modes of therapy, for example, through altering the microenvironment, interfering with deranged signal transmission, or introducing antioncogenes.
急性髓系白血病和骨髓增生异常综合征的克隆性恶性肿瘤与众多染色体及致癌异常相关。尽管几乎没有证据表明仅癌基因激活就会导致二倍体细胞发生恶性转化,但癌基因激活已得到证实。随着患者从骨髓增生异常综合征发展为急性髓系白血病,可观察到异常模式,但尚未描述出独特或不变的发现。除某些易位外,染色体变化既非疾病特异性也非谱系特异性。目前,数据为癌症发生的多步骤观点提供了有力支持,并且有间接或旁证表明5号染色体长臂和7号染色体长臂上存在肿瘤抑制基因。对这些克隆性血液系统疾病的持续研究将为肿瘤发生机制提供相当多的见解,并可能导致新的治疗模式,例如通过改变微环境、干扰紊乱的信号传导或引入抗癌基因。