Lee Christina R, Cervi Dave, Truong Amandine H, Li You-Jun, Sarkar Aloke, Ben-David Yaacov
Sunnybrook and Women's College Health Sciences Centre, Toronto Sunnybrook Regional Cancer Centre, Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Anticancer Res. 2003 May-Jun;23(3A):2159-66.
Retroviruses lacking oncogenes have been known to induce various types of cancer when inoculated into animals. Among these, Friend virus, discovered by Charlotte Friend in 1957, is capable of inducing erythroleukemias when injected into susceptible strains of mice. Since its discovery, this murine model of leukemogenesis has been extensively used to study the multistage nature of cancer. In the past two decades, several oncogenes and tumour suppressor genes, which play critical roles in the induction and progression of Friend erythroleukemia, have been identified. Retroviral insertional activation of Fli-1 and Spi-1/PU.1, as well as loss of tumour suppressor genes such as p53 or p45 NFE2 have been shown to be critical for the induction and progression of Friend virus-induced erythroleukemias. The majority of these genetic changes have also been implicated in various types of human neoplastic transformations. In this review we will discuss the genetic changes associated with Friend Disease, the temporal order during induction and progression of disease, and the function of these genes in both normal erythroid development as well as malignant transformation.
已知缺乏癌基因的逆转录病毒接种到动物体内时可诱发各种类型的癌症。其中，夏洛特·弗里德于1957年发现的弗里德病毒，注入易感品系小鼠后能够诱发红白血病。自发现以来，这种白血病发生的小鼠模型已被广泛用于研究癌症的多阶段性质。在过去二十年中，已经鉴定出几种在弗里德红白血病的诱导和进展中起关键作用的癌基因和肿瘤抑制基因。Fli-1和Spi-1/PU.1的逆转录病毒插入激活，以及p53或p45 NFE2等肿瘤抑制基因的缺失，已被证明对弗里德病毒诱导的红白血病的诱导和进展至关重要。这些基因变化中的大多数也与各种类型的人类肿瘤转化有关。在这篇综述中，我们将讨论与弗里德病相关的基因变化、疾病诱导和进展过程中的时间顺序，以及这些基因在正常红系发育和恶性转化中的功能。
