Nesbit C E, Tersak J M, Prochownik E V
Department of Pediatrics, Children's Hospital of Pittsburgh, Pennsylvania 15213, USA.
Oncogene. 1999 May 13;18(19):3004-16. doi: 10.1038/sj.onc.1202746.
c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, we first summarize data, derived mainly from non-clinical studies, indicating that these oncoproteins actually serve quite different roles in vivo. This concept necessarily lies at the heart of the basis for the observation that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences. We also review evidence implicating each of the above MYC genes in specific neoplastic diseases and have attempted to identify unresolved questions which deserve further basic or clinical investigation. We have made every attempt to review those diseases for which significant and confirmatory evidence, based on studies with primary tumor material, exists to implicate MYC members in their causation and/or progression.
c-myc、N-myc和L-myc是myc癌蛋白家族的三个成员，它们在许多人类肿瘤性疾病发病机制中的作用已获得广泛的经验支持。在本综述中，我们首先总结主要来自非临床研究的数据，这些数据表明这些癌蛋白在体内实际上发挥着相当不同的作用。这一概念必然是以下观察结果的核心基础：每个MYC基因的失调表达仅与人类某些自然发生的恶性肿瘤可重复相关，并且这些基因在其异常功能后果方面不可互换。我们还综述了上述每个MYC基因与特定肿瘤性疾病相关的证据，并试图确定值得进一步基础或临床研究的未解决问题。我们已尽一切努力综述那些基于对原发性肿瘤材料的研究而存在重要且确凿证据表明MYC成员参与其病因和/或进展的疾病。
