Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Cancer Cell. 2012 Aug 14;22(2):141-2. doi: 10.1016/j.ccr.2012.07.018.
Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.
导致 c-MYC 表达失控的染色体易位在大多数 Burkitt 淋巴瘤病例中均可检测到。然而，对于淋巴瘤发生所必需的其他病变知之甚少。现在，两项独立的研究，其中一项由 Sander 等人在本期《癌细胞》中进行，确定了组成性 PI3K 信号和 CyclinD3 突变是在小鼠和人类中均起作用的合作病变。这些结果具有直接的治疗意义。
