Langdon W Y, Harris A W, Cory S, Adams J M
Cell. 1986 Oct 10;47(1):11-8. doi: 10.1016/0092-8674(86)90361-2.
Transgenic mice bearing a c-myc oncogene subjugated to the lymphoid-specific immunoglobulin heavy chain enhancer (E mu) develop clonal B lymphoid malignancies, but most young E mu-myc mice lack malignant clones. Their prelymphomatous state has allowed us to examine how constitutive c-myc expression influences B cell development. We find that early stages are overrepresented, even before birth. Pre-B cells of polyclonal origin increase greatly, while B cells develop in reduced number. Both the pre-B and the B cells appear to be in an active state, since they are larger than normal and a greater fraction are in the cell cycle. Enforced myc expression has thus favored proliferation over maturation. Hence, a normal function of c-myc may be to regulate differentiation as well as to promote cell cycling.
携带受淋巴特异性免疫球蛋白重链增强子(Eμ)调控的c-myc癌基因的转基因小鼠会发生克隆性B淋巴细胞恶性肿瘤,但大多数年轻的Eμ-myc小鼠缺乏恶性克隆。它们的淋巴瘤前期状态使我们能够研究组成型c-myc表达如何影响B细胞发育。我们发现,甚至在出生前,早期阶段就过度存在。多克隆起源的前B细胞大量增加,而B细胞数量减少。前B细胞和B细胞似乎都处于活跃状态,因为它们比正常细胞大,且有更大比例处于细胞周期中。因此,强制表达myc有利于增殖而非成熟。因此,c-myc的正常功能可能是调节分化以及促进细胞周期运转。