在转基因小鼠中通过myc和bcl-2之间的合作引起的新型原始淋巴瘤
A Strasser1, A W Harris, M L Bath
1Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Nature
|November 22, 1990
概括
bcl-2 瘤基因促进细胞存活,而 myc 驱动细胞增殖. 它们在转基因小鼠中的联合作用导致原始造血细胞的快速瘤发育,揭示了淋巴发育中的协同相互作用.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 在t(14;18) 转位调节bcl-2表达在毛囊B细胞淋巴瘤.
- bcl-2 增强了细胞存活率,在压力下提供了生长优势.
- myc转位促进B淋巴细胞的增殖和恶性瘤.
研究的目的:
- 为了研究bcl-2和myc在淋巴发育中的协同作用.
- 在双重转基因小鼠中描述瘤的细胞起源.
主要方法:
- 产生具有E mu-bcl-2和E mu-myc转基因的双重转基因小鼠.
- 对B细胞增殖和瘤发展的分析.
- 瘤细胞起源的特征.
主要成果:
- 双重转基因E mu-bcl-2/myc小鼠表现出B前和B细胞的过度增殖.
- 与Emu-myc小鼠相比,Emu-bcl-2/myc小鼠的瘤发育显著加快.
- 瘤来自于原始的造血细胞,潜在的淋巴细胞干细胞.
结论:
- bcl-2和myc在促进B细胞淋巴发育方面表现出明显的协同作用.
- bcl-2和myc之间的相互作用加速了瘤的形成.
- 淋巴瘤可以源于原始的造血干细胞,突出显示它们在癌症发展中的作用.
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