Allen J D, Verhoeven E, Domen J, van der Valk M, Berns A
Division of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Oncogene. 1997 Sep 4;15(10):1133-41. doi: 10.1038/sj.onc.1201288.
Evidence from proviral tagging experiments has suggested that pim-2 is similar in oncogenic behavior to its well characterized relative pim-1. While the basal expression in tissues differs, both genes are highly expressed in mitogenically stimulated hematopoietic cells and their transcription is induced in response to the same cytokines. Expression of a pim-2 transgene in lymphoid cells predisposed mice to T-cell lymphomas like those promoted by pim-1 transgenes. Moreover, strong collaboration with an E mu-myc transgene was manifested as pre-B cell leukemia in neonate bi-transgenic animals. Remarkably, this collaboration was attenuated but not prevented by X-inactivation of one of the transgenes. The addition of pim-2 to the fold increases the prominence of the pim proto-oncogene family in tumorigenesis.
前病毒标记实验的证据表明,pim-2在致癌行为上与其特征明确的相关基因pim-1相似。虽然组织中的基础表达有所不同,但这两个基因在有丝分裂原刺激的造血细胞中均高度表达,并且它们的转录会因相同的细胞因子而被诱导。pim-2转基因在淋巴细胞中的表达使小鼠易患T细胞淋巴瘤,就像pim-1转基因所引发的淋巴瘤一样。此外,与Eμ-myc转基因的强烈协同作用在新生双转基因动物中表现为前B细胞白血病。值得注意的是,其中一个转基因的X染色体失活会减弱但不会阻止这种协同作用。将pim-2加入其中会增加pim原癌基因家族在肿瘤发生中的显著程度。