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A bcr-v-abl oncogene induces lymphomas in transgenic mice.

机译:bcr-v-abl癌基因在转基因小鼠中诱导淋巴瘤。

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In chronic myeloid leukemia and some cases of acute lymphoblastic leukemia, a 9;22 chromosome translocation has fused most of the c-abl oncogene to a gene designated bcr. To explore in vivo the biological effects of the chimeric gene, we introduced a facsimile of the translocation product, a bcr-v-abl gene, into the mouse germ line under the control of the immunoglobulin heavy-chain enhancer or a retroviral long terminal repeat. Some transgenic mice bearing either construct developed clonal lymphoid tumors. T lymphomas predominated, but some pre-B lymphomas developed. The transgenes were expressed in the tumors but not detectably in the lymphoid tissues of nontumorous transgenic animals, implying that transcription is activated by a low-frequency somatic event. These results demonstrate that bcr-v-abl is tumorigenic in vivo and provide a new animal model for lymphomagenesis.
机译:在慢性粒细胞白血病和某些急性淋巴细胞白血病病例中,9; 22染色体易位已将大多数c-abl癌基因融合至一个称为bcr的基因。为了在体内探索嵌合基因的生物学效应,我们在免疫球蛋白重链增强子或逆转录病毒长末端重复序列的控制下,将易位产物bcr-v-abl基因的传真引入小鼠生殖细胞系。一些带有任一种构建体的转基因小鼠都会出现克隆性淋巴瘤。 T淋巴瘤占主导地位,但一些B前淋巴瘤发展。转基因在肿瘤中表达,但在非肿瘤转基因动物的淋巴组织中未检测到,这表明转录是由低频体细胞事件激活的。这些结果表明,bcr-v-abl在体内具有致瘤性,并为淋巴瘤的形成提供了新的动物模型。

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