STRAIN DEPENDENCY OF CELL-TYPE SPECIFICITY AND ONSET OF LYMPHOMA DEVELOPMENT IN E-MU-MYC TRANSGENIC MICE

STRAIN DEPENDENCY OF CELL-TYPE SPECIFICITY AND ONSET OF LYMPHOMA DEVELOPMENT IN E-MU-MYC TRANSGENIC MICE
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DOI:
10.1111/j.1349-7006.1992.tb00099.x
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发表时间:
1992-03-01
期刊:
JAPANESE JOURNAL OF CANCER RESEARCH
影响因子:
--
通讯作者:
YAMAMURA, K
YAMAMURA, K
中科院分区:
其他
文献类型:
--
作者:
AKAGI, K;MIYAZAKI, J;YAMAMURA, K

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c-myc 是一种核原癌基因,激活后会诱发多种组织的恶性肿瘤。 大多数鼠浆细胞瘤和人伯基特淋巴瘤已被证明携带涉及 c-myc 和免疫球蛋白基因的染色体易位。 为了研究影响 myc 诱导的淋巴细胞肿瘤的遗传或表观遗传因素,我们之前将缺乏自己的启动子和第一个外显子的 E-mu-myc-DELTA 基因引入两种近交系小鼠 C57BL/6 和 C3H/HeJ 中。 我们在转基因小鼠中观察到了三个特征。 首先,T细胞淋巴瘤在C3H背景中占主导地位。 其次,C57BL/6 转基因小鼠中前 B 细胞淋巴瘤和 B 细胞淋巴瘤的发生频率相同。 第三,平均发病年龄比其他研究者报道的要早。 为了测试这些特征是否是由于构建体中缺少 c-myc 基因的启动子区域和第一个外显子,或者是由于小鼠的遗传背景,我们将包含完整 c-myc 基因的 E-mu-myc 基因引入 C57BL/6 和 C3H/HeJ 小鼠的受精卵中。 细胞类型特异性、分化阶段特异性和淋巴瘤发展的平均年龄不受转基因构建体的影响。
c-myc is a nuclear proto-oncogene that, when activated, induces malignancies in a variety of tissues. Most murine plasmacytomas and human Burkitt's lymphomas have been shown to carry a chromosomal translocation involving c-myc and immunoglobulin genes. To study genetic or epigenetic factors that affect myc-induced lymphoid cell tumors, we previously introduced the E-mu-myc-DELTA gene lacking its own promoter and first exon into two inbred strains of mice, C57BL/6 and C3H/HeJ. We observed three characteristic features in our transgenic mice. First, T cell lymphoma predominated in the C3H background. Second, both pre-B and B cell lymphoma developed at equal frequency in C57BL/6 transgenic mice. Third, the average age of onset is earlier than that reported by other investigators. To test whether these characteristics are due either to the lack of the promoter region and first exon of the c-myc gene in the construct or to the genetic background of the mice, we introduced E-mu-myc gene containing the complete c-myc gene into fertilized eggs of C57BL/6 and C3H/HeJ mice. The cell-type specificity, differentiation-stage specificity and the average age at onset of lymphoma development were not affected by the transgene construct.