Saggioro D, D'Andrea E, Chieco-Bianchi L
Institute of Oncology, Interuniversity Center for Cancer Research (C.I.R.C.), Padova, Italy.
Tumori. 1989 Aug 31;75(4):341-4. doi: 10.1177/030089168907500408.
The Abelson and Moloney murine leukemia virus complex (A-MuLV/M-MuLV) induces rapidly growing thymic lymphomas following direct injection into the thymus of newborn BALB/c and C57BL/6 mice. Southern blot analysis with a v-abl specific probe not only demonstrated that primary tumors are clonal, but also that the pattern of A-MuLV provirus integration is quite stable in primary tumor cells, as well as in their derived cell lines and clones. Most of the cell samples were able to rearrange the immunoglobulin heavy chain genes in culture, whereas in two cases the T cell receptor gamma chain genes also underwent rearrangement. Since the recombination mechanism is operative only in very immature lymphoid cells, these data provide indirect evidence for the lack of differentiation of A-MuLV cell targets in the thymus.
将艾贝尔森和莫洛尼鼠白血病病毒复合体（A-MuLV/M-MuLV）直接注射到新生BALB/c和C57BL/6小鼠的胸腺中后，会诱发快速生长的胸腺淋巴瘤。用v-abl特异性探针进行的Southern印迹分析不仅表明原发性肿瘤是克隆性的，而且还表明A-MuLV前病毒整合模式在原发性肿瘤细胞及其衍生的细胞系和克隆中相当稳定。大多数细胞样本在培养中能够重排免疫球蛋白重链基因，而在两例中，T细胞受体γ链基因也发生了重排。由于重组机制仅在非常不成熟的淋巴细胞中起作用，这些数据为胸腺中A-MuLV细胞靶标的未分化提供了间接证据。
