Earl C D, Scher C D
J Cell Physiol. 1980 Aug;104(2):153-62. doi: 10.1002/jcp.1041040204.
BALB/c or DBA/2 mice were infected with Abelson murine leukemia virus (A-MuLV), pseudotype Molony murine leukemia virus (M-MuLV). Infection of these mice with 10(4) focus-forming units of A-MuLV(M-MuLV) induced overt leukemia, detectable grossly or microscopically in 90% of the mice at 20-38 days. However, these methods did not detect leukemia at 17 days or before. Bone marrow cells from A-MuLV-infected leukemic or preleukemic mice were placed in tissue culture in a soft agarose gel. Cells from leukemic or preleukemic BALB/c mice grew to form colonies of 10(3) cells or more, composed of lymphoblasts, whereas marrow cells from normal uninfected mice did not. Cells from these colonies grew to form ascitic tumors after intraperitoneal inoculation into pristane-primed BALB/c recipients. Colony-forming leukemia cells could be detected in the marrow of A-MuLV-infected mice as early as 8 days after virus inoculation. The number of colony-forming leukemia cells increased as a function of time after virus inoculation. Colony-forming leukemia cells require other cells in order to replicate in tissue culture. Normal bone marrow cells, untreated or after treatment with mitomycin-C, provide this "helper" function. Only in the presence of untreated or mitomycin-C treated helper cells was the number of colonies approximately proportional to the number of leukemia cells plated. Marrow cells from leukemic BALB/c mice form more colonies than those from leukemic DBA/2 mice. The number of colonies formed per 10(3) microscopically identifiable leukemia cells plated was determined to be 2-3 for leukemic BALB/c mice and 0.3 for DBA/2 mice. Cocultivation of leukemic DBA/2 marrow cells with mitomycin-C treated normal BALB/c cells did not increase the number of colonies formed by the DBA/2 leukemic cells. Thus, the decreased ability of DBA/2 leukemia cells to form colonies appears to be a property of the leukemia cell population.
将BALB/c或DBA/2小鼠感染艾贝尔逊鼠白血病病毒（A-MuLV）、莫洛尼鼠白血病病毒假型（M-MuLV）。用10⁴个A-MuLV（M-MuLV）集落形成单位感染这些小鼠会诱发明显的白血病，在20至38天时，90%的小鼠在大体或显微镜下可检测到。然而，这些方法在17天或之前未检测到白血病。将来自感染A-MuLV的白血病或白血病前期小鼠的骨髓细胞置于软琼脂糖凝胶的组织培养中。来自白血病或白血病前期BALB/c小鼠的细胞生长形成由成淋巴细胞组成的10³个或更多细胞的集落，而来自未感染的正常小鼠的骨髓细胞则不能。将这些集落中的细胞腹腔接种到经 pristane 预处理的BALB/c受体小鼠后，生长形成腹水瘤。早在病毒接种后8天，就可在感染A-MuLV的小鼠骨髓中检测到集落形成白血病细胞。集落形成白血病细胞的数量随病毒接种后的时间而增加。集落形成白血病细胞在组织培养中复制需要其他细胞。未处理或经丝裂霉素-C处理的正常骨髓细胞提供这种“辅助”功能。只有在存在未处理或经丝裂霉素-C处理的辅助细胞时，集落数量才大致与接种的白血病细胞数量成比例。白血病BALB/c小鼠的骨髓细胞形成的集落比白血病DBA/2小鼠的多。每接种10³个显微镜下可识别的白血病细胞形成的集落数量，白血病BALB/c小鼠为2至3个，DBA/2小鼠为0.3个。白血病DBA/2骨髓细胞与经丝裂霉素-C处理的正常BALB/c细胞共培养，并未增加DBA/2白血病细胞形成的集落数量。因此，DBA/2白血病细胞形成集落的能力下降似乎是白血病细胞群体的一种特性。
