Boniver J, Humblet C, Rongy A M, Delvenne C, Delvenne P, Greimers R, Thiry A, Courtoy R, Defresne M P
Department of Pathology, University Hospital of Liège, Belgium.
In Vivo. 1990 Jan-Feb;4(1):41-3.
Radiation-induced thymic lymphomas in C57Bl/Ka mice are interesting models for studying the successive steps of carcinogenesis. Irradiation initiates "preleukemic" cells, which are promoted to become neoplastic. Studies in mice in which lymphoma development is inhibited by a bone marrow transplantation after irradiation suggest that radiation--induced alterations to the T cell lineage, and particularly to thymic microenvironment, are critical for the promotion of preleukemic cells. It is proposed that the lack of physiological differentiation signals within the thymus, as a result of irradiation, allows these cells to escape the normal controls of thymocyte production and pushes them towards neoplastic transformation. A disturbance in the production of cytokines may be involved, since exogenous cytokines, such as Interferon gamma or Tumor Necrosis Factor a, can inhibit radiation-induced lymphomagenesis, reproducing the effects of bone marrow transplantation. The model is thus suitable for studying the mechanisms of carcinogenesis and designing biological manipulation devoted to cancer prevention in individuals who have been exposed to oncogenic agents.
C57Bl/Ka小鼠辐射诱导的胸腺淋巴瘤是研究致癌作用连续步骤的有趣模型。辐射引发“白血病前期”细胞，这些细胞会发展成为肿瘤细胞。对辐射后通过骨髓移植抑制淋巴瘤发展的小鼠的研究表明，辐射诱导的T细胞谱系改变，特别是胸腺微环境的改变，对于白血病前期细胞的发展至关重要。有人提出，由于辐射导致胸腺内缺乏生理分化信号，使得这些细胞能够逃脱胸腺细胞产生的正常控制，并促使它们发生肿瘤转化。细胞因子产生的紊乱可能与之有关，因为外源性细胞因子，如干扰素γ或肿瘤坏死因子α，可抑制辐射诱导的淋巴瘤发生，重现骨髓移植的效果。因此，该模型适合用于研究致癌机制，并设计针对接触致癌剂个体的癌症预防生物操作。
