Fey F
Arch Geschwulstforsch. 1978;48(8):705-11.
Strain XVII mice with Graffi virus induced leukemia of various hematological types showed a pronounced thrombocytopenia which was severe in erythroblastic leukemia and weaker in lymphatic ones. The thrombocytic reactions shortly following Friend and Rauscher virus applications and occurred 3 weeks after birth in AKR mice are not found in Graffi virus system. A significant preleukemic thrombocytopenia did appear only 8 weeks after Graffi virus infection. The origin of both the preleukemic and the secondary thrombocytic reactions are discussed. (XVII X AKR) F1 hybrids, neonatally treated with N-nitroso-N-methylurea (NMU), resulted also in a decline in the number of thrombocytes after manifestation of leukemia. In contrast to the expection following NMU treatment a preleukemic thrombocytopenia appeared as in viral leukemogenesis too. The possibility of a co-operation of oncogenic viruses in chemical carcinogenesis is considered.
感染格拉菲病毒的17系小鼠诱发了各种血液学类型的白血病，表现出明显的血小板减少，在成红细胞性白血病中严重，在淋巴细胞性白血病中较轻。在格拉菲病毒系统中未发现接种弗瑞德和劳舍尔病毒后不久以及AKR小鼠出生3周后出现的血小板反应。仅在格拉菲病毒感染8周后才出现明显的白血病前期血小板减少。讨论了白血病前期和继发性血小板反应的起源。用N-亚硝基-N-甲基脲（NMU）对（17系×AKR）F1杂种新生小鼠进行处理，在白血病表现出来后也导致血小板数量下降。与NMU处理后的预期相反，白血病前期血小板减少也如病毒致白血病过程中一样出现。考虑了致癌病毒在化学致癌过程中协同作用的可能性。
