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牛3型腺病毒转化的肿瘤细胞的病毒特异性抗原性研究。

Studies of virus-specific antigenicity of tumour cells transformed by bovine adenovirus type 3.

作者信息

Strizhachenko N M, Graevskaya N A, Karmysheva V Y, Syurin V N

出版信息

Arch Geschwulstforsch. 1975;45(4):324-34.

PMID:1200779
Abstract

The present paper deals with the study of immunologic relationship between tumours induced by bovine adenovirus type 3 and the organism of the tumour-bearing hamster. The experiments showed that primarily induced tumours were not virus-specifically antigenic as a result of non-expression of weak TSTA presumably due to the presence of more potent antigens of cellular origin. It was only after repeated passages of tumour cells in vivo or in vitro, as a result of tumour progression, that the loss of potent antigens of cellular origin occurs which contributes to expression of weak virus-specific antigens. The findings obtained can explain unsuccessful attempts at detecting virus-specific antigens in spontaneous tumours. Antigenicity of spontaneous tumour and its immunologic relationship with the organism are probably associated with antigens of cellular origin occurring on cell membrane as a result of malignization rather than with antigens induced by an etiological agent. Consequently, the more profound development of immunological methods for diagnosis, therapy and prophylaxis of oncogenic processes irrespective of their etiology seems to be expedient.

摘要

本文探讨了牛3型腺病毒诱导的肿瘤与荷瘤仓鼠机体之间的免疫关系研究。实验表明,由于可能因存在更强的细胞源性抗原而导致弱肿瘤特异性移植抗原(TSTA)不表达,原发性诱导肿瘤并非病毒特异性抗原。只有在体内或体外对肿瘤细胞进行反复传代后,由于肿瘤进展,细胞源性强抗原才会丢失,这有助于弱病毒特异性抗原的表达。所获得的研究结果可以解释在检测自发肿瘤中病毒特异性抗原时的失败尝试。自发肿瘤的抗原性及其与机体的免疫关系可能与细胞恶变后细胞膜上出现的细胞源性抗原有关,而非与病原体诱导的抗原有关。因此,无论致癌过程的病因如何,进一步深入发展用于诊断、治疗和预防致癌过程的免疫学方法似乎是适宜的。

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