Basolo F, Fontanini G, Serra C, Dolei A, Proietti E, Belardelli F, Conaldi P G, Bistocchi M, Squartini F, Toniolo A
Institute of Pathological Anatomy, University of Pisa, Italy.
Int J Cancer. 1992 Jul 30;51(6):956-61. doi: 10.1002/ijc.2910510620.
Low levels of anti-viral activity, mainly interferon alpha/beta (IFN-alpha/beta), are regularly found in lymphoid tissues of BALB/c mice infected with the C3H strain of mammary tumor virus. At the time of tumor development, significant amounts of anti-viral activity were detected in homogenates of spleen and mammary tumors, but not in blood and normal mammary glands. This activity is pH2-resistant and neutralized by antibody to IFN/alpha-beta. The pathogenetic role of IFN in mammary carcinogenesis was investigated in 2 ways: (a) by treating virus-infected newborn mice with antibody to IFN-alpha/beta, and (b) by giving either the latter antibody or IFN-alpha/beta to virus-free animals transplanted with pre-neoplastic lesions. Mice were treated only for 2 months, starting either 1 week after birth or immediately after tumor transplant. In case (a), treatment with antibody to IFN-alpha/beta shortened the incubation period of mammary carcinomas and decreased the mean survival time. In case (b), anti-IFN antibody did not significantly affect the development of mammary tumors. However, exogenous IFN-alpha/beta markedly reduced both tumor incidence and mortality rate. These results indicate that endogenous IFN-alpha/beta plays a crucial role in the in vivo restriction of the early infectious phase of spontaneous carcinogenesis and that relatively high doses of IFN-alpha/beta may inhibit the progression of pre-neoplastic lesions.
在感染了乳腺肿瘤病毒C3H株的BALB/c小鼠的淋巴组织中，经常发现低水平的抗病毒活性，主要是α/β干扰素（IFN-α/β）。在肿瘤发生时，在脾脏和乳腺肿瘤的匀浆中检测到大量抗病毒活性，但在血液和正常乳腺中未检测到。这种活性对pH2有抗性，并可被抗IFN-α/β抗体中和。通过两种方式研究了IFN在乳腺癌发生中的致病作用：（a）用抗IFN-α/β抗体处理病毒感染的新生小鼠，以及（b）给移植有肿瘤前病变的无病毒动物注射后一种抗体或IFN-α/β。小鼠仅在出生后1周或肿瘤移植后立即开始治疗2个月。在情况（a）中，用抗IFN-α/β抗体治疗缩短了乳腺癌的潜伏期并降低了平均存活时间。在情况（b）中，抗IFN抗体对乳腺肿瘤的发展没有显著影响。然而，外源性IFN-α/β显著降低了肿瘤发生率和死亡率。这些结果表明，内源性IFN-α/β在体内限制自发致癌的早期感染阶段起着关键作用，并且相对高剂量的IFN-α/β可能抑制肿瘤前病变的进展。
