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Interferon‐α/β in virus‐induced mouse mammary carcinogenesis: Effects on the spontaneous process and on the progression of transplanted pre‐neoplastic lesions
Author(s) -
Basolo F.,
Fontanini G.,
Serra C.,
Dolei A.,
Proietti E.,
Belardelli F.,
Conaldi P. G.,
Bistocchi M.,
Squartini F.,
Toniolo A.
Publication year - 1992
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910510620
Subject(s) - carcinogenesis , antibody , spleen , virus , interferon , biology , mammary tumor , mouse mammary tumor virus , mammary gland , endogeny , in vivo , immunology , pathology , cancer , medicine , endocrinology , genetics , microbiology and biotechnology , breast cancer
Low levels of anti‐viral activity, mainly interferon α/β (IFN‐α/ β), 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/ α‐β. The pathogenetic role of IFN in mammary carcinogenesis was investigated in 2 ways: (a) by treating virus‐infected newborn mice with antibody to IFN‐α/β, and (b) by giving either the latter antibody or IFN‐α/β to virus‐free animals transplanted with pre‐neoplastic lesions. Mice were treated only for 2 months, starting either I week after birth or immediately after tumor transplant. In case (a), treatment with antibody to IFN‐α/β 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‐α/β markedly reduced both tumor incidence and mortality rate. These results indicate that endogenous IFN‐α/β plays a crucial role in the in vivo restriction of the early infectious phase of spontaneous carcinogenesis and that relatively high doses of IFN‐α/β may inhibit the progression of pre‐neoplastic lesions. © 1992 Wiley‐Liss, Inc .