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Action of recombinant alpha interferon against experimental and spontaneous metastases in a murine model
Author(s) -
Ramani P.,
Balkwill F. R.
Publication year - 1989
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.2910430126
Subject(s) - cancer research , lung , alpha (finance) , alpha interferon , stimulation , cell , ratón , metastasis , mechanism of action , medicine , immunology , interferon , biology , in vitro , cancer , construct validity , genetics , nursing , patient satisfaction , biochemistry
The therapeutic potential of rHuIFN‐α A/D, a hybrid human IFN molecule with equal activity on murine cells, was studied in experimental and spontaneous metastatic models of a murine colon carcinoma COLON 26. rHuIFN‐α A/D inhibited experimental pulmonary metastases of COLON 26 and prolonged the survival of BALB/c mice. Dose scheduling, survival and tumour‐cell clearance studies showed that the first 5 days were critical in the inhibition of pulmonary metastases. However, it is unlikely that lung NK cells were involved in the anti‐metastatic effect of rHuIFN‐α A/D because inhibition of pulmonary metastases and a decrease in radio‐labelled tumour‐cell survival was seen in BALB/c mice depleted selectively of their NK cells by prior treatment with rabbit antiasialoGM 1 serum. Although rHuIFN‐α A/D stimulated Nit‐cell activity in BALB/c mice, it was ineffective in abrogating the NK suppressant action of rabbit anti‐asialoGM 1 serum on murine lung NK cells. Thus, IFN may mediate its early antimetastatic effect via a mechanism independent of NK‐cell stimulation. IFN also inhibited the development of lung metastases from s.c. COLON 26 tumours in normal, NK‐depleted and T‐cell‐deficient mice.