Premium
Enhancement or inhibition of tumor growth by interferon: Dependence on treatment protocol
Author(s) -
Murasko Donna M.,
Fresa Kerin,
Mark Raymond
Publication year - 1983
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.2910320616
Subject(s) - in vivo , radioresistance , interferon , cancer research , sarcoma , population , in vitro , biology , growth inhibition , primary tumor , immunology , pathology , cell culture , medicine , cancer , metastasis , biochemistry , microbiology and biotechnology , environmental health , genetics
MSC cells are tumor cells originally induced in BALB/c mice by Moloney sarcoma virus. In these studies we demonstrated that, although these tumor cells are sensitive in vitro both to lysis by NK or NK‐like cells and to the growth‐inhibitory effect of murine L‐cell interferon (IFN), the growth of the tumor in vivo could be either inhibited or enhanced by IFN. The outcome of in vivo IFN treatment was dependent on the timing and route of IFN administration relative to tumor challenge. IFN given systemically at the same time as tumor challenge resulted in enhancement of primary tumor formation, rate of tumor growth and subsequent progressive tumor growth. In contrast, IFN administered at the site of tumor inoculation on days 1–3 after tumor challenge inhibited tumor formation and growth. Histopathology of tissue sections obtained from the site of tumor challenge confirmed these results. Similar studies performed in mice given 450 rads of X‐irradiation showed that IFN could still inhibit tumor growth when administered at the site of tumor inoculation on days 1‐3 after tumor challenge. IFN administered simultaneously with tumor challenge, however, did not enhance tumor growth in irradiated mice. These results are consistent with the interpretation that 1) inhibition of MSC‐induced tumor growth by IFN has a radioresistant component and 2) the enhancement of MSC‐induced tumor formation by IFN is dependent on interaction with a radiosensitive population of cells, possibly lymphoid cells.