The concept that the immune system recognizes and controls cancer was first postulated over a century ago, and cancer immunity has continued to be vigorously debated and experimentally tested. Mounting evidence in humans and mice supports the involvement of cytokines in tumor initiation, growth, and metastasis. The idea that the immune system detects stressed, transformed, and frankly malignant cells underpins much of the excitement currently surrounding new cytokine therapies in cancer treatment. In this review, we define the contrasting roles that cytokines play in promoting tumor immunity, inflammation, and carcinogenesis. We also discuss the more promising aspects of clinical cytokine use in cancer patients.

Cytokines in cancer immunity and immunotherapy

Cotylenin A, a novel inducer of the differentiation of leukemia cells, and IFN-alpha synergistically inhibited the growth of and induced apoptosis in several human non-small cell lung carcinoma cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptor DR5 were the early genes induced by the combination of cotylenin A and IFN alpha in lung carcinoma cells. Neutralizing antibody to TRAIL inhibited apoptosis, suggesting that cotylenin A and IFN alpha cooperatively induced apoptosis through the TRAIL signaling system. This combined treatment preferentially induced apoptosis in human lung cancer cells while sparing normal lung epithelial cells and significantly inhibited the growth of human lung cancer cells as xenografts without apparent adverse effects, suggesting that this combination may have therapeutic value in treating lung cancer.

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Cotylenin A, a Differentiation-inducing Agent, and IFN-α Cooperatively Induce Apoptosis and Have an Antitumor Effect on Human Non-Small Cell Lung Carcinoma Cells in Nude Mice

Pharmacodynamic aspects of peptide administration biological response modifiers

CD59 is a 18-25 kDa glycoprotein which, by inhibiting the formation of the membrane attack complex, protects homologous cells from complement mediated damage. We have described recently the expression and complement regulatory function of CD59 on colonic adenocarcinoma cells both in vivo and in vitro. In this study we have examined the influence of cytokines on the expression and complement regulatory function of CD59 on the colonic adenocarcinoma cell line HT29. CD59 expression on the HT29 cells was up-regulated after stimulation by mononuclear cells activated by mixed lymphocyte reaction and by culture supernatants from activated mononuclear cells. Similarly, a dose-dependent increase in CD59 expression was observed after stimulation with both tumour necrosis factor-alpha and interleukin-1 beta. A dose-dependent increase in the level of CD59 expression was also seen using low concentrations of interferon-gamma (IFN-gamma), while CD59 expression on cells cultured with high IFN-gamma concentrations was comparable to non-stimulated cells. Cytokine treated cells were more resistant to lysis by homologous complement than non-stimulated cells, and the increase in CD59 expression was shown to be partially responsible for this. The present data strengthen the role of CD59 as a possible participant in tumour escape.

The influence of tumour necrosis factor-alpha, interleukin-1 beta and interferon-gamma on the expression and function of the complement regulatory protein CD59 on the human colonic adenocarcinoma cell line HT29.

A low concentration of differentiation inducers such as dimethylsulphoxide (DMSO), sodium butyrate, hexamethylene bisacetamide and sodium phenylacetate greatly enhanced the antiproliferative effect in vitro and in vivo of interferon alpha (IFN-alpha) to several human lung adenocarcinoma cells. The agents induced morphological changes in the adenocarcinoma cells and the agents together with IFN-alpha-induced alkaline phosphatase activity, which is a typical marker of type II pneumocyte maturation. To understand the mechanism of the DMSO-enhanced interferon sensitivity, we examined the effect of DMSO on high-affinity IFN-alpha receptor and interferon-stimulated promoter-binding factors. The lung adenocarcinoma cells were not impaired in IFN-alpha receptor and interferon-stimulated gene transactivation factor 3 (ISGF-3). Our data suggest that the enhancement of interferon sensitivity in the lung adenocarcinoma cells acts downstream of the activation of ISGF-3.

Enhancement of sensitivity of human lung adenocarcinoma cells to growth-inhibitory activity of interferon alpha by differentiation-inducing agents.

Belonging to the vast family of cytokines, interferons (IFN) have recently been widely investigated concerning their possible clinical applications, both in virology and oncology. In this field results have been quite mixed but definitely encouraging. The best achievements have been obtained in hematology, and particularly in the treatment of hairy cell leukemia and chronic myelogenous leukemia, but new perspectives have also opened in the therapy of solid tumors, especially in the local treatment of superficial bladder cancer and ovarian cancer, AIDS-related Kaposi's sarcoma and malignant melanoma. IFN have in certain cases showed an efficacy comparable to that of classic treatments but with lower toxicity, and in some tumors they have even improved the results obtained so far, especially in combined therapy. We have here gathered the most recent results concerning the use of IFN in the therapy of solid tumors in order to highlight the new therapeutic opportunities available to clinical oncology.

Interferons in the therapy of solid tumors

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Interferons in the therapy of solid tumors