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H Mugitani

Publications and source records attributed to H Mugitani.

7 recordsLinked to original sources
PubMed1988

[Interferon-alpha].

Among interferon (IFN)-alpha, beta, gamma, there are no differences in its clinical effects and toxicities. As to IFN-alpha, there are leukocyte IFN, lymphoblastoid IFN, recombinant IFN-alpha 2a, 2b, and 2c. Now we have largely completed the process of surveying for anticancer effects over the broad range of malignancies. However, the adequate method of administration, route, dose, and interval are not yet fully established. Dose response remains unanswered question with some contradictory results in in vitro and clinical reports. The actual mechanism responsible for its anticancer activity is still not known. The question of what variables to monitor in assessing adequate dosages of IFN remains unsolved. Several trials have examined the possibility of combining IFN with other treatment modalities including anticancer agents, BRMs, radiation, etc. It should be acknowledged that we remain at a very early stage in our understanding of IFN. In future, IFN may play an even larger role when used in an adjuvant setting or as part of multimodality cancer treatment.

Drug Evaluation↗
PubMed1987

[Interferon production in vitro].

Interferon production in vitro was induced by poly I: C and PHA in leukocytes obtained from patients with cancer, benign diseases and control subjects. The interferon response per lymphocyte was relatively constant in all groups. However, interferon production was slightly inhibited in patients receiving cancer chemotherapy. The peak response of interferon occurred at 48 hours after the initiation of the combined culture in each specimen. From our observations, it was suggested that interferon production in vitro seems to be useful marker for evaluation of effect of chemotherapy and or immunotherapy, and, furthermore, in the treatment of cancer patients with interferon inducers, there seems to be optimum BRM dose and optimum timing of administration.

Cell Wall Skeleton↗
PubMed1986

[Host factors in cancer chemotherapy].

Cancer grows in interaction with the host, that is, a host-tumor relationship exists. Investigations of host factors in patients receiving cancer chemotherapy are important, as they reveal the conditions in which a tumor response can develop. Furthermore, reliable host factors, if present, will be useful for quantitative evaluation of the effects of treatment. We have investigated the following three categories of host factors in relation to the effects of cancer chemotherapy and/or immunotherapy. CBC, and blood chemistries (44 parameters). Tumor markers; sialic acid, RNase, lysozyme, ferritin, IAP (immunosuppressive acidic protein), elastase I, AFP, CEA, POA, CA 19-9, CA 125, etc. Immunological parameters; lymphocyte, active T cell, T cell, B cell, IgG Fc receptor-positive T cell, lymphocyte blastogenesis stimulated by PHA, or concanavalin-A, ADCC activity, interferon production in vitro induced by poly I: C, or PHA, PPD skin test, immune complex, immunoglobulin G, A, and M, OKT series 3, 4, 8, 11, 4/8 ratio, antihuman HLA-DR, Leu 11, NK cell activity, etc. From our clinical observations, there were no significant differences in the pretreatment levels of these parameters between responders and non-responders. In responders, there was a tendency for the host factors to show greater degrees of improvement following treatment than in non-responders, but none proved to be reasonably reliable parameters for evaluating therapeutic effects. On the other hand, from our clinical observations on the advanced gastric cancer cases, life span showed a close correlation with tumor regression induced by cancer chemotherapy. Because of these facts, it is only natural that the clinical effects of chemotherapy are currently determined by definite tumor regression.

Humans↗