Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past decade, much has been learned about the pathophysiology of ACH--yet much remains to be determined. Although LC, IL-1, IL-2, IFN-gamma, and the T effector circuits have been extensively studied, it is still not clear whether it is LC- or keratinocyte-derived IL-1 that is crucial in ACH, whether IL-1 acts primarily on T-cells or the APC, whether other cytokines are involved in the circuit (TNF, KTGF?), the exact relationships between T effector, T memory, and other T helper cells, what the functions of mast cells and basophils are in the allergic reaction, and how the regulatory circuits (including prostaglandins and eicosanoids) affect the outcome of ACH. The mechanism of suppression remains even less well understood despite the potential application of this knowledge to the treatment of diseases caused by Type IV hypersensitivity. A better understanding of the ACH mechanism will lead not only to more sophisticated ACH treatment, but also to a better understanding of the cell-mediated events of cutaneous viral replication, organ transplantation, and tumor growth.
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PMID:The pathophysiology of allergic contact hypersensitivity. 269 Oct 41

The recent progress in immunology has shown depression of immunological competence, especially cellular immunity in tumor bearing host due to anesthesia, blood transfusion and operative trauma itself and disappearance of host's concomitant immunity caused by removal of primary tumor, resulting the enhancement of growth of residual tumor or metastatic foci. The prophylactic lymph node dissection in cancer operation must be reconsidered through immunological studies of lymph node as immunological surveillance system. Splenectomy combined with the operation of stomach cancer must also be reconsidered. Therefore, the main aims of this society are to suppress the negative aspect in connection with the cancer operation by means of immunotherapeutic approach and to prevent the recurrence and/or metastasis of cancer. Research society, met for the first time in 1980, and has since discussed the following main themes at 9 occasions of meetings up to 1988: 1. Pre- and postoperative immunological competence in cancer patients. 2. Surgery and immunological competence for cancers. 3. Antitumor activity of regional lymph nodes. 4. Splenectomy and tumor growth. 5. Surgical treatment and immunochemotherapy. 6. Serum immunosuppressive factors in cancer patients. 7. BRM and immunotherapy. 8. Diagnosis and treatment of cancer using monoclonal antibody. 9. Cancer treatment using IL-2, TNF. 10. Host defense factors and cancer metastasis. In addition, 14 educational lectures dealing with recent immunology have been given by immunological specialists.
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PMID:[On the activity of the Japanese Research Society for Surgical Cancer Immunology]. 273 30

Sensitized T lymphocytes can mediate potent antitumor effects when transferred to tumor-bearing animals. Employing the MCA 105 and MCA 106 sarcomas, we were able to generate antitumor effector cells by immunization of syngeneic mice with tumor cells admixed with Corynebacterium parvum. These immune splenocytes could be further sensitized and expanded in culture by the in vitro sensitization (IVS) method utilizing tumor stimulator cells and IL-2. Adoptive immunotherapy of pulmonary metastases mediated by noncultured splenocytes from immunized mice or immune IVS cells showed exquisite specificity between the two sarcomas. These results demonstrate the presence of tumor-specific antigens on MCA 105 and MCA 106 tumor cells which can serve as target molecules for immunotherapy. Recently, we have generated therapeutic T lymphocytes from mice bearing progressively growing tumors by the IVS method. However, IVS cells from tumor-bearing mice showed cross-reactivity between the MCA 105 and 106 sarcomas in adoptive immunotherapy experiments. Since these IVS cells did not affect other control tumors, the limited cross-reactivity suggests the presence of common tumor-associated antigens on MCA 105 and MCA 106 tumor cells which can also serve as the target for tumor rejection. Therefore, immune responses to progressive tumor growth and to immunization are distinct with respect to antigen recognition by T lymphocytes.
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PMID:Distinct immunologic specificity of tumor regression mediated by effector cells isolated from immunized and tumor-bearing mice. 278 60

Cimetidine (CMT), cyclosporine A (CsA), interleukin 2 (IL 2), were used to characterize the anticancerous effect of a polyantigenic immunodulator (PAI). PAI consists of a mixture of inactivated bacteria and influenza virus in a peanut oil-arlacel A-aluminum monoesterate emulsion. Antitumoral activity was tested on Ehrlich's ascites tumor (EAT) implanted into Swiss-Webster (allogeneic) or C57BL/6J (syngeneic) mice. PAI antitumor activity was enhanced by CMT acting synergistically by reducing substantially the tumor growth and increasing the percentage of surviving mice, while CsA suppressed this activity. PAI or its individual components were able to induce significant lymphocyte blastogenesis in mouse (C57BL/6J)-spleen lymphocytes and IL-2 enhanced considerably this lymphoproliferative response. The results suggest that PAI acts at the level of cellular immunity.
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PMID:Characterization of the antitumor activity of a polyantigenic immunomodulator (PAI): I--Utilization of cimetidine and cyclosporine A. 278 52

Elvax pellets containing interleukin 1 (IL-1) or 2 (IL-2) were assessed for their ability to alter the growth of transplanted C6 cells in rat. C6 cells were injected into the left caudate of Sprague Dawley rats. At the time of tumor cell injection, or 9 days later, Elvax pellets containing either 50 or 200 units of interleukin were inserted into the dorsal aspect of the caudate. Animals were killed 16 days later and the volume of tumors determined. Results showed that introduction of low-dose IL-2 pellets at time of C6 cell injection virtually prevented establishment of tumors, whereas low-dose IL-1 pellet insertion resulted in nearly a threefold increase in tumor size relative to control preparations. Insertion of high-dose IL-2 pellets 9 days after C6 cell injection decreased tumor growth relative to controls by nearly twofold, low-dose pellets having no effect. These effects appear to be mediated by alterations in host brains, vs interleukin-moderating effects on growth of C6 cells themselves, since (a) no effect of IL-2 on C6 cell growth in vitro could be demonstrated and IL-1 appeared to enhance their proliferation in culture, and (b) IL-1 pellets diminished and IL-2 pellets enhanced infiltration of inflammatory cells into brain when implanted into brain after a "stab" wound.
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PMID:Exogenous interleukin regulates growth of C6 tumors in vivo. 322 15

T lymphocytes isolated from a bulk culture of splenocytes exposed in vitro to polyoma TAA and IL-2, taken from CBA mice with transplanted polyoma tumors, exhibited both antitumor and DTH activity to polyoma TAA, associated with the Lyt 1+ phenotype, and also showed an increased affinity to TAA. The antitumor efficacy of adoptive immunotherapy, consisting in the i.p. administration of these TAA-driven lymphocytes, showed time and IL-2 dependence, while transferred cells were capable of eliciting DTH independently of IL-2. The suppression of tumor growth observed in 70% of the animals in the optimal variant seems to result from the cooperation of transferred lymphocytes with the recipients own lymphocytes.
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PMID:Polyoma antigen driven T lymphocytes with antitumor and DTH activity in CBA mice. 326 95

Adoptive immunotherapy with LAK-cells in conjunction with high-dose IL-2 has recently been introduced in the treatment of patients with advanced cancer. This therapeutic modality has thus far proved to be of limited efficacy, severe toxicity and entails complicated logistics. Our present study is aimed at establishing a model system to test for increasing efficacy and reducing toxicity by using AIT cojointly with chemotherapy. Mice implanted i.v. or i.p. with weakly immunogenic tumors (M109 lung carcinoma, MCA-105 sarcoma) were treated 7 to 20 days after tumor inoculation with or without CTX, with and without recombinant human IL-2, and with and without syngeneic/allogeneic LAK-cells. Whereas IL-2 or IL-2 + LAK-cells without CTX was largely ineffective, and CTX alone cured 0 to 20% of the animals with an i.p. tumor and only slightly reduced pulmonary tumor mass, the combination of CTX + IL-2 cured 50 to 80% of the mice bearing i.p. tumors and reduced pulmonary tumor growth by greater than or equal to 80%. The combination of CTX + IL-2 + LAK-cells proved no more beneficial than CTX + IL-2 without LAK-cells. Also relevant were the observations that murine LAK-cells are transiently sensitive to moderate doses of CTX (greater than or equal to 100 mg/kg body weight) and X-irradiation (greater than equal to 400 rad), and that administration of IL-2 by the i.v. or i.p. route variously affects LAK-cell activation in different tissues and eradication of growths localized at different sites. With the regimens used, no signs of toxicity were detected. It is proposed that instillation of IL-2 (and perhaps of additional immunostimulating cytokines as well) as an adjunct to chemotherapy (or chemoradiotherapy), each given at a subtoxic dose, is both safe and effective in the treatment of metastatic advanced tumors, and that the additional administration of LAK-cells may not be required.
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PMID:Therapy of advanced solid tumors in mice using chemotherapy in combination with interleukin-2 with and without lymphokine-activated killer cells. 326 51

The murine leukemia L1210-specific cytotoxic T-cell clone K7 was established by repeated antigenic stimulation of spleen cells of L1210-immune CD2F1 mice in long-term culture. K7 possessed L1210-specific cytolytic activity detectable by the 51Cr-release test, but lost its cytolytic activity about 100 days after initiation of culture (designated as clone K7L). Clone K7L retained its L1210-specific tumor-growth-inhibitory activity independently of culture supplementation with IL-2. K7L possessed the cell-surface antigenic phenotype of cytotoxic T cells, Thy-1+, Lyt-1-, Lyt-2+. This clone K7L displayed surprisingly strong activity in specifically inhibiting in vivo tumor growth of L1210 by day 5 in the peritoneal cavity of CD2F1 mice when injected together with 10(5) tumor cells (more than 90% inhibition at E/T = 5), and prolonged survival times of most of the mice for more than 60 days, whereas control mice inoculated with L1210 alone died on day 9-17. This unique in vivo anti-tumor activity was not correlated to the in vitro cytolytic activity. Nevertheless, bystander inhibitory effect on the growth of third-party tumor cells (P388) was not seen in mice injected with a mixture of L1210 and P388 together with K7L, suggesting that K7L inhibited L1210 growth by direct cell-to-cell interaction. Host cells such as X-irradiation (800R)-sensitive lymphocytes and Carrageenan-sensitive macrophages were not involved in the early growth inhibition of L1210 by K7L.
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PMID:Establishment of a murine leukemia L1210-specific T-cell clone displaying novel in vivo anti-tumor activity. 349 92

Highly purified natural IL-2, obtained from induced human PBL's, was used to treat tumor-bearing mice. 3 X 10(6) vital cells of chemically induced fibrosarcoma BALB/c female Meth A were transplanted subcutaneously to female mice. Repeated injections of 10,000 U IL-2 into established tumors of 7-8 mm diameter led to complete rejections in 75% of the treated animals. Single intratumoral injections and other routes of the application of IL-2 did not significantly influence the tumor growth rate.
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PMID:Inhibition of tumor growth in a mouse fibrosarcoma after interleukin 2 application. 349 35

The in vivo anti-tumor activity of 2 recombinant cytokines, interleukin-2 (rIL-2) and human hybrid interferon alpha (rHuIFN-alpha A/D), were tested using the murine reticulum cell sarcoma M5076. Experimental hepatic metastases, following i.v. injection of tumor cells, and tumor growth and spontaneous metastases, following s.c. injection of tumor cells, were inhibited to a greater extent in mice treated with a combination of these cytokines than in animals treated with either one alone. When used in conjunction with surgical removal of the s.c. tumor, treatment of mice with both cytokines significantly prolonged survival of tumor-bearing animals. Injection of normal mice with a combination of cytokines, but not with either cytokine alone, resulted in a marked increase in cytotoxic activity of hepatic effector cells. The effector cells in these mice appeared to be NK cells since this enhanced cytotoxicity was markedly reduced in animals treated in vivo with anti-asialo GM1 or in NK-deficient beige mice. Furthermore, no in vivo efficacy was observed in M5076-bearing beige mice treated with these cytokines. Thus, injection of mice with rIL-2 and rHuIFN-alpha A/D results in the induction of an NK-cell-like population in the liver with enhanced cytotoxic activity that correlates with the observed anti-tumor activity in vivo in this murine model. These results suggest that combinations of cytokines, in particular IFN-alpha and IL-2, can be effectively used in combination for the treatment of tumors and/or metastases.
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PMID:In vivo anti-tumor activity of combinations of interferon alpha and interleukin-2 in a murine model. Correlation of efficacy with the induction of cytotoxic cells resembling natural killer cells. 349 83


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