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)

The hazards and complications of BCG immunotherapy, as well as the potential for enhanced tumor growth, make it imperative that the clinician know the clinical setting in which BCG can offer therapeutic benefit. This would include the intratumor injection of localized intradermal tumor deposits of melanoma and breast cancer, chemoimmunotherapy with BCG to prolong remission in acute myelogenous leukemia, and possibly the use of BCG as an adjuvant to control minimal residual disease. Aside from these situations, it is advisable to treat patients only on clearly defined experimental protocols.
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PMID:Hazards and complications of BCG immunotherapy. 127 90

In this series, 25 adult patients with intramedullary astrocytomas were treated by radical excision alone. Six patients proved to have anaplastic astrocytoma; five of them died within approximately 2 years and the sixth has demonstrated disease progression. The other 19 patients were diagnosed as having low-grade astrocytoma (16 cases) or ganglioglioma (three cases); two of these had advanced preoperative neurological disability and died of medical complications. Fifteen of the remaining 17 patients have no clinical evidence of tumor recurrence after a mean follow-up period of 50.2 months; the other two have a small residual neoplasm that demonstrates no progression. Of these 17 patients, seven had previously received radiation therapy, but had clear evidence of tumor growth subsequently. This experience suggests that surgery is not beneficial for anaplastic spinal astrocytoma. However, in cases of low-grade tumor, radical excision is associated with minimal morbidity and an excellent long-term prognosis when carried out before significant disability occurs.
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PMID:Adult intramedullary astrocytomas of the spinal cord. 150 81

Female C3H mice aged 8-10 weeks with transplanted KHT sarcoma or SCCVII tumor were used to investigate the antitumor effect of SPG (Sonifilan, Schizophyllan) alone and in combination with local irradiation of pions with 4 fractions of 400 cGy (total 1600 cGy). Daily doses of 10 mg/kg of SPG were given intramuscularly to the mice bearing KHT sarcoma for 14 consecutive days from day 7, and to mice bearing SCCVII tumor for 20 consecutive days from day 7 and thereafter three times a week for another 2 weeks. The antitumor effect was evaluated by the changes in tumor volume, survival curves, and the number of pulmonary metastatic nodules on the surface of the lungs. SPG failed to exert any antitumor effect and any life-prolonging effect for the KHT sarcoma. As for SCCVII tumor, in the group treated with pions and SPG, tumor growth decreased significantly (p less than 0.01) compared with the group treated with pion only, and life prolonging effect and metastasis-suppressing effect were also observed (p less than 0.04). In conditions of minimal residual disease brought about by pion irradiation, the adjuvant effect of a Biological Response Modifier (BRM) SPG may prove to be a promising method of cancer therapy for some tumors.
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PMID:Combination therapy of pions and SPG (Sonifilan, Schizophyllan), a biological response modifier for mouse tumor systems. 214 85

The therapeutic effect of intradermal (i.d.) injection of tumor cells mixed with VCN on growth of spontaneous metastases in transplantable tumors in mice (3-Lewis lung adenocarcinoma; B16-melanoma) and rats (R-3230 mammary adenocarcinoma) was investigated. Intradermal injection was done in a chessboard-like manner; increasing numbers (10(5), 10(6) and 10(7)) of Mitomycin-treated tumor cells (M-TC) were each mixed with increasing amounts (10, 50 and 100 mU) of Vibrio cholerae Neuraminidase (VCN). These different mixtures were injected i.d. at different sites one day after resection of the primary tumor graft to mice and rats, suffering from minimal residual disease. The therapeutic effect of this so-called chessboard vaccination on minimal residual disease was compared to that of the subcutaneous or i.d. injection of VCN-treated M-TC (10(5), 10(6), 10(7) or 10(8) cells) or of single mixtures of M-TC and VCN. The results show that compared to VCN-treated M-TC or single mixtures of M-TC and VCN, chessboard vaccination is the only procedure that is therapeutically effective on metastasation of Lewis lung adenocarcinoma. The therapeutic effect could be abrogated by heat-inactivation of VCN. Incomplete chessboard vaccinations (10(5), 10(6), 10(7) tumor cells, each mixed with 5 mU VCN only) were likewise ineffective. However, treatment with incomplete chessboard vaccinations in combination with a low dose of cyclophosphamide (which is not immunosuppressive, but partly inhibits tumor growth) had a synergistic therapeutic effect on minimal residual disease of Lewis lung adenocarcinoma. In contrast, growth of metastases of B16-melanoma and R-3230 adenocarcinoma could not significantly be influenced by any of those treatments. The DTH response of tumor bearing animals against i.d. applied tumor cells was neither significantly enhanced by the admixture of enzymatically active VCN nor did the DTH response seem to be predictive for a tumor-therapeutic effect. Thomsen-Friedenreich antigens could serologically be detected on untreated cells of Lewis lung adenocarcinoma, B16-melanoma and R-3230 adenocarcinoma. Exposure of Thomsen-Friedenreich antigens after treatment with VCN was enhanced on cells of all tumors except Lewis lung adenocarcinoma. As chessboard vaccination only proved to be successful in Lewis lung adenocarcinoma, but not in the other tumors, it can be concluded that the exposure of Thomsen-Friedenreich antigen plays no decisive role in tumor therapy with tumor cells and VCN. Chessboard vaccination was tolerated without any side effects. Tumor enhancement was not observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tumor therapy of neoplastic diseases with tumor cells and neuraminidase: experimental studies on chessboard vaccination in transplantation tumors. 342 76

It is clear, then, that cryosurgery augments immunity that is specifically directed against the tumor in several murine tumor systems. Both cell-mediated and humoral immunity are involved. The degree of augmentation of immunity is greater than that following a period of tumor growth and cold-knife excision and that following electrocoagulation of tumor. The degree of tumor-specific immunity after cryosurgery is not sufficient to alter growth rates of recurrent tumors, however. Although immunity is not markedly potentiated, it is sufficiently augmented to be effective in protecting against small doses of tumor cells of up to 10(6) cells, and presumably in the presence of minimal residual disease. It is possible that immunity could be potentiated further by the injection of accessible tumors with a nonspecific immunoadjuvant one to five days before cryosurgery.
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PMID:Immunotherapeutic effect of cryosurgical tumor necrosis. 697 55

The therapeutic effects of the low and high affinity mAbs 17-1A and 323/A3 were investigated in nude mice xenografted with LS 180 human colorectal carcinoma cells. Treatment of mice grafted with dispersed tumor cells, before formation of a tumor nodule, was started 1 day after s.c. injection of tumor cells and consisted of a single i.p. injection of murine 17-1A or 323/A3 mAb. Tumor appearance after a single injection of either 17-1A or 323/A3 was delayed as compared to injection of an irrelevant mAb. Both 17-1A and 323/A3 reduced the tumor growth rate, and both mAbs decreased the total number of mice that eventually developed a tumor. In all experiments, 323/A3 showed consistently better treatment effects on xenografted mice than mAb 17-1A. For treatment of established tumors with mAb 17-1A or 323/A3 therapy was delayed until a tumor nodule was macroscopically detectable. One single i.p. injection of mAb 17-1A had no effect on further tumor growth and mean tumor size as compared to the control group injected with irrelevant mAb. One single i.p. injection with mAb 323/A3 reduced the tumor growth rate in some mice with established tumors and resulted in a significant difference of mean tumor size of this group as compared to the 17-1A treated mice and the control groups. Multiple injections with mAb 17-1A also had no effects on established tumors, in contrast to mAb 323/A3, where serial injections resulted in tumor growth reduction and, eventually, in some mice reduction in tumor size. In summary, we showed that in nude mice mAb 323/A3 (Ka = 2 x 10(9) M-1) is much more potent than mAb 17-1A (Ka = 5 x 10(7) M-1) in eradication of nonestablished tumor cells and treatment of small established tumors. These results suggest that high affinity mAbs like 323/A3 might dramatically improve the clinical results obtained thus far with the low affinity mAb 17-1A in the adjuvant treatment of surgically resected Dukes C colorectal cancer patients with minimal residual disease.
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PMID:Immunotherapy with low and high affinity monoclonal antibodies 17-1A and 323/A3 in a nude mouse xenograft carcinoma model. 767 Dec 52

The use of differentiation-inducing agents has been proposed for the purging of bone marrow and for the treatment of minimal residual disease prior to autologous bone marrow transplantation in patients with metastatic neuroblastoma. The present studies examine the effects of the enediyne differentiation inducer neocarzinostatin (NCS) on tumor development from subcutaneous implants of murine (Neuro-2A) neuroblastoma cells. Prior in vitro treatment with NCS results in a concentration- and drug exposure time-dependent decrease in the incidence of tumors from subcutaneously implanted cells. In vivo treatment results in a dose-dependent decrease in the rate of tumor growth. These results imply that enediynes such as NCS may be useful in ex vivo purging regimens and in in vivo treatment of microscopic residual disease in patients with neuroblastoma.
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PMID:Effects of neocarzinostatin upon the development of tumors from murine neuroblastoma cells. 798 86

The potential of interleukin 2-gene-transfected tumor cells to prevent tumor growth and cure established tumors was evaluated using cells from a spontaneous, invasive, and metastasizing mouse mammary adenocarcinoma. Tumor cells engineered to secrete interleukin 2 initially trigger a local inflammatory reaction that leads to inhibition of established parental adenocarcinomas, as well as an antigenically unrelated fibrosarcoma. The ensuing systemic immunity selectively inhibits subsequent parental cell challenges and cures established parental adenocarcinomas and their lung metastases, although less effectively as the neoplastic mass increases. Multiple injections of interleukin 2-gene-transfected tumor cells may thus be considered a new form of vaccination in the management of minimal residual disease and incipient metastases.
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PMID:Protective and curative potential of vaccination with interleukin-2-gene-transfected cells from a spontaneous mouse mammary adenocarcinoma. 822 36

One of the major limitations to the immunotherapy of ovarian carcinoma based on the use of anti-CD3/antitumor bispecific monoclonal antibodies (bi-mAb) is the need for preactivation of effector cells ex vivo, because cross-linking of the T cell receptor-CD3 complex per se may lead to T-cell unresponsiveness or even apoptosis. The bi-mAb OC/TR, which recognizes the folate-binding protein (FBP) overexpressed in 90% of ovarian carcinomas and the CD3 molecule on T cells, has demonstrated efficacy in a clinical setting. Here we investigated the possibility of delivering accessory signals to OC/TR-retargeted peripheral blood mononuclear cells (PBMCs) via an anti-CD28 mAb or an anti-FBP/anti-CD28 bi-mAb. Coculture of resting PBMCs from healthy donors with OC/TR, anti-FBP/anti-CD28 bi-mAb, and FBP+ tumor cell lines resulted in a highly activated phenotype of effector cells and in a dramatic in vitro growth inhibition of the target cells without an increase in OC/TR-redirected lysis. Whereas both the CD4 and CD8 T cell subsets were involved in the growth inhibition, only the CD8 subpopulation accounted for the cytotoxic activity. The in vitro tumor growth inhibition was mediated mainly by soluble factors, which were active on both FBP+ and FBP- ("bystander effect") cell lines. Activation and antitumor activity were also observed, albeit to a lesser extent, using OC/TR and monospecific bivalent anti-CD28 mAb. In vitro analysis demonstrated that cross-linking between tumor and effector cells for at least 24 h was needed to achieve T-cell activation and development of antitumor activities. Thus, ex vivo CD3-CD28 costimulation on resting PBMCs might be of therapeutic utility for local treatment of minimal residual disease.
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PMID:CD3-CD28 costimulation as a means to avoiding T cell preactivation in bispecific monoclonal antibody-based treatment of ovarian carcinoma. 896 99

The effect of allogeneic cell therapy on tumor growth was studied in a murine model of mammary carcinoma (4T1) as an experimental model of solid tumors in humans. i.v. inoculation of 4T1 (H-2d) cells into syngeneic mice [BALB/c or (BALB/cXC57BL/6)F1] (F1) carrying the H-2d histocompatible antigens results in tumor colonies in the lungs that finally cause the death of all of the mice. Sublethally irradiated F1 mice were inoculated with 4T1 cells to simulate minimal residual disease and with immunocompetent splenocytes derived from naive donors of F1 (syngeneic), BALB/c (syngeneic to the tumor but semiallogeneic to the host), or C57BL/6 (allogeneic to the tumor and semiallogeneic to the host) mice. The survival of F1 tumor-bearing mice that were treated with allogeneic C57BL/6 splenocytes was significantly prolonged (P < 0.02) compared with hosts given F1 or BALB/c-derived splenocytes that are syngeneic to 4T1 tumor cells. Adoptive transfer of lung cells that were isolated from F1 primary mice inoculated with 4T1 cells and syngeneic BALB/c or F1 splenocytes led to local tumor growth and death in secondary recipients. In contrast, only 1 of 22 secondary recipients developed tumors when inoculated with lung cells derived from F1 mice given allogeneic C57BL/6 splenocytes. All of the 21 secondary hosts survived disease-free for a follow-up time of >200 days. These results indicate that immunocompetent cells allogeneic to the mammary carcinoma cells were able to inhibit tumor development in the primary hosts and to prevent tumor growth in the adoptive recipients, which suggests that allogeneic cell therapy may be an efficient antitumor tool to eradicate minimal residual disease in human solid tumors.
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PMID:Allogeneic cell therapy for a murine mammary carcinoma. 973 99


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