Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two children with advanced (Stage III and IV) neuroblastoma have been treated in a nonrandomized fashion, half with a three-drug regimen consisting of vincristine, adriamycin, and cyclophosphamide, and half with this same drug combination plus the nonspecific immunostimulatory agent, MER/BCG. The addition of MER to the three-drug combination appeared to improve the duration of survival in this pilot study. The median duration of response was less than one year in the combination chemotherapy alone arm. The median duration of complete remission in children treated with the addition of MER has yet to be reached at 24 months.
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PMID:Immunochemotherapy in advanced neuroblastoma. 63 92

One hundred forty-four Wistar-Furth rats in 12 therapeutic groups have been studied in a long-term comparison of the effectiveness of nonspecific immunotherapy with MER (methanol extraction residue) vs active-specific immunotherapy with neuraminidase-modified tumor cells. Six months after surgical adjuvant immunotherapy a 100% improvement in survival was achieved with MER immunotherapy compared to untreated control animals. In addition, the use of MER enhanced the value of active-specific immunotherapy where both modalities were combined in sequence. The predicted value of MER-BCG (Bacillus Calmette-Guerin) for the immunotherapy of solid tumors was borne out by these results suggesting that present ongoing clinical trials of MER as adjuvant therapy for large bowel cancer should prove to be successful if properly controlled. The pattern of survival in these experiments suggests that surgical adjuvant immunotherapy is cytostatic rather than cytocidal, and implies the need for long-term, repeated immunizations.
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PMID:Surgical adjuvant immunotherapy for colorectal cancer. 73 27

A pronounced vitiliginous reaction developed at the sites of MER/BCG injections given as an adjuvant immunotherapy to a patient with malignant melanoma. To our knowledge, this is the third report on patients exhibiting vitiligo apparently induced by immunotherapy and the first in association with MER. This association may be a sign for an antimelanocytic effect and may offer a further confirmation for the autoimmune nature of vitiligo.
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PMID:Vitiligo associated with BCG-methanol extraction residue in malignant melanoma. Report of a case. 76 93

The data reviewed in this paper indicate that immunotherapy is effective in prolonging remission and survival in acute and chronic leukemia. The acute lymphocytic leukemias may or may not respond to immunotherapy and further work is needed in this area. No studies of immunotherapy in chronic lymphocytic leukemia have been done, but this will be an important area for investigation, since there is often profound immunodeficiency in this disease. The malignant lymphomas are another fertile area for this type of research, since they have a high response rate, tumor-associated immunodeficiency, and at least differentiation antigens if not tumor-specific antigens. The scientific basis for the use of immunotherapy in leukemia includes the demonstration of a relationship of rate and duration of remission and survival to immunocompetence, the demonstration of unique tumor-associated antigens on leukemia cells, and the demonstration of immune responses to these antigens which can be boosted by immunization. At the present time, active nonspecific immunotherapy with BCG and MER and active specific immunotherapy have been proved effective in acute myelogenous leukemia. Careful attention should be given to dose, schedule, route, and so forth. Other types of immunotherapy remain to be explored.
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PMID:Immunotherapy of leukemia. 78 12

An immunosuppressed mouse model was devised to test the effects of immunopotentiators on the prevention of bacterial and fungal infections. The effects of BCG and Corynebacterium were tested against Staphylococcus aureus and Candida albicans infection. The effect of methanol-extraction residue (MER-BCG) was tested against S. aureus septicemia. CDF mice were given various doses of BCG, 1.0 mg of C. parvum, or 0.5 mg of MER intraperitoneally at varying intervals before injection of an intravenous bacterial challenge. Four days before challenge, 300 mg of cyclophosphamide per ml was given intraperitoneally. BCG (106 colony-forming units) reduced mortality due to S.aureus at pretreatment intervals of 3, 7, 14, and 28 days. Isonicotinic acid hydrazide treatment elimated the protective effect of the live BCG. C. parvum was as effective as BCG against S. aureus septicemia when given 3 days before infection, but lost most of its protective effect after that time. MER protected at doses as small as 0.25 mg when given 25 days prior to challenge. Both BCG and C. parvum exerted a protective effect against Candida albicans infection.
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PMID:Effects of BCG, Corynebacterium parvum, and methanol-extration residue in the reduction of mortality from Staphylococcus aureus and Candida albicans infections in immunosuppressed mice. 110 24

The experimental treatment of a rat sarcoma (McFiFi 2) by intratumoral injection of BCG2 is described. Tumors which have a mean diameter of less than 10 mm at the beginning of treatment are fully susceptible to BCG, although spontaneous regression is not observed at this stage. The effective dose of living BCG ranges from two injections of 0.1 mg to two injections of 1 mg, given IT at an interval of 7 days. The permanent cure of a proporation of the tumors may also be induced by IT injection of a similar dose of heat-killed BCG or of MER, or of 10(9) heat-killed C. parvum, according to the same schedule. Preimmunization of the rats with living BCG does not improve the efficiency of heat-killed BCG. Direct contact between the therapeutic material and the tumor cells is critical. If rats are grafted with two pieces of the same tumor in widely separated sites, the intratumoral treatment of only one of these tumors with living BCG is sufficient to induce regression of both tumors in 50% of the animals. The effect of BCG is counteracted by injection of silica or by ingestion of polaramine. The same intratumoral treatment with living BCG was applied to different rat and mouse tumors. Only McFiFi 2 tumors were cured by intralesional BCG. C3H mouse plasmocytoma 5563 was not cured by intratumoral BCG but its growth could be prevented by mixing BCG and tumor cells at the time of grafting; this tumor was considered to be of medium susceptibility. However, until there is definite proof that the two mechanisms are identical, one should consider the regression and cure of a growing tumor, and the prevention of tumor growth, as two different phenomena. The clinical treatment of human tumors resembles the first experimental procedure more closely than the second.
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PMID:Therapeutic effect of intratumoral injection of bcg and other substances in rats and mice. 117 5

Systemic administration of the synthetic immunopotentiator pyran, was as effective as the use of the biologic immunopotentiator BCG in activating macrophages and in inhibiting the Lewis lung carcinoma and MCA 2182 sarcoma. Several other synthetic polyanions also activated macrophages and exhibited some anti-tumor activity, but none were as effective as pyran. Cell-wall fractions such as the Ribi vaccine and MER were considerably less effective than BCG. The anti-tumor activity of pyran against the virtually non-immunogenic Lewis lung carcinoma involved non-specifically activated macrophages, and both anti-tumor activity and macrophage activating ability persisted over a 100-fold range of drug from 0.5 mg/kg to 50 mg/kg. The ability of activated macrophages to destroy tumor cells was abrogated by treatment with trypan blue, an inhibitor of macrophage lysosomal enzymes. In addition, preincubation of tumor cells with activated peritoneal cells at effector-cell:target-cell ratios of 20:1 and 5:1 markedly decreased tumor incidence and mortality. Glycogen-stimulated or unstimulated peritoneal cells were completely inactive in inhibiting tumor growth in vivo or exhibiting cytotoxicity in vitro, demonstrating the requirement for activated macrophages selective for tumor-cell destruction.
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PMID:Macrophage activation and anti-tumor activity of biologic and synthetic agents. 124 2

Patients with limited-stage small-cell carcinoma of the lung (SCCL) were randomly assigned to a four-drug chemotherapy program consisting of methotrexate, doxorubicin, cyclophosphamide, and CCNU (MACC) or to a regimen consisting of cyclophosphamide, CCNU, and vincristine alternated with Adriamycin (Adria Laboratories, Columbus, Ohio) and vincristine (CCV/AV). All patients received 4,500 cGy, in a split course, to the primary tumor, mediastinum, and supraclavicular lymph node drainage areas and 3,000 cGy to the whole brain. After four cycles of chemotherapy, patients were randomly assigned to chemotherapy plus methanol extractable residue of BCG (MER-BCG) or no MER-BCG. The complete response frequencies were similar for the two regimens (54% and 48%) as were the median survivals (12.0 and 11.5 months) and the two-year survival rates (15% and 17%). Immunotherapy with MER-BCG did not prolong the time to disease progression or improve survival. Women had a greater chance of achieving a complete remission independent of performance status. There was a complex interaction between sex and the chemotherapy regimens that may have important implications for the design and stratification of future trials in SCCL.
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PMID:Combined modality therapy with radiotherapy, chemotherapy, and immunotherapy in limited small-cell carcinoma of the lung: a Phase III cancer and Leukemia Group B Study. 299 78

The present study was designed to study the effect of dietary fat intake on the modulation of dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis in rats injected with the methanol extract residue of Bacillus Calmette-Guerin (MER-BCG). Rats were maintained on either a 5% or a 20% corn oil diet for the entire duration of the experiment. When MER-BCG was administered 2 and 3 weeks before DMBA, mammary tumorigenesis was suppressed in the 2 dietary groups with different levels of fat intake. This was in contrast to when MER-BCG was administered 3 and 5 weeks after DMBA; in this case the development of mammary tumors was noticeably enhanced regardless of the fat intake of the host. The magnitude of inhibition or increase by MER-BCG was similar in animals fed either fat level, although a high fat diet consistently stimulated mammary tumorigenesis in the 2 experiments. In vitro assays on T cell mitogen-induced blastogenesis and natural killer cell activity in splenocytes isolated from the untreated rats showed that dietary fat failed to elicit any differential response in these immune functions.
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PMID:BCG-modulated mammary carcinogenesis is dependent on the schedule of immunization but is not affected by dietary fat. 308 63

Forty-four patients with previously untreated advanced lung cancer were randomized to receive radiochemotherapy (RC) or radiochemotherapy plus MER/BCG (RCM). Prior to immunotherapy administration cutaneous reactivity to 5 log dilutions of MER/BCG was determined starting at 100 micrograms per injected site to 10 sites. Reactive patients were injected with 10, 1.0, or 0.1 micrograms while anergic patients were given 200 or 100 micrograms to each of 10 cutaneous sites, the dose being inversely related to the strength of the pretreatment reaction. Injected doses were subsequently further increased or decreased to achieve tolerable local erythema and induration. This modification resulted in a marked reduction in cutaneous toxicity previously observed, and made it possible to nearly double the mean number of MER courses per patient. It is suggested that intradermal MER/BCG may prove to be a considerably more useful therapeutic agent if doses are adjusted to patients' individual cutaneous responsiveness.
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PMID:Novel approach to MER/BCG administration in cancer patients. 358 Sep 42


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