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)

Subcutaneous growth of immunogenic chemically induced rat sarcomata and a hepatoma was restricted when cells were injected into syngeneic animals in admixture with MER. Rats rejecting mixed inocula were immune to further challenge with the same tumour. Growth of a chemically induced mammary carcinoma which lacks detectable immunogenicity was suppressed when low cell inocula were injected in admixture with MER or intact BCG organisms, although animals were not immune to re-challenge. These studies indicate that clinically MER may be a suitable alternative to BCG for contact suppression of tumour growth or incorporation into tumour cell:adjuvant vaccines for active immunotherapy.
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PMID:Methanol extraction residue of BCG in the treatment of transplanted rat tumours. 16 61

The local reaction to gingival injections of methanol extraction residue of BCG (MER/BCG) was investigated in guinea pigs to help determine the potential of this agent in treating oral carcinoma. The drug was used in a standard and diluted form. Both concentrations were well tolerated and caused no ulceration or necrosis. Histological examinations performed at predetermined intervals showed an inflammatory response to the standard and the diluted solution. This reaction was more pronounced when the higher concentration was used. No changes in the alveolar bone were found in either of the groups. Complete healing with scar formation was evident four to six weeks later. The absence of severe reactions after injections of MER should encourage further investigations of this agent in the local treatment of neoplastic processes in the oral cavity.
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PMID:Local reaction to gingival injections of MER/BCG in guinea pigs. 28 60

The combination of vincristine, methyl-CCNU, and methotrexate with or without MER-BCG achieved a 2% complete response (CR) and a 11% partial response (PR) with a median duration of 25-29 weeks in 124 evaluable patients with advanced adenocarcinoma of the colon and rectum. Responses were seen in previously untreated patients and in patients refractory to 5-fluorouracil. The median survival of these objective responders (CR + PR) was 57 weeks. The addition of MER-BCG did not appear to influence response rate or duration of survival and was accompanied by significant toxicity. Response was significantly correlated with performance status, sex, and disease free interval and survival with alkaline phosphatase and performance status. Patients with advanced colorectal carcinoma should be stratified according to these variables.
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PMID:Chemotherapy versus chemoimmunotherapy in advanced adenocarcinoma of the colon and rectum: a prospective randomized study. 36 76

Isografts of two mammary carcinomas, one spontaneously arising in a BALB/cfC3H female infected with MTV and one free of MTV (tumor D7T4S), were removed surgically from Balb/c (MTV free) female hosts, and fragments of each tumor were immediately reimplanted in situ (simulated local recurrence challenge). The animals were then subjected to treatment with the MER fraction of tubercle bacilli, with one of three chemotherapeutic drugs (5-FU, cyclophosphamide, and methotrexate), or with both MER and one of the chemotherapeutic agents (chemoimmunotherapy). The incidence of progressively developing recurrence tumors and the longevity of the animals were determined. The therapeutic effects of treatment with MER alone were ascertained by comparing groups of mice that received the fraction by various schedules with saline-injected control groups; the efficacy of chemoimmunotherapy was assassed by comparing groups that received MER plus one of the drugs with groups subjected to drug intervention by itself. MER administered alone did not reduce the incidence of recurrent tumors but was consistently efficacious in prolonging the lives of animals challenged with the MTV (+) carcinoma, although considerably less so in animals tested with the weakly immunogenic tumor D7T4S. A negative effect by MER on tumor frequency did not occur and was seen only once with regard to host life duration. Combined intervention with MER and 5-FU proved to be significantly and consistently superior to similar treatment with only 5-FU in animals challenged with the MTV(+) carcinoma. No such additive action by MER plus 5-FU was seen in mice challenged with D7T4S, however, nor did the other two chemoimmunotherapeutic regimens differ significantly in therapeutic efficacy from the corresponding chemotherapy alone in most of the trials with both tumors.
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PMID:Chemoimmunotherapy of syngeneic mouse mammary carcinomas employing methanol extraction residue. 79 79

Skin tumour development was studied in groups of mice painted once with 125 mug of 3-methylcholanthrene (MCA) either at 12:00 or at 24:00 MET. Eight animals were kept in each box. The animals were observed weekly for 20 months and all tumours were registered. There was no difference between the two groups of mice as regards tumour induction time or number of papilloma-bearing mice. In the groups of mice treated at 24:00 the number of skin tumours to develop was 9 per cent higher than in groups of mice treated at 12:00. This difference in papilloma yields is not statistically significant. Among female mice painted at 24:00 carcinoma-bearing animals were significantly more numerous (50 per cent) than among those painted at 12:00, whereas there was no difference between the groups of male mice. Considering the groups collectively (males + females), the intergroup difference (17 per cent) in advantage of painting at 24:00 was barely significant (0.5 less than p less than 0.10). There was no difference between the groups as regards the total number of carcinomas to occur. When the tumour yields in individual boxes were found to vary greatly. The slight increase in tumour yield after night painting correlates with the circadian variation in proliferative activity of the epidermidis. Previous reports in the literature have shown similar differences. Further investigations and better methods seem necessary before a definite conclusion can be drawn concerning a possible diurnal variation in the susceptibility of mouse skin to chemical carcinogenesis. It is also emphasized that it is necessary to exercise great caution when the results of classical epidermal chemical carcinogenesis experiments are to be interpreted. It seems necessary to observe animals for at least 15 months before any conclusion can be drawn.
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PMID:Is there a diurnal variation in the susceptibility of mouse skin to the tumorigenic action of methylcholanthrene? A study of tumour yield with special reference to the variation between cages. 98 89

The TEAG rosette test was not devised as an immediate diagnostic indicator, but in order to detect gross differences over a period of time between the lymphocytes of patients with conditions where immune complexes may be formed, and those of normal people. In summary these results indicate that:- 1. Percentage TEAG rosettes were highly significantly increased in patients with SLE, active chronic hepatitis and carcinoma of lung compared with normal controls, when the tests were performed on suspensions, containing over 90% lymphocytes, separated from peripheral blood. 2. Estimates of mean B lymphocytes plus blood monocytes in the separated suspensions, as measured by EAC rosettes (and peroxidase and differential counts for monocytes) are exceeded by TEAG-rosetting cells in the patients tested. 3. Tests on patients with chronic autoimmune conditions (e.g. ACH and SLE) do not show a highly significant difference from normal controls with respect to mean total cells forming E-rosettes. 4. It may be speculated that some TEAG rosettes are formed by T-cells which could have immune complexes or autologous anti-lymphocyte globulin on their surface and that such a condition may account for the depressed T-cell function found in these conditions.
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PMID:Lymphocyte surface-attached immunoglobulins in some clinical conditions. 108 63

Correlation between the expression of growth factor/receptor systems or the alterations of tumor suppressor genes and biological malignancy of gastric cancer was described. Overexpression of many growth factors/receptors, such as EGF, TGF alpha, EGF receptor and ERBB2, and reduction of type I receptor for TGF beta may be linked with new prognostic factors of gastric carcinomas. The expression of cripto, a novel gene of EGF family, shows a tendency to correlate with tumor staging of well differentiated gastric adenocarcinomas. p53 gene abnormalities take place in 60% of gastric carcinomas including early stage carcinoma. Loss of heterozygosity on chromosomes 1q, 7p and 7q is frequently observed in advanced gastric carcinomas of well differentiated type. Molecules which regulate tumor invasion and metastasis such as nm23, tissue inhibitor of metalloproteinase (TIMP) and endogenous galactoside-binding lectin may provide for prognostic factors of gastric cancer.
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PMID:[New prognostic factors in human gastric carcinomas]. 134 86

DNA content, proliferative activity (Ki-67 immuno-staining and S-phase fraction by flow cytometry), and neu-oncogene overexpression were studied in 135 patients with invasive breast carcinoma. Image analysis and flow cytometry of fresh tumors showed good correlation between the two methods and yielded 39% diploid tumors and 61% aneuploid tumors. Aneuploidy, including tetraploidy, was significantly related to the loss of estrogen (p = 0.0002) and progesterone (p = 0.03) receptors, high histologic (p = 0.014) and nuclear (p less than 0.0001) grades, and mitotic rate (p = 0.0001). Immunohistochemical evaluation of proliferation by staining with Ki-67 monoclonal antibody and of neu-oncogene protein overexpression was performed in fresh frozen tissue from 83 tumors. The Ki-67 score, quantitated by the CAS-200 image analyzer, correlated only moderately with S-phase fraction obtained by flow cytometry by linear regression analysis (r = 0.39, p less than 0.001). However, both of these proliferation markers correlated strongly with the mitotic rate (p less than 0.0001). Aneuploid and tetraploid tumors demonstrated higher Ki-67 scores and S-phase fractions than diploid tumors. Neu-oncogene protein overexpression was seen in 24 tumors (29%) overall and was much higher in aneuploid tumors (38%) and tetraploid tumors (50%) than in diploid tumors (7%). However, the concentration of neu-oncogene protein positive tumors in the tetraploid region reported by others was not observed. Neu-oncogene protein overexpression was also associated with higher Ki-67 scores (p = 0.016) and S-phase fractions (p = 0.037).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:DNA ploidy, proliferation, and neu-oncogene protein overexpression in breast carcinoma. 134 24

The mechanism by which HER2/neu overexpressing tumor cells resist NK, LAK, and LDCC cytotoxic lymphocytes was investigated. Resistance was not explained by a delay in kinetics of lysis, concurrent resistance to TNF, or a diminished expression of the transferrin receptor. HLA-class I expression, however, was markedly elevated compared to HER2 nonexpressing targets suggesting a reason for resistance. To test the role of class I, we selectively decreased expression by incubation of targets with beta-2 microglobulin anti-sense oligonucleotides. Anti-sense-treated HER2+ targets, displaying levels of class I comparable to HER2- targets, were still markedly resistant to cytotoxic effectors. Down-regulation of class I expression in HER2- carcinoma cells also had no effect on sensitivity to cytotoxicity by anti-sense treatment of Raji and U937 targets resulted in enhanced sensitivity to NK and LAK effectors but not to T cells mediating LDCC. These data indicate resistance to cytotoxicity in HER2-expressing targets cannot be solely explained by heightened expression of class I. The data also support the concept that class I expression regulates sensitivity to NK and LAK cells (but not LDCC effectors) in selected targets.
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PMID:Effects of beta-2 microglobulin anti-sense oligonucleotides on sensitivity of HER2/neu oncogene-expressing and nonexpressing target cells to lymphocyte-mediated lysis. 134 16

To determine whether the sporadically occurring amplification of the oncogene erbB2/HER2 in gastrointestinal carcinomas is associated with additional changes of this sequence, DNA from 17 colorectal and 5 stomach carcinomas was analyzed for copy number, sequence rearrangement and DNA methylation by Southern blot hybridization. Amplification was detected in two cases. By applying the isochizomers Hpall and Mspl we tested for alterations in the DNA methylation status. Whereas in colon tumors with non-amplified erbB2 this status was unchanged, one case with erbB2 amplification showed additional MspI bands indicating a methylation of the amplified gene sequences. In stomach carcinoma, however, we detected differences between tumor and mucosa samples but not between amplified and non-amplified tumor samples. Independent of the DNA methylation status, significant amounts of the erbB2 oncoprotein were detected in the cases with gene amplification; weaker immunostaining of erbB2 was also seen in a few additional tumors.
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PMID:Tumor-specific methylation patterns of erbB2 (HER2/neu) sequences in gastro-intestinal cancer. 135 39


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