Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By using DNCB delayed hypersensitivity test, the reaction of spontaneous rosette formation (RSRF) and the reaction of inhibition of leucocytes migration the authors examined 55 female patients with different forms of trophoblastic tumors of the uterus and 15 females following the removal of the mole without any signs of the disease concerned. Forty three patients showed a positive DNCB test, 93 of them were completely cured, a negative test was noted in 12 patients, only a 50% cure being observed. RSRF indicated the increased level of rosette-forming cells from 4,7--28% up to 10,3--73% in a successful treatment and its decrease down to 0--5% in the tumor progression, except 7 patients showing reduced RFC levels after the recovery. The reaction of leucocytes migration inhibition has revealed a considerable depression of leucocytes migration (MI--from 0.35 to 0.78) in 18 of 25 patients with manifestations of an acute tumor process (72%). In 7 cases no inhibition was noted, in 6--the treatment being insignificantly effective or time-consuming. In 21 (47.8%) of 27 patients without any signs of the affection there was no inhibitory effect. Leucocytes of healthy donors failed to respond to the tumor extract in either of 24 cases.
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PMID:[Immunological reactivity study of patients with uterine trophoblastic tumors]. 22 75

Cell factors of nonspecific immunity were estimated in 99 patients with different stages of melanoblastoma by delayed hypersensitivity skin test to tuberculin and DNCB (2,4-dinitrochlorobenzene). The skin test to DNCB is found to correlate with the clinical manifestations of the disease, while the skin test to tuberculin is not related with the degree of tumor spread. It is considered not rational to use the test concerned to define one of the immune cell factors in patients with melanoblastoma during the tumor progression.
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PMID:[Skin reactions of delayed hypersensitivity in melanoblastoma]. 43 14

In 137 patients with different kinds of cancer and different cancer stage, cell-mediated immunity was investigated by DNCB (dinitrochlorobenzene) and tuberculin test. These two skin tests were performed before and after cytostatic drug combination therapy. For a collective of cancer patients we found a positive correlation between skin reactions and prognosis and a negative correlation between skin reactions and cancer stage. After cytostatic drug therapy skin reactions could be significantly stronger. This could be observed in 50% when one test was positive before chemotherapy and in only 20% when both tests were negative before chemotherapy. There existed a significant correlation between an increased reaction after cytostatic drug therapy and objective tumor regression. When skin reactions decreased, tumor progression was seen in all cases. Due to these observations we use skin reactions as a good parameter for therapy results. When delayed cutaneous hypersensitivity impairs 2--3 weeks after chemotherapy, we then change the cytostatic drug combination immediately. We cannot say at this moment, whether an improvement of cytostatic drug therapy can be reached in this way.
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PMID:Tuberculin and dinitrochlorobenzene (DNCB) tests in cancer patients before and after cytostatic drug therapy. 71 20

It is generally accepted that cell mediated immunity is impaired in melanoma patients. Several studies, however, could not confirm this thesis, especially in early malignancy. Therefore, it was the aim of our study to evaluate the results of the DNCB skin tests in melanoma patients of the literature. DNCB sensitization lineally decreased with increasing tumor progression. The difference of the sensitization rates between controls and stage I patients and between melanoma stage I and stage II was significant (p less than 0.001). The difference between stage II patients and stage III melanoma was apparent; statistical analysis, however, could not be done, because the results of three out of six evaluated studies where contradictory. The results confirm the thesis of impaired delayed type immunity in the course of tumor progression and support the therapeutic approaches of immune modulation in tumor patients: BCG vaccination, DNCB sensitization, interferon application.
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PMID:[Decrease in immunoreactivity in melanoma. Analysis of DNCB tests in the literature]. 382 18

There are definite immunologic abnormalities associated with the cancer bearing state which are apparent on both in vitro and in vivo testing. The weight of evidence presented suggests an increasing loss of immunocompetence with increasing disease stage and a degree of positive correlation of immunologic responsiveness with prognosis. Unfortunately the correlation is not absolute for any one individual, although it is often fairly well defined for a large group of patients. This is a failure of all other prognostic studies as well. The critical question as to whether or not this loss of immune integrity reported represents a cause or a result of cancer progression remains largely unanswered. The data suggests that the measured impairment of immunologic responsiveness stems from conditions brought about by the tumor bearing state. Regardless of which precedes the other, the cancer or the immunoincompetence, the additional question as to the effect of immune impairment on the disease progression also remains uncertain. Results of tests to monitor immunocompetence appear to be of some value if used as additional data on which to base prognostic conclusions. Dinitrochlorobenzene skin testing is an assay that is easily performed and probably yields the most easily obtained significant prognostic information.
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PMID:Assays of immunocompetence in the staging and prognosis of cancer. 702 61

Serial magnetic resonance imaging (MRI) was used to evaluate the influences of dietary deoxycholic acid (DCA) on the rate of progression of chemically induced hepatocellular neoplasms in rats. Male Fischer-344 rats with established persistent hepatocellular nodules generated by the Solt-Farber protocol were exposed to dietary DCA (0.3%) between 6 and 12 mo of age. Growth of nodules and carcinomas in vivo was measured by morphometric quantification of tumor images obtained every 6 wk. The final stages of neoplastic progression were determined by terminal histopathological examination and by expression and functional evaluation of glutathione S-transferase (GST) isoenzyme phenotypes. Dietary DCA increased the number of hepatocellular neoplasms per rat, accelerated the rate of growth of persistent nodules, and increased the histological progression of liver tumors. Expression of immunoreactive GST subunits Yf, Ya, and Yb1 was induced in early persistent nodules, a pattern that was maintained throughout the study in both basal diet and DCA-fed groups. However, 5% of early nodules and about 75% of advanced neoplasms were partially or completely deficient in GST Yb2 expression in both groups. DCA did not alter the cytosolic activity for the GST substrates 1-chloro-2,4-dinitrobenzene (CDNB) or trans-4-phenyl-3-buten-2-one (tPBO) in tumors or surrounding liver. However, in both groups, CDNB activity was increased in the tumors relative to the surrounding nonneoplastic tissue, whereas activity for tPBO, a substrate more specific for the Yb2 subunit, was reduced in the tumors. All advanced neoplasms were similarly more resistant than surrounding liver to DNA-binding metabolites of aflatoxin B1 or benzo[a]pyrene. These data demonstrate that DCA can increase the progression of established hepatocellular nodules to larger, more advanced neoplasms but does not preferentially select for a specific GST phenotype. Preferential loss of constitutively expressed GST Yb2 in both basal diet and DCA-fed groups may be an important aspect of progression from resistant nodules to advanced cancers in this model. These studies also demonstrate that serial MRI is a useful tool for measuring the rates of enlargement and patterns of growth in established hepatocellular neoplasms.
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PMID:Influences of dietary deoxycholic acid on progression of hepatocellular neoplasms and expression of glutathione S-transferases in rats. 773 75

We followed the expression of several glutathione S-transferase subunits in altered foci, liver neoplasms and metastases produced in male Fischer 344 rats by a modified Solt-Farber protocol, to determine whether components of the resistant phenotype are lost during neoplastic progression. At 6 mo after initiation, altered foci and persistent nodules displayed increased immunohistochemical expression of glutathione S-transferase subunits Yf (pi-class), Ya (alpha-class) and Yb1 (mu-class) in comparison with normal or surrounding liver tissue. However, although most altered foci exhibited little change in glutathione S-transferase Yb2 (mu-class) subunit expression, 5% of Yf-positive foci and nodules were partially or completely deficient in Yb2 expression. At 12 and 18 mo after initiation, most grossly visible hepatocellular tumors retained induced expression of glutathione S-transferase subunits Yf, Ya and Yb1, but 63% of the carcinomas, 88% of the primary metastatic carcinomas and 94% of the pulmonary metastases were deficient in Yb2 expression. These differences in glutathione S-transferase subunit expression were confirmed by quantitative analysis by reverse-phase HPLC of S-hexylglutathione affinity-purified glutathione S-transferases from advanced tumors. Cytosolic glutathione S-transferase activity for trans-4-phenyl-3-buten-2-one in advanced tumors ranged from 42% to 66% of the activity in matched surrounding liver, whereas glutathione S-transferase activities for 1-chloro-2,4-dinitrobenzene were increased by 140% to 161%. These studies demonstrate that progression of hepatocellular carcinomas in the resistant hepatocyte model of carcinogenesis in which several glutathione S-transferase subunits are induced is associated with the loss of a major constitutive mu-class hepatic glutathione S-transferase. Although the mechanism and role of the reduction or loss of glutathione S-transferase Yb2 during malignant progression are unknown, we propose that loss of glutathione S-transferase Yb2 in some preneoplastic populations of hepatocytes might be conducive to further DNA damage by presently unknown environmental or endogenous compounds that are normally detoxified preferentially by glutathione S-transferase isoenzymes containing this subunit.
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PMID:Reduced expression of glutathione S-transferase Yb2 during progression of chemically induced hepatocellular carcinomas in Fischer 344 rats. 802 Aug 84

The potential to metabolize endogenous and exogenous substances may influence breast cancer development and tumor growth. Therefore we investigated GST activity and the protein expression of glutathione S-transferases (GSTs) isoenzymes known to be involved in the metabolism of endogenous and exogenous carcinogens in breast cancer tissue to obtain new information on their possible role in tumor progression. The interindividual variation in the conjugation of 1-chloro-2,4-dinitrobenzene (CDNB) and of 1,2-epoxy-3-(p-nitrophenoxy) propane (EPNP) with glutathione (GSH) by cytosolic glutathione S-transferases (GSTs) were investigated in human breast matched normal and tumor samples. The GSTA, GSTM, GSTP and GSTT isoenzymes from the crude extracts of matched breast normal and tumor tissues in terms of their immunological properties using western blotting were compared. In most of the samples, the GST activities were higher in the tumor than in the normal cytosolic fractions against both CDNB and EPNP. In the western blotting analysis, it was proved statistically that in normal and tumor epithelial cells, there was difference between GST pi and theta isoenzymes expressions (p0.05). In normal epithelium there was a stronger GST theta expression than in invasive tumor tissues (p=0.013). However, the stronger GST pi expression was observed in tumor epithelium than in normal epithelium in human breast cancers (p=0.000). We found the GSTP protein level and GST activities were higher in the breast tumor than in the normal cytosolic fractions against both CDNB and EPNP, thus implicating a certain biological importance.
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PMID:GST isoenzymes in matched normal and neoplastic breast tissue. 2152 Sep 86