Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the effects of glucose on the development of cell heterogeneity and the occurrence of necrotic areas in the center of tumor spheroids, a procedure (combining microdissection of small tissue samples from frozen-dried cryosections and microchemical analysis) was developed to measure glucose in distinct, concentrically arranged, microregions of tumor spheroids: the outermost area of proliferating cells, the area of nonproliferating cells and 2 central "necrotic" areas, with either abundant or little intercellular space. Since glucose levels, for analytical reasons, had to be expressed on a dry weight basis, and because of the morphological heterogeneity of the microregions of tumor spheroids, it was necessary to measure and take into account the regional differences in cell density (water content), in order to obtain adequate estimates of the glucose levels in the various microregions. At glucose concentrations of 5.5 and 3.6 mM in the culture medium, the glucose levels varied between 3.5 and 1.4 mmoles/kg wet weight and were lowest in those central areas where the cell density was lowest. Histochemical demonstration of the distribution of lactate and succinate dehydrogenase activity indicates a considerably higher capacity of tumor cells for anaerobic than for aerobic energy production.
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PMID:Glucose levels and succinate and lactate dehydrogenase activity in EMT6/Ro tumor spheroids. 777 14

In order to study the mechanism of the effects of M phi on tumor cells, enzyme cytochemistry and morphometry were used to investigate the activities of cytochrome oxidase (CO), succinate dehydrogenase (SD), lactate dehydrogenase (LDH) and acid phosphatase (ACP) in A549 pulmonary alveolar cell carcinoma cells which had been interacted with normal and CP-activated macrophages respectively. It was found that when E/T = 10:1, the enzyme activity of the cancer cell mitochondria, CO, SD, LDH were decreased, and when E/T = 20:1, the activity of the lysosomal enzyme ACP was increased. These results indicate that when the E/T ratio was appropriate, activated M phi may injure the mitochondria and lysosomes and affect the aerobic respiration and oxidative phosphorylation of cancer cells. This may be one of the cytostatic and cytotoxic mechanisms of activated M phi on tumor cells.
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PMID:[Enzyme cytochemistry and morphometric study of the effects of macrophages on A549 pulmonary alveolar cell carcinoma cell line]. 780 50

Mouse renal cell tumors (RCTs) were induced in male CBA mice by 5 subcutaneous injections of 8 mg 1,2-dimethylhydrazine (DMH)/kg body weight once a week. After a lag period of 2 yr kidneys were removed, and serial cryostat sections of the kidneys were histochemically analyzed for the following parameters: glycogen content, basophilia, and the activities of glycogen synthase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), glucose-6-phosphate dehydrogenase (G6PDH), hexokinase (HK), pyruvate kinase (PK), lactate dehydrogenase (LDH), malic enzyme (ME), succinate dehydrogenase (SDH), alkaline phosphatase (ALPase) and gamma-glutamyltranspeptidase (GGT). RCTs displayed the same histochemical profile irrespective of their size and growth pattern. In comparison with the normal kidney epithelium, the neoplastic cells exhibited elevated activities of enzymes for glycolysis (HK, PK, LDH) and the pentose phosphate pathway (G6PDH), while negative G6Pase and low SDH activity were observed in these cells. The majority of RCTs showed high PHO activity and weak staining for SYN. Activities of ALPase and GGT were negative in most of the RCTs. Markedly enlarged cells with atypical nuclei were detected in some advanced RCTs. Higher activities of glycolytic and mitochondrial enzymes and G6PDH were found in these enlarged cells than in other tumor cells. Tubular preneoplastic lesions were similar to neoplastic lesions in morphological and histochemical characteristics. The present study revealed that a markedly elevated capacity for glycolysis and the pentose phosphate pathway occurred in RCTs in mice. A similar histochemical pattern in the few preneoplastic tubular lesions observed suggests that these metabolic aberrations emerge early during carcinogenesis, but additional studies on early stages of renal carcinogenesis are needed to substantiate this assumption.
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PMID:Enzymic pattern of preneoplastic and neoplastic lesions induced in the kidney of CBA mice by 1,2-dimethylhydrazine. 781 30

Cellular DNA content and succinate dehydrogenase activity of 92 human head and neck (34 laryngeal, 24 pharyngeal, 21 oral cavity, 13 maxillary) squamous cell carcinomas were examined, and DNA ploidy status and chemosensitivity were analyzed and compared. DNA aneuploidy was observed in 54 tumors (58.7%). The aneuploid pattern was most common in tumors of the maxillary sinus (84%), and least common in tumors of the larynx (41.3%). Histologically, aneuploidy was detected in 71.4% of poorly-differentiated, 63.8% of moderately-differentiated and 37.5% of well-differentiated squamous cell carcinomas. There was a statistically significant difference between the survival rates of patients with diploid and aneuploid patterns. Chemosensitivity was determined by exposing fresh tumor material to five antitumor drugs: adriamycin (ADM), cisplatin (CDDP), carboquone (CQ), 5-fluorouracil (5-FU) and mitomycin C (MMC). The average decrease in succinate dehydrogenase (SD) activity was 49.8% with ADM, 33.6% with CDDP, 39.9% with CQ, 68.4% with 5-FU and 45.5% with MMC. Histologically, poorly-differentiated squamous cell carcinomas were most sensitive to these five antitumor drugs. We also compared average SD activity in tumors from different organs and found that pharyngeal tumors tend to be most sensitive to these drugs, except for MMC. The chemosensitivity of a tumor with DNA diploidy tended to be higher among well- and moderately-differentiated squamous cell carcinomas. In contrast, tumors with DNA aneuploidy tended to have higher chemosensitivity in the poorly-differentiated type. The results of this study indicate that simultaneous analysis of DNA ploidy and chemosensitivity will be helpful in understanding the characteristics of tumors as well as in predicting the most effective chemotherapy agents for head and neck cancer patients.
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PMID:[Flow cytometric DNA analysis and chemosensitivity in squamous cell carcinoma of the head and neck]. 786 Dec 97

In 58 human gastric cancers, the expression of P-glycoprotein (P-gp) was evaluated immunohistochemically and chemosensitivity was determined using the in vitro succinate dehydrogenase inhibition (SDI) test. Tumors which contained over 75% stained cells were scored as positive, and 14 of 58 cases (24%) were positive. There was no significant correlation between P-gp expression and clinicopathologic features. The succinate dehydrogenase (SD) activity for each drug of P-gp positive and negative tumors was as follows: 81.8 +/- 15.2% vs. 66.3 +/- 16.1% for Adriamycin (ADM), 75.5 +/- 14.2% vs. 59.1 +/- 17.6% for aclacinomycin A (ACR), 71.7 +/- 15.0% vs. 61.1 +/- 14.0% for mitomycin C (MMC), and 57.5 +/- 18.4% vs. 47.0 +/- 16.7% for cisplatin (CDDP). The increase in SD activity was evident in P-gp positive tumors compared with negative ones in cases of ADM (P = 0.0044), ACR (P = 0.0105), and MMC (P = 0.0353). We suggested that P-gp expression is closely related to chemosensitivities of human gastric cancers to anthracyclines.
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PMID:Expression of P-glycoprotein influences resistance against anthracyclines in clinical gastric carcinomas. 791 78

Lactobacillus casei, which shows antitumoral activity mediated by the stimulation of cellular defence mechanisms, and its peptidoglycan were tested for their ability to inhibit in vitro the viability of various murine (Yac-1, P815, Ehrlich ascites tumor, mammary carcinoma) and human (K562, KB) tumor cell lines through primary cytotoxic activity. Treatment of these tumor line with L. casei or its peptidoglycan at different doses and for different times demonstrated a decrease in viability by 25-30%. This cytotoxic activity was revealed by 51Cr release, succinate dehydrogenase (SDH) activity, ATP assays and morphological alterations in the treated tumor cells. Immunoenzymatic assays (ELISA) showed a precise ratio of binding between Ehrlich ascites or YAC-1 cell membranes and peptidoglycan. This binding is discussed with regard to the structure of the peptidoglycan molecule. The results suggest that L. casei and its derivative peptidoglycan have both a stimulating activity in normal cells and an inhibiting activity in tumor cells, as has been found for other immunomodulatory complexes.
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PMID:Non-immunologically-mediated cytotoxicity of Lactobacillus casei and its derivative peptidoglycan against tumor cell lines. 792 9

Glutathione-S-transferase (GST) in one of several factors that are proposed to affect tumor sensitivity to anticancer drugs, including cisplatin (CDDP). Attempts are made herein to evaluate the significance of the enzymes in resistance to CDDP in clinical samples of gastric cancer. A total of 22 gastric cancer specimens, 16 of which were obtained with matching normal mucosae, underwent immunoblotting with polyclonal antibodies against GST-alpha and GST-pi. At the same time, the chemosensitivity of 15 gastric cancer specimens to CDDP was evaluated by the succinic dehydrogenase inhibition (SDI) test. The expression of GST-pi was detected in all the specimens, and its content in the neoplasms exhibited a significant positive correlation with that in the matched normal mucosae. The expression of GST-alpha was detected in 18 of 22 cancer specimens (82%), but its content in the neoplasms did not correlate with that in the matched mucosae. A comparison of the drug-sensitivity findings with the results of immunoblotting revealed a weak but interesting correlation between the protein levels of GST-alpha and CDDP resistance. The cellular content of GST-alpha correlated weakly with CDDP resistance in gastric cancer, and its quantification could contribute to prediction of the clinical effects of CDDP in patients with gastric cancer.
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PMID:Expression of glutathione-S-transferases alpha and pi in gastric cancer: a correlation with cisplatin resistance. 800 52

In an analysis of nitric oxide (.NO) production and toxicity, chicken macrophage-generated .NO inhibited mitochondrial activity in both .NO-producing macrophages themselves and lymphoid tumor targets. However, differences in targeting of mitochondrial toxicity were observed among these cells. Two chicken macrophage cell lines, HD11 and MQ-NCSU, produced .NO (measured as nitrite) dependent upon concentrations of L-arginine and bacterial endotoxin (lipopolysaccharide). Mitochondrial activity was negatively correlated with the amount of .NO produced. Using a modified MTT assay, .NO induced suppression in two mitochondrial complexes. Mitochondrial activity was significantly suppressed among HD11 cells receiving LPS alone (complex I, 63.0 +/- 5.5% suppression; complex II, 27.9 +/- 5.2%). In contrast, mitochondrial activities in samples receiving LPS plus inhibitor, NG-nitro-L-arginine methyl ester (NAME; 5 mM) or 2,4-diamino-6-hydroxypyrimidine (DAHP; 5 mM), were not significantly different from control values. When HD11 macrophages were cocultured with lymphoblastoid tumor targets, RECC-CU60 (T cell) or LSCC-RP9 (B cell), adding LPS (1 microgram/ml), tumor cell mitochondrial activity was significantly suppressed. In the generator macrophages, complex I was more suppressed than complex II, whereas in lymphoid targets no such difference was observed. These results indicate that .NO inhibits complex I and II mitochondrial activity but that differential targeting can occur among chicken leukocyte populations.
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PMID:Nitric oxide (.NO)-induced mitochondrial injury among chicken .NO-generating and target leukocytes. 802 70

Metallothioneins (MTs) are small cysteine-rich, metal-binding proteins involved in resistance to heavy-metal toxicity, and are known to bind cisplatin. Several experiments suggest possible involvement of MT in cellular resistance to cisplatin. To investigate the relationship between MT expression and cisplatin resistance in urinary tract transitional cell carcinoma (TCC), immunohistochemical staining for MT was performed in 31 untreated TCCs of the urinary tract. The results were compared with the sensitivity of the tumors to cisplatin as assessed by the microtiter succinate dehydrogenase inhibition (mSDI) test. Variable MT expression was observed in all 31 TCCs, but there was no specific correlation between histopathological parameters and MT expression. Fourteen (87.5%) of the 16 TCCs with less than 10% of their tumor cells positive for MT were sensitive to cisplatin. On the other hand, 6 (75.0%) of the 8 TCCs with MT expression by more than 30% of their tumor cells were resistant to cisplatin, and there was a significant correlation between MT expression and cisplatin resistance (p < 0.01). These results suggest the possible involvement of MT in the intrinsic cisplatin resistance of urinary tract TCC and that immunohistochemical investigation of MT may be useful for predicting the response of these tumors to cisplatin therapy.
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PMID:Metallothionein expression is correlated with cisplatin resistance in transitional cell carcinoma of the urinary tract. 807 17

A particulate fraction consisting of heavy organelles such as nuclei and mitochondria was prepared from Ehrlich ascites tumor cells. From this fraction we have purified a GTP-binding protein with a molecular mass of 33 kDa (MTG33) by guanidine hydrochloride extraction followed by four steps of column chromatography. The Kd value of MTG33 for GTP was 17 nM. [alpha-32P]GTP-binding to MTG33 was inhibited by GTP and GDP, but not appreciably by ATP, CTP, UTP, or GMP. MTG33 hydrolyzed GTP to GDP at a rate of 4.5 mmol/min/mol protein. Subcellular fractionation analysis of mouse liver revealed that the heavy mitochondrial fraction contained the highest level of MTG33. Furthermore, dual immunofluorescence examination indicated that the staining of NIH 3T3 cells with anti-MTG33 antibody is coincident with the distribution of mitochondrial succinate dehydrogenase. Of the mouse organs examined, the heart contained the highest level of MTG33. These results strongly suggest that MTG33 is a GTP-binding protein located in mitochondria.
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PMID:Purification of a GTP-binding protein localized in mitochondria. 811 21


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