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)

Three squamous cell carcinoma cell lines, YES-1, YES-2, and YES-3, were established from human esophageal carcinoma. Two cell lines, YES-1 and YES-2, were established from the surgically removed tumor and YES-3 was established from pleural effusion of the pleuritis carcinomatosa by esophageal carcinoma. These three cells not only resembled the original esophageal carcinoma tissue on microscopic examination, but also produced same tumor marker, such as SCC antigen, CEA, TPA, CA125 and CA19-9. However, the secretion patterns of tumor markers were different. The doubling times of YES-1 cells, YES-2 cells and YES-3 cells were 35.2 hours, 22.9 hours, and 61.0 hours, respectively. Chromosomal studies show that chromosomal number of YES-1 cells ranges 47 to 54 with a mode of 51, that of YES-2 cells ranges 53 to 62 with a mode of 60 and that of YES-3 cells ranges 48 to 52 with a mode of 50. These three cells grow both in serum-containing medium and in serum free medium. When YES-1, YES-2, and YES-3 cells were injected into athymic nude mice subcutaneously, they introduced tumors which resembled the original esophageal carcinoma tissue histologically. These 3 cell lines may provide useful models for the study of human esophageal carcinoma.
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PMID:[Establishment and characterization of human esophageal carcinoma cell lines--especially the role of the serum-free culture]. 177 Sep 30

The usefulness of tumor-associated trypsin inhibitor (TATI) in the diagnosis of various solid tumors was compared to other tumor markers occurring in serum and urine (CEA, CA19-9, CA125, CA72-4, CA50, CA15-3, CA72-4, NSE, TPA, AFP, CK-BB and ferritin). TATI was particularly well suited for the diagnosis of tumors of the pancreas, ovary, oesophagus and bladder. For tumors of these organs TATI may be considered the marker of choice. TATI was also a good marker for distinguishing between disease with or without liver metastasis in cancer of the colon and the breast.
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PMID:Evaluation of TATI and other markers in solid tumors. 178 Jun 86

Esophageal carcinoma has a catastrophic clinical course with a very low 5 year survival rate of 5%. A circulating tumor marker with good specificity and sensitivity would be useful in the management strategy of the disease. So far, no tumor marker effective in esophageal carcinoma has been identified. Preliminary reports suggest satisfactory positivity rates of tumor-associated trypsin inhibitor (TATI) in esophageal carcinoma. We measured TATI levels in 71 patients with primary squamous cell esophageal carcinoma as well as in 30 tissue samples from both carcinoma and normal esophageal mucosa. Detectable TATI levels were not found in tumor tissue samples. The marker showed significantly higher serum levels in patients than in controls, with an overall positivity rate of 28%. TATI levels were significantly lower in patients with a high number of tumor-positive lymph nodes. No relationship was found between TATI and several other clinical and pathological parameters. High TATI levels correlated with a lower probability of overall survival as well as in cases without clinical evidence of lymph node metastases. TATI did not show any relationship with CEA, TPA, ferritin or SCC. The results of the present study suggest that TATI shows a satisfactory positivity rate in esophageal carcinoma, and TATI levels are related to local disease spread and prognosis.
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PMID:Tumor-associated trypsin inhibitor (TATI) in primary esophageal carcinoma. 178 Jun 88

To evaluate the usefulness of tumor-associated trypsin inhibitor (TATI) as a marker for the diagnosis of lung cancer we determined serum levels of this peptide in 255 patients with lung cancer and in 74 patients with chronic obstructive lung disease. A reference population consisting of 151 healthy volunteers was also studied. TATI concentrations were measured by radioimmunoassay. As a cut-off point we used the 99th percentile of the TATI concentrations in a reference population, which was 32 micrograms/l. TATI does not appear to be a good tumor marker in lung cancer. Its sensitivity is poor in comparison with CEA and TPA. The correlation between TATI levels and stage of the disease and histological type was weak.
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PMID:Tumor-associated trypsin inhibitor (TATI) in the diagnosis of lung cancer. 178 Jun 95

Basic and clinical research has led to a better understanding of bladder tumor disease. Better characterization of host and tumor has made it possible for the clinician to choose appropriate treatment and follow-up and to better predict prognosis. Therefore, at tumor presentation a number of variables should be determined to reach the goal. Tumor factors: T-category, grade, size, number and appearance of the primary tumors, time to first recurrence and for invasive tumors also N- and M-categories, small vessel invasion, recurrence pattern, papillary stalk or true lamina propria invasion, the presence of secondary carcinoma in situ, ureteric obstruction and response to specific treatment. Host factors: Immune status, age, performance status, sex, pretreatment length of history and hemoglobin. However, in the individual patient bladder tumor disease may not always follow the predicted course, so that we are still in need of more accurate biological predictors. A number of markers (cytogenetic and cytomorphometric characteristics, such as flow-cytometry, immunohistochemical markers such as ABH expression, T-antigen, CEA, TPA and cytokeratins, and finally ultrastructural changes, proliferative indices and morphometric analysis) have been evaluated. Some have been shown to be of clinical value, but have as yet not been included into routine clinical use. Thus, we are steadily approaching the goal to disclose the true biological potential of each individual tumor and its relation to the host.
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PMID:Prognostic factors in bladder carcinoma. 178 99

A Chinese herb, wikstroemia Chamaedaphen (WC) extract, recently has been shown to be a potential tumor promoting agent on uterine cervical carcinoma induced by HSV-2 or MCA in mice. To determine whether the tumor promoting effects of WC extract were mediated through inhibition of gap junctional intercellular communication (GJIC) with relation to cellular growth, experiments were conducted on Chinese hamster V79 cells and rat WB liver cells by utilization of SLDT method for GJIC detection and cell growth curve examination, 3H-TdR incorporation, mitotic index (MI) and Flow Cytometry (FCM) methods. TPA was used for comparative purpose. WC extract inhibited GJIC and stimulated cell growth in a dose (2-200 micrograms/ml) and time (0-72 hr)-dependent manner in both cell lines. Both WC extract and TPA treatments increased V79 cell growth rate. The average cell doubling-time was decreased from 36.5 hr in control V79 cells to 28.2 hr in WC extract (10 micrograms/ml) and 20.9 hr in TPA (50 ng/ml) treatment by the 3rd day. Stimulating effect of both drugs on DNA synthesis of V79 cells was demonstrated. The results of FCM and MI indicated that the cell number of M-phase cells was increased after drug treatment. It is suggested that (1) tumor promoting effect of WC extract might be mediated through inhibition of GJIC: (2) inhibition of GJIC is closely correlated with increased cell growth rate and entry of cell division cycle.
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PMID:[Effects of tumor promoting herb Wikstroemia chamaedaphne extract on V79 cells and WB liver cells: I. Correlation between cellular growth and gap junctional intercellular communication]. 179 15

The gene structures of rat cathepsins H and L have been determined. Cathepsin H gene spans more than 21.5 Kbp and comprises more than 12 exons. On the other hand, cathepsin L gene spans 8.5 Kbp and comprises 8 exons. In both genes, two intron insertion positions are conserved at the amino acid level. Both enzymes, therefore, diverged from a common ancestral gene. In the 5'-upstream region of the cathepsin L gene, no TATA box, one CAAT box and some SP-1 binding sites exist, common with other lysosomal enzyme genes. Furthermore, two AP-2 binding sites exist: a promoter under the control by the tumor promoter (TPA) and cAMP, and a cAMP response element (CRE). These results suggest that the cathepsin L gene expression is controlled by these factors.
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PMID:Gene structures of rat cathepsins H and L. 180 20

c-jun is a protooncogene associated with neoplastic transformation and is transcriptionally induced by ionizing radiation. To examine the possible mechanisms of radiation-induced c-jun transcription, we analyzed RNA from human tumor cell lines RIT-3 and STSAR-5 following x-irradiation in the presence of protein kinase inhibitors, or the absence of serum and calcium. Protooncogene c-jun expression increased several fold following irradiation of these radiation-induced human sarcoma cell lines. The expression of c-jun was not altered following irradiation in conditioned medium containing serum as compared to that of cells in serum free medium. Depletion of PKC by prolonged TPA treatment resulted in inhibition of c-jun expression. In addition, nonspecific protein kinase inhibitors, staurosporin and H7 attenuated c-jun expression, whereas the analogue of ATP (sangivamycin) did not. Furthermore, the selective inhibitor of cAMP dependent protein kinase HA 1004 did not alter radiation-mediated c-jun induction. These data indicate that ionizing radiation exposure results in c-jun induction which is dependent upon the activation of PKC. Protein kinase C activation and the subsequent expression of the protooncogene c-jun by ionizing radiation may further define the molecular mechanisms of radiation-induced neoplastic transformation.
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PMID:Mechanisms of X-ray-mediated protooncogene c-jun expression in radiation-induced human sarcoma cell lines. 180 83

An antioxidative fraction was extracted from green tea and the major compounds in the fraction identified as epicatechins. Experimental results showed that green tea epicatechin compounds (GTEC) inhibited the mutagenicity and/or chromosomal damage caused by different carcinogens in both bacterial and mammalian cells. In vitro, GTEC inhibited transformation of BALB/3T3 cells induced by BP, X-rays, or MCA/TPA. In vivo, green tea extract decreased the incidence of carcinoma in the forestomach and esophagus of mice induced by sarcosine and NaNO2. GTEC inhibited the development of gamma-glutamyl transpeptidase-positive foci in the livers of rats treated with diethyl nitrosamine (DEN) or DEN/phenobarbital. Our investigations indicate that the antimutagenic and anticarcinogenic mechanisms of GTBC are related to the following: increased glutathione-S-transferase activity; inhibition of edema, hyperplasia, and ODC activity induced by TPA; free radical scavenging; blocked tumor promoter-induced inhibition of intercellular communication; and enhanced cell-mediated immunity. GTEC might be useful in the prevention of some kinds of cancer and a variety of oxidation-related diseases.
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PMID:Progress in studies on the antimutagenicity and anticarcinogenicity of green tea epicatechins. 181 62

Papillomas induced by DMBA initiation-TPA promotion protocols are necessary precursor lesions of squamous cell carcinomas. The papillomas are heterogeneous in their potential for progression to carcinomas, a property apparently induced at the time of initiation. The probability of conversion to malignancy is highest for the papillomas most easily promoted, by either the first few TPA treatments or by "weak" promoters such as mezerein or chrysarobin. The conversion frequency is lowest for TPA-dependent papillomas and those papillomas which appear late in a TPA promotion protocol. The spontaneous rate of malignant conversion is not altered by continued TPA treatment; TPA promotion may simply expand clones of initiated cells which are already programmed with a given probability of conversion. Treatment of papilloma-bearing mice with a genotoxic agent, such as 4-NQO, urethane or cisplatin, increases the rate of malignant conversion. The properties of active converting agents differ markedly from those of the phorbol ester promoting agents, suggesting differences in the mechanisms of action of these two classes of compounds. A genetic mechanism appears likely to explain conversion. The differences between the two stages are further emphasized by the finding that inhibitors of tumor promotion are not inhibitory when given during malignant conversion. The converting agent urethane also affects the subsequent discrete stage in tumor progression, tumor metastasis. Differences in metastatic potential have been found between carcinomas which progress spontaneously after TPA promotion and carcinomas induced in TPA-promoted papillomas by urethane. The multistage nature of experimental epidermal carcinogenesis is well established. The mouse skin model will continue to be valuable for mechanistic studies since similar stages have been described in other tissues as well as in man.
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PMID:Malignant conversion, the first stage in progression, is distinct from phorbol ester promotion in mouse skin. 181 91


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