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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diagnostic value was assessed of serum testosterone concentration and compared with that of serum assay of CEA and CA 19-9 in the differential diagnosis of pancreatic cancer (PC) and chronic pancreatitis (CP). Thirty-six patients with PC were compared with thirty-two CP patients. The sensitivity of CA 19-9 (76.9%) in detecting PC was greater than that of testosterone and CEA (30.6% and 30.8%, respectively). The specificity of testosterone and CA 19-9 were comparable (93.7% and 96.4%, respectively). The combination of tests did not enhance the sensitivity and specificity of each test when used alone. The serum CA 19-9 concentration in PC patients was significantly higher then in patients with colon cancer, gastric cancer and benign gastrointestinal diseases.
Pol Arch Med Wewn 1992 Nov
PMID:[Value of plasma testosterone, carcinoembryonic antigen and CA 19-9 in the differential diagnosis of pancreatic carcinoma and chronic pancreatitis]. 130 May 50

Tumor markers known to date are not sensitive and specific enough to detect malignant tumors. Therefore, attempts to find new markers have led to sialic acid assays in cancer patients. Serum sialic acid, CEA and ESR have been determined in 33 patients with the cancer of the colon. All patients have been divided into four groups, according to TNM cancer staging. Serum sialic acid levels have been increased by 100% of patients in groups I and IV. The most significant correlation was noted between sialic acid levels and ESR. No significant relationship between serum sialic acid and CEA have been noted. No correlation of the colon cancer stage, according to TNM staging, and sialic acid and CEA levels in the peripheral blood has been observed. It seems, however, that serum sialic acid assay may be useful auxiliary technique in the detection and monitoring of patients with colon cancer.
Pol Tyg Lek
PMID:[Sialic acid and carcinoembryonic antigen (CEA) as markers of colon cancer: Preliminary report]. 166 62

The study aimed at assessing a degree of low serum cholesterol relationship to carcinoma of the colon. The study involved 137 patients with carcinoma of the colon and 54 patients serving as a control group. Serum cholesterol and total proteins levels were assayed and nutritional status of the patients was analysed. It was found that serum cholesterol was significantly lower in patients with both advanced and mild cancer of the colon in comparison with a control group. Similar tendency was noted in the group of female patients with cancer of the colon but the difference between the patients with not advanced cancer and control group was statistically insignificant. Serum total proteins did not differ in patients with cancer of the colon and control group. In the group of male patients (with both stages of the cancer) in whom low serum cholesterol was noted (below 5.2 mM/L) a risk of cancer was 3-7 times higher. In female patients relative risk of cancer was significantly higher only in the advanced stages of the disease.
Pol Tyg Lek
PMID:[Low serum cholesterol level and the risk of cancer of the colon]. 207 37

In the present paper we analyzed cathepsin D activity in digestive tract cancers. Cathepsin D activity was estimated in 10% homogenates of oesophageal cancer, gastric cancer and colon cancer tissues and in the blood serum and expressed as the amount of liberated tyrosine which was assayed acc. to Folin-Ciocalteau. Mean cathepsin D activities in neoplastic tissues and normal counterparts were as follows: oesophaged cancer (218.5 mM Tyr/1/2 h vs 145.0 mM Tyr/1/2 h), gastric cancer (285.4 mM Tyr/1/2 h vs 142.3 mM Tyr/1/2 h) and colon cancer (233.7 mM Tyr/1/2 h vs 159.5 mM Tyr/1/2 h). In all examined neoplastic tissues cathepsin D activity was almost too-fold higher than in the normal counterparts. Cathepsin D activity in the sera of cancer patients was too a lesser degree higher than in the sera of normal subjects. The data indicate that estimating of cathepsin D activity in the neoplastic tissues homogenates and in the blood serum may be of diagnostic value and may constitute an information which is complementary to the analysis of other tumor markers and histopathologic examination.
Pol Merkur Lekarski 1997 May
PMID:[Activity of cathepsin D in some neoplasms of the gastrointestinal tract]. 937 76

Carcinoid is a slowly developing neuroendocrine tumour. It appears with frequency of 1.5/100,000 persons. Usually it is localized in appendix, small intestine, rectum and bronchi. Clinical sings. of carcinoid syndrome develop in only 10% cases of tumour. We present three cases of carcinoid: the first one with evidences of heart insufficiency, the second one with evidences of colon cancer, the third one coexisting with Graves-Basedow disease.
Pol Merkur Lekarski 1999 Dec
PMID:[Carcinoid: unusual clinical course]. 1071 Sep 52

This study aimed at evaluating diagnostic significance of cancer procoagulant (CP) activity in the homogenates of colon cancer tissues and in blood serum of patients with this neoplasm. Procoagulant activity, depending of specific cancer procoagulant, has been found in all examined tissues as well as in blood serum of cancer patients. CP activity in homogenates of colon cancer tissues as well as in blood serum of the examined cancer patients has been markedly higher than in the normal subjects. These data indicate that CP activity in the neoplastic tissue homogenates and in blood serum may be of value in the diagnosis of cancer.
Pol Merkur Lekarski 2000 Mar
PMID:[Diagnostic significance of cancer procoagulant activity in colorectal cancer]. 1087 Apr 14

Recent reports suggest that the beta-catenin-T-cell factor (Tcf) (BCT) signaling pathway is important in the progression of prostate cancer. Evidence suggests that the androgen receptor (AR) can repress BCT-mediated transcription both in prostate cancer and colon cancer cells (Chesire and Isaacs, 2002). In this study, we validate such findings and show that repression of BCT signaling is facilitated by competition between the AR and Tcf. Measurements of the Tcf transcriptional reporter (TOPFLASH) indicated that AR+DHT-mediated repression can inhibit BCT transcription in the presence of WT and exogenous activating beta-catenin (Delta1-130 bp). Transient transfections in SW480 cells (APC(mut/mut)) showed that this mode of repression is functionally independent of APC-mediated beta-catenin ubiquitination. Using a recently developed red flourescent protein (HcRed), we demonstrate novel observations about the nuclear distribution of Tcf. Furthermore, with the use of red (HcRed-AR and HcRed-Tcf) and green fusion proteins (beta-catenin-EGFP), we provide morphological evidence of a reciprocal balance of nuclear beta-catenin-EGFP (BC-EGFP). By cotransfecting in LNCaP prostate tumor cells and using quantitative imaging software, we demonstrated a 62.0% colocalization of HcRed-AR and BC-EGFP in the presence of DHT and 63.3% colocalization of HcRed-Tcf/BC-EGFP in the absence of DHT. Costaining for activated RNA Pol II (phosphoserine 2) and HcRed-Tcf suggested that Tcf foci contain transcriptional 'hotspots' validating that these sites have the capacity for transcriptional activity. Given this apparent androgen-dependent competition for nuclear BC-EGFP, we chose to assess our hypothesis by in vivo and in vitro binding assays. SW480 cells transiently transfected with an AR expression construct, treated with DHT and immunoprecipitated for Tcf showed less associated beta-catenin when compared to Tcf precipitates from untreated cells. Furthermore, by treating cells with DHT+Casodex, we were able to abrogate the androgen-sensitive AR/beta-catenin interaction, in addition to relieving transcriptional repression of the TOPFLASH reporter. In vitro binding assays, with increasing amounts of AR(S35), resulted in decreased Tcf(S35) association with immunoprecipitated recombinant beta-catenin-HIS. These data suggest that in steady-state conditions, AR has the ability to compete out Tcf binding for beta-catenin. Finally, using SW480 cells, we show that AR-mediated repression of the BCT pathway has implications for cell cycle progression and in vitro growth. Using FACs analysis, we observed a 26.1% increase in accumulation of cells in the G1 phase of the cell cycle, while in vitro growth assays showed a 35% reduction in viable cells transfected with AR+DHT treatment. Together, our data strongly suggest that a reciprocal balance of nuclear beta-catenin facilitates AR-mediated repression of BCT-driven transcription and cell growth.
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PMID:Functional localization and competition between the androgen receptor and T-cell factor for nuclear beta-catenin: a means for inhibition of the Tcf signaling axis. 1294 8

Butyric acid, a short chain fatty-acid derived from bacterial fermentation of complex carbohydrates in the large intestine has been shown to be a growth inhibitory in many colon cancer cell lines. Butyrate induced inhibition of cellular proliferation is considered to result from the induction of P21 gene expression through the activation of this gene transcription. P21 is an inhibitor of cyclin-dependent protein kinases that are required for the cells to enter the DNA synthesis phase. In the present study the kinetics of the changes of the P21 transcription in Caco-2 colon adenocarcinoma cells treated with various concentrations of sodium butyrate was determined using a novel real-time quantitative RT-PCR (TaqMan) technique. Beta-actin mRNA and GAPDH mRNA levels were used as the endogenous references. Colonocytes were incubated with sodium butyrate at concentrations of 5 mM, 10 mM and 20 mM for 3, 6, 12, 24 and 48 h. The results of this study indicated that butyrate strongly induced P21 gene expression as early as 3 h after treatment. Characteristic patterns of time-dependent changes of the target gene expression were observed. The increases in P21 mRNA level were generally more pronounced at higher butyrate concentrations. Because Caco-2 cells are lacking the wild allele of the P53 gene, the present results support the hypothesis that butyrate induces P21 gene expression by P53-independent mechanism.
Acta Pol Pharm
PMID:Quantification of p21 gene expression in Caco-2 cells treated with sodium butyrate using real-time reverse transcription-PCR (RT-PCR) assay. 1367 14

Recent small-scale studies have shown that 30% of human tumors examined to date express DNA polymerase beta variant proteins. One of the DNA polymerase beta colon cancer-associated mutants, K289M, has been shown to synthesize DNA with a lower fidelity than wild-type Pol beta. Thus, the K289M protein could confer a mutator phenotype to the cell, resulting in genomic instability. Another DNA polymerase beta variant identified in colon carcinoma interferes with base excision repair in cells. This may result in unfilled gaps which can serve as substrates for recombination and result in genomic instability. DNA polymerase beta has also been shown to be overexpressed in a variety of tumors. In some cases, overexpression of polymerase beta in cells confers a transformed phenotype to the cells. In other cases, overexpression results in telomere fusions. Thus, mutant forms or aberrant quantities of polymerase beta confer a mutator phenotype to cells. Combined with the small-scale tumor studies, these mechanistic studies implicate variant forms of DNA polymerase beta in the etiology of human cancer.
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PMID:Is there a link between DNA polymerase beta and cancer? 1528 Jun 58

Recent studies have suggested that carcinoembryonic antigen (CEA)-promoter sequences are active only in CEA-positive cells, filing in the criteria for tumor specific targeting of suicide genes. However, the present study on gene therapy of colon cancer and cell-specificity of CEA promoter, provide evidence that CEA-positive and CEA-negative cells transfected with E. coli cytosine deaminase (CD) gene under the control of CEA promotor sequence are sensitive to enzyme/pro-drug therapy with 5-fluorocytosine (5-FC). Individual clones derived from the CEA-negative cell lines: melanoma Hs294T and glioblastoma T98G after transfection with CD differed profoundly in their sensitivity to 5-FC. The IC50 values for several clones of the CEA-negative cells were almost the same as for CEA-positive colon cancer cells. Such 5-FC-sensitive clones derived from the population of CEA-negative cells, present even in small number, because of the very effective bystender effect of this enzyme/pro-drug system can cause severe problems during therapy by efficiently killing surrounding normal cells. Safety is the major issue in gene therapy. Our data suggest that the safety of gene-directed enzyme pro-drug therapy (GDEPT) with CEA promoter driven expression of therapeutic genes is not so obvious as it has originally been claimed.
Acta Biochim Pol 2004
PMID:CEA-negative glioblastoma and melanoma cells are sensitive to cytosine deaminase/5-fluorocytosine therapy directed by the carcinoembryonic antigen promoter. 1544 34


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