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

The purpose of this study was to evaluate the CT characteristics of metastatic pulmonary tumor. The study included 163 cases. Analysis of the distribution of 1265 metastatic nodules observed the conventional and helical CT with 10 mm slice thickness showed that they were distributed mainly below the carina and external peripheral lung field. The relationship between the characteristics of the margins of the metastatic nodules and primary tumors was evaluated in 280 nodules with high-resolution CT(HRCT). The margins were smooth in 88% of thyroid cancers, 85% of hepatocellular carcinomas and 75% of renal cell carcinomas, and irregular in 75% of pharyngolaryngeal cancers, 62% of colon cancers and 58% of breast cancers. HRCT findings were correlated with histology in 23 surgically resected metastatic nodules. The well-defined smooth margin on HRCT histologically corresponded to the expanding type, while the irregular margin corresponded predominantly to the alveolar space-filling type. Among other CT findings calcification was seen in colon cancer and osteosarcoma, and cavitation in pharyngolaryngeal cancer, colon cancer angiosarcoma, pancreatic cancer and endometrial uterine cancer. The author concludes that CT is useful for observing the morphologic features of metastatic pulmonary nodules which seem to reflect the underlying pathologic characteristics and thus contributes to the diagnosis.
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PMID:[CT of metastatic pulmonary tumor: morphology, HRCT and histological correlation]. 901 64

We used a yeast functional assay (functional analysis of separated alleles in yeast: FASAY) to determine the p53 gene status of human cell lines maintained in our laboratory. This assay enables the researcher to score wild-type p53 expression on the basis of the ability of expressed p53 to transactivate the reporter gene HIS 3 via the p53-responsive GAL 1 promoter in Saccharomyces cerevisiae. The cell lines examined were ten hepatoma, two hepatoblastoma, three in vitro immortalized fibroblast, two osteosarcoma, a chondrosarcoma, an ovarian teratocarcinoma and a colon cancer cell line. Out of 20 cell lines, 11 cell lines had mutations in both alleles of the p53 gene, and another 8 cell lines had no mutation in the p53 gene. Thus, 55% of the cell lines examined had mutations in the p53. Interestingly, PA-1 cells had both the normal and the mutant p53 alleles, showing that FASAY is a useful method for detecting the wild-type and mutated p53 genes simultaneously. As for the three liver cell lines harboring HBsAg, there was no relationship between their p53 gene status and the presence of HBsAg. Two cell lines were normal for p53 status, while the other had a mutation of the p53 gene.
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PMID:Yeast functional assay of the p53 gene status in human cell lines maintained in our laboratory. 935 23

The expression of Bfl-1 gene, a novel Bcl-2 related gene, was determined by Northern blot analysis using a radiolabeled cDNA specific for Bfl-1 gene in 82 surgically resected tissue specimens of 28 gastric cancers, 15 colon cancers, nine breast cancers, eight bone and soft tissue sarcomas, five ovarian cancers, nine colon adenomas and eight gastric adenomas. A high rate of expression was observed in gastric and colon cancer, at 86 and 93%, respectively. In breast cancer, bone and soft tissue sarcoma and ovarian cancer, the expression rate was 33, 25 and 40%, respectively. In stomach cancer, the expression rate of Bfl-1 gene in metastatic lymph nodes was 82%, which was higher than 50% of the primary sites (p < 0.02). The intensity of RNA bands of the gastric cancer specimens was compared according to the stage, demonstrating that there was no difference in the expression levels of Bfl-1 gene between the stages in both primary sites and metastatic lymph nodes. Bfl-1 gene was expressed in three (33%) out of nine adenomas of the colon, while it was not detected in all eight gastric adenomas, We also examined the RNA expression of Bfl-1 gene in 22 human cancer cell lines consisting of five stomach cancer, four squamous cell carcinoma, three lung cancer, three cervical cancer, two colon cancer, two brain cancer, two leukemia and one osteosarcoma cell lines. Bfl-1 gene band was detected in one (5%) cervical cancer cell line, SiHa. The results of cancer tissue specimens indicate that Bfl-1 gene may play an important role in carcinogenesis of human cancers and may be involved in a relatively early phase of the adenoma-carcinoma sequence in colon cancer development. However, the mechanism responsible for the very low rate of expression in established cell lines is not clearly understood and further investigation is necessary to clarify the mechanism involved.
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PMID:Expression of a novel Bcl-2 related gene, Bfl-1, in various human cancers and cancer cell lines. 949 79

The physiologically active metabolite of the vitamin D seco-steroid hormone, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is a major regulator of mineral homeostasis. Recent evidence also suggests its role in regulating proliferation and differentiation of cells, including cancer cells. Therapeutic application of 1,25(OH)2D3 to hyperproliferative disease, such as cancer, is thwarted by its hypercalcemic activity. To overcome this problem, analogs of 1,25(OH)2D3 have been produced which retain growth regulating properties and exhibit decreased hypercalcemic activity. In the present study, the efficacy of the vitamin D2 analog, 1,24(S)-dihydroxyvitamin D2 (1,24(S)-(OH)2D2) in the inhibition of cancer cell proliferation and in inducing differentiation of cancer cells was compared to that of 1,25(OH)2D3. By the [3H]-thymidine incorporation procedure, 1,24(S)-(OH)2D2 is as equipotent as 1,25(OH)2D3 in inhibiting the proliferation of five different cell lines, ROS 17/2.8, the rat osteosarcoma cell line, MCF-7, the human breast cancer cell line, HD-11, the chick bone marrow v myc transformed cell line, HT-29, the human colon cancer cell line and HL-60, the human leukemia cell line. The inhibitory action was dose and time-dependent. The NBT reduction method indicated that 1,24(S)-(OH)2D2 induces the differentiation of the human leukemia cell (HL-60) to the same extent as 1,25(OH)2D3. Notwithstanding the vast similarity between 1,24(S)-(OH)2D2 and 1,25(OH)2D3 with regard to the above activities, they differ in their effects on calcium regulation. In conclusion, the present results encourage the use of 1,24(S)-(OH)2D2 for the treatment of cancer disease in vivo.
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PMID:The novel analog 1,24(S)-dihydroxyvitamin D2 is as equipotent as 1,25-dihydroxyvitamin D3 in growth regulation of cancer cell lines. 967 3

A novel mRNA isoform (meprin beta') of the cell-surface protease subunit meprin beta was previously identified in human colon cancer cells. The study reported here revealed that this mRNA isoform was identical within the protein coding region and at the 3' end to the beta isoform of normal intestine but that it contained an extended 5' untranslated region. Meprin beta' mRNA was expressed in the human breast cancer cell lines MCF-7 and SK-BR-3, in the human osteosarcoma cell line U2 Os, and in the human pancreatic cancer cell line BxPC-3. Meprin beta mRNA, but not beta' mRNA, was expressed in human fetal kidney cells. We cloned and sequenced genomic DNA encoding portions of the promoter region of the meprin beta gene. The unique sequences present in the beta' mRNA were present in the human genomic DNA immediately upstream of the transcription start site for the beta mRNA. The human meprin promoter sequence was searched for potential transcription-factor binding sites, and putative activator protein-1, polyoma enhancer activator 3 (PEA3), CCAAT enhancer-binding protein beta, and estrogen-receptor binding sites were identified along with binding sites for the intestine-specific cdx-2 transcription factor. The activity of meprin promoter/luciferase reporter gene constructs transfected into U2 Os cells was highest with constructs containing 83 and 639 bp of promoter DNA. These regions of the promoter each contain a putative PEA3 element. Treatment of the human colon adenocarcinoma cell line HT29-18C1 with 50 or 100 ng/mL phorbol myristal acetate for 8 h increased meprin beta' mRNA levels. Likewise, U2 Os cells transfected with the -639/luciferase or -1800/luciferase constructs showed a phorbol myristal acetate-inducible increase in reporter gene activity, indicating that the PEA3 element within the -639 construct or other elements further upstream respond to phorbol ester.
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PMID:Expression and regulation of the meprin beta gene in human cancer cells. 1041 Nov 43

The transcription factor YB-1 is expressed in a wide range of cell types and has been implicated in the regulation of various genes involved in cell proliferation. Nuclear expression of YB-1 is correlated with MDR-1 gene expression in breast cancer and osteosarcoma. In this study, we asked whether YB-1 expression is enhanced in human colorectral carcinoma and if it is associated with the expression of target genes such as MDR-1, DNA topoisomerase II alpha and PCNA. YB-1, DNA topoisomerase II alpha, PCNA and MDR-1 expression were assessed by Western blotting, Northern blotting and immunohistochemistry in 26 human colorectal carcinomas. The involvement of YB-1 in DNA topoisomerase II alpha gene expression was examined by transient DNA transfection assays. YB-1 was overexpressed in almost all cancerous lesions in comparison with normal mucosa in surgically resected colorectal carcinomas of 26 patients. YB-1 expression correlated well with both DNA topoisomerase II alpha and PCNA expression. In contrast, no correlation was observed between YB-1 and MDR-1 expression. We also found that a transient co-transfection with a DNA topoisomerase II alpha promoter-luciferase plasmid and an antisense YB-1 expression construct resulted in a significant reduction of the promoter activity in KM12C human colon cancer cells. YB-1 may be an excellent proliferation-associated marker and may be a transcription factor regulating DNA topoisomerase II alpha gene expression in human colorectal carcinoma.
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PMID:Enhanced coexpression of YB-1 and DNA topoisomerase II alpha genes in human colorectal carcinomas. 1059 87

The human INK4a gene locus encodes two structurally unrelated tumor suppressor proteins, p16(INK4a) and p14(ARF), which are frequently inactivated in human cancer. Whereas p16(INK4a) acts through engagement of the Rb-cdk4/6-cyclin D pathway, both the pro-apoptotic and cell cycle-regulatory functions of p14(ARF) were shown to be primarily dependent on the presence of functional p53. Recent reports have also implicated p14(ARF) in p53-independent mechanisms of cell cycle regulation and apoptosis induction, respectively. To further explore the pro-apoptotic function of p14(ARF) in relation to functional cellular p53, we constructed a replication-deficient adenoviral vector for overexpression of p14(ARF) (Ad-p14(ARF)). As expected, Ad-p14(ARF) efficiently induced apoptosis in p53/Rb wild-type U-2OS osteosarcoma cells at low multiplicities of infection. Interestingly, Ad-p14(ARF) also induced apoptosis in both p53-deleted SAOS-2 osteosarcoma cells and HCT116 colon cancer cells with a bi-allelic knock-out of p53 (HCT116-p53(-/-)). Similarly, adenovirus-mediated overexpression of p14(ARF) induced apoptosis in p53/Bax-mutated DU145 prostate cancer cells as well as in HCT116 cells devoid of functional Bax (HCT116-Bax(-/-)). Restoration of Bax expression by retroviral gene transfer in DU145 cells did not further enhance p14(ARF)-triggered cell death. Infection with Ad-p14(ARF) induced activation of mitochondrial permeability shift transition, caspase activation and apoptotic DNA fragmentation irrespective of the presence or absence of either Bax or functional cellular p53. Nevertheless, overexpression of the anti-apoptotic Bcl-2 homolog Bcl-x(L) markedly inhibited p14(ARF)-induced apoptosis. This may indicate that p14(ARF) triggers a so far unknown activator of mitochondrial apoptosis which can be inhibited by Bcl-2 but which acts either independently or downstream of Bax. Taken together, this report demonstrates the participation of signaling pathways apart from the p53/Mdm-2 rheostat and Bax in p14(ARF)-mediated apoptosis.
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PMID:Adenovirus-mediated overexpression of p14(ARF) induces p53 and Bax-independent apoptosis. 1208 30

MUC2 is one of the major components of mucins that provide a protective barrier between epithelial surfaces and the gut lumen. We investigated possible alterations of MUC2 gene expression by p53 and p21(Sdi1/Waf1/Cip1) in a human colon cancer cell line, DLD-1, establishing subclones in which a tetracycline-regulatable promoter controls exogenous p53 and p21 expression. MUC2 mRNA more significantly increased in response to p53 than to p21. Unexpectedly, MUC2 expression was also induced in human osteosarcoma cells, U-2OS and Saos-2, by exogenous p53. We next performed a reporter assay to test the direct regulation of MUC2 gene expression by p53. Deletion and mutagenesis of the MUC2 promoter region showed that it contains two sites for transactivation by p53. Furthermore, an electrophoretic mobility shift assay indicated that p53 binds to those elements. We analyzed MUC2 expression in other cell types possessing a functional p53 after exposure to various forms of stress. In MCF7 breast cancer and A427 lung cancer cells, MUC2 expression was increased along with the endogenous p53 level by actinomycin D, UVC, and x-ray, but not in RERF-LC-MS lung cancer cells carrying a mutated p53. These results suggest that p53 directly activates the MUC2 gene in many cell types.
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PMID:Transcriptional activation of the MUC2 gene by p53. 1237 98

We have cloned and characterized the cDNA, expression pattern, and subcellular localization of the human and murine orthologs of the centrosomal colon cancer autoantigen protein (CCCAP). We identified both the transcriptional start site of murine CCCAP (mCCCAP) and its TATA-less promoter within BAC genomic clones of the mCCCAP 5' region. The mCCCAP transcript is ubiquitously present in mouse tissues, but at very low copy number. The 2151 bp open reading frame of mCCCAP encodes an 83 kDa protein that possesses a large C-terminal coiled-coil domain, which is able to homo-oligomerize in the yeast 2-hybrid system. Endogenous mCCCAP localizes to the centrosomes of murine BALB/c 3T3 fibroblasts during both interphase and mitosis. This centrosomal localization was not disrupted by nocodazole-induced depolymerization of the microtubule cytoskeleton, suggesting that mCCCAP is an integral component of the centrosome rather than simply a microtubule-associated protein. We also cloned human CCCAP (hCCCAP). The 2139 bp open reading frame of hCCCAP encodes an 82.5 kDa protein that is 71% identical to mCCCAP at the amino acid level and has the same predicted secondary structure. Ectopically expressed full-length hCCCAP in human U2-osteosarcoma cells also displayed centrosomal localization during interphase and mitosis. This pattern of localization was abolished by truncations of the N- and C-terminus of the protein. We further discovered that the C-terminal portion of hCCCAP is identical to the human colon cancer autoantigen NY-CO-8 (Human Gene Nomenclature symbol SDCCAG8).
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PMID:Identification and characterization of the novel centrosome-associated protein CCCAP. 1255 64

Survival of patients aged 15-24 years, diagnosed with cancer during the period of 1990-1994, is described within Europe. Data on 15101 patients, extracted from the files of the 56 adult cancer registries included in the EUROCARE-3 database, representing 20 European countries, were analysed and compared. Five-year survival for 'all cancers combined' was 75% in males (ranging from 59% in Estonia to 89% in Iceland), and 78% in females (ranging from 59% in Estonia to 89% in Norway). The Northern European countries (except Denmark) and Austria had the highest survival figures, while survival in the Eastern European countries was lower than the European average. Denmark, UK, and the pool of the central European countries, had intermediate survival figures. Haemopoietic tumours were the most common malignancies: 5-year survival was high for Hodgkin's disease (89%), intermediate for non-Hodgkin's lymphoma (68%) and lower for acute lymphoblastic leukaemia (ALL) (47%) and acute myeloblastic leukaemia (AML) (39%). Five-year survival for gonadal germ cell cancers, the second most common malignancy in young adults, was 90%. Five-year survival for the other cancers under consideration was as follows: 89% for skin melanoma, 66% for all Central Nervous System (CNS) tumours, 57% for bone tumours, 58% for osteosarcoma, 42% for Ewing's sarcoma, 57% for soft-tissue sarcomas, 99% for thyroid carcinoma, 82% for uterine cervical carcinoma, and 83% for ovarian carcinoma. For more 'adult-specific tumours', 5-year survival was good for colon (77%) and lung (60%) cancers, and less favourable, compared with adults, for breast cancer (68%). Adolescents (15-19 years) had significantly worse survival than young adults (20-24 years) for all malignancies combined. Survival for Hodgkin's lymphoma, CNS tumours, melanoma and colon cancer showed marked regional variability. Since many of the tumours occurring in young adults are curable, these results should encourage, without delay, efforts to identify obstacles to improving outcome and reducing geographical inequalities in survival for this group of patients.
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PMID:Cancer survival in European adolescents and young adults. 1464 22


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