Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basic evaluation of SPan-1 assay (SPan-1 RIA. BEAD) and clinical significance of serum SPan-1 levels for the diagnosis of pancreatic cancer were studied. This assay was reproducible, reliable and simple to perform. It required minimal samples (duplicate 50 microliters) and may be done within 4 hrs. Normal subjects (N = 1182) had serum SPan-1 antigen levels which ranged 0 to 42.8 units/ml with a mean of 7.5 units/ml and above 40 units/ml was considered to be positive. SPan-1 antigen levels in cultured medium of four out of five pancreatic cancer cell lines showed more than 1000 units/ml by this assay. While over 90% of pancreatic cancer patients had elevated levels of serum SPan-1 antigen, only 0-17% of patients with other malignant and non malignant gastrointestinal diseases such as pancreatitis (chronic or acute), gastric cancer or colon cancer had above normal levels. Furthermore, levels of serum SPan-1 antigen correlated well with treatment and recurrence of disease in patients with pancreatic and gastric cancer. These results suggest that determination of serum SPan-1 antigen levels by this assay kit is useful for the diagnosis and monitoring of pancreatic cancer.
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PMID:[Basic and clinical evaluation of measurement of pancreatic cancer associated antigen, SPan-1]. 232 7

Anticarcinoembryonic antigen (CEA) antisera which showed no reactions with normal adult feces were prepared in guinea pigs. Using these, levels of CEA in feces from patients with colorectal carcinoma were measured by gel diffusion and rocket immunoelectrophoresis. Sixteen of 22 (73 percent) patients with carcinoma of the colon or rectum (Dukes' A4/6, B6/8, C6/7, D0/1) had detectable CEA in their feces, while none was detected in the feces of four patients with gastric ulcers or in those of 22 normal volunteers. Five of the 16 fecal CEA-positive patients showed no elevation of plasma CEA levels. Measurements using a commercial CEA kit (Abbott Laboratories) could not detect the differences between fecal CEA values of patients with colorectal carcinoma and benign diseases, or those of normal volunteers. These results suggest that measurement of fecal CEA by specific anti-CEA antisera will be valuable in screening and diagnosis of colorectal carcinoma.
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PMID:Usefulness of carcinoembryonic antigen measurement in feces of patients with colorectal cancer. 362 64

Heat inactivation has been proposed as an alternative to perchloric acid (PCA) precipitation for the extraction of carcinoembryonic antigen (CEA) from human plasma. We examined a commercial RIA kit using heat inactivation, and compared results with those obtained with PCA precipitation. Adequate sensitivity (1.5 micrograms CEA/l plasma), satisfactory analytical recovery of CEA added to plasma, and dilutional linearity of samples found to have elevated CEA concentrations, were demonstrated for the heat-inactivation assay. Between-assay precision was better with the heat inactivation than with the PCA assay. Although the absolute concentration of CEA estimated after heat inactivation was consistently lower than that estimated after PCA extraction of plasma specimens, there was excellent correlation between results obtained with the two methods in colon cancer patients free of disease, colon cancer patients with residual or recurrent disease, patients with benign gastrointestinal disease, and in patients with chronic renal failure. We conclude that the heat-inactivation assay is an excellent alternative to the PCA assay.
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PMID:Carcinoembryonic antigen: assay following heat compared with perchloric acid extraction in patients with colon cancer, non-neoplastic gastrointestinal diseases, or chronic renal failure. 631 99

99Tcm is the optimum radionuclide for imaging in nuclear medicine due to its superior physical properties (E gamma of 140 keV and t1/2 of 6 h). Several techniques have recently been developed for labelling monoclonal antibodies with 99Tcm for immunoscintigraphy of human malignancies. These techniques primarily consist of either direct labelling of endogenous sulphydryl groups on the immunoglobulin with 99Tcm or indirect labelling through conjugation of a preformed 99Tcm-chelate. Direct methods offer the best promise for a one-step labelling kit but the 99Tcm-antibody may be unstable in vivo. This instability has been advantageous, however, in reducing blood background radioactivity and achieving sufficiently high tumour/blood ratios for clinical imaging. Over 1200 patients have been studied with 99Tcm-labelled monoclonal antibodies in the past decade. The majority of studies have been carried out in melanoma or colon cancer but other malignancies have also been investigated. The sensitivity has been variable and depended both on the size of the lesion and its location. Single photon emission computed tomographic imaging was helpful in some instances. Further study of labelling techniques and their effect on the pharmacokinetics of 99Tcm-labelled monoclonal antibodies as well as additional clinical evaluation of these agents is indicated.
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PMID:Immunoscintigraphy of tumours using 99Tcm-labelled monoclonal antibodies: a review. 851 Aug 74

Surveillance colonoscopy and biopsy are inaccurate methods of predicting the likelihood of ulcerative colitis patients to develop colon carcinoma. We examined uPA and PAI-1 as potential markers for assessing these patients and those with familial polyposis who are at risk of developing colon cancer. For comparison, biopsies of normal colon and Crohn's disease were evaluated. We examined 77 colonic mucosa specimens taken from patients undergoing elective resection for benign and malignant colonic disease. uPA and PAI-1 were measured using a monoclonal antibody-based ELISA kit (American Diagnostica, Greenwich, CT) and expressed as ng/mg extract protein. Intra- and interassay controls of uPA gave CV = 3-4% and CV = 8-9%, respectively, while those for PAI-1 were 6-7% and 10-11%, respectively. The Mann-Whitney test showed that both uPA and PAI-1 expression were significantly higher in colon cancer, chronic ulcerative colitis, and Crohn's disease than in normal colon. uPA in familial polyposis samples was similar to that of normal colon, while PAI-1 was much lower than in normal colon. Neither patient age nor sex appeared to influence the expression of these potential markers in any tissue. The pattern of uPA and PAI-1 expression in normal, benign and malignant colon suggests these proteins deserve further consideration as markers for assessing colon carcinoma risk.
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PMID:Expression of urokinase-type plasminogen activator and plasminogen activator inhibitor in colon disease. 858 11

A freeze dried kit formulation for the preparation of 99mTc-labelled IOR-CEA1, a monoclonal antibody (MoAb) against a human colorectal cancer, was developed. Methods of analysis were also established permitting identification of radiochemical impurities which may be present in radiopharmaceutical solution. 99mTc-EHDP-MoAb-IOR CEA1 prepared by the kit method was evaluated in human volunteers to apply the radioimmunodetection of human colon cancer. Data demonstrated that the complex formed after kit-reconstitution shows excellent stability and tumor seeking properties. Colon carcinoma in patients was successfully detected 6-8 and 20-28 h post administration.
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PMID:A freeze dried kit formulation for the preparation of 99mTc-EHDP-MoAb-IOR CEA1 complex. 923 58

Germline mutations in the adenomatous polyposis coli gene cause familial adenomatous polyposis, a colon cancer predisposition syndrome. More than 95% of the identified mutations result in the generation of stop codons or reading frame shifts and encode a truncated gene product, a mutation profile also found in other tumor predisposition genes such as the breast cancer or the hereditary non-polyposis coli. Therefore the protein truncation test is ideally suited for screening of mutations in these genes, starting from simple blood samples. Gene segments of interest are amplified from genomic DNA or mRNA, thereby incorporating a T7 promoter at the 5'-end. After in vitro transcription and translation of the PCR products, the resulting protein is analysed by gel electrophoresis. Truncated translation products indicate the presence of a stop mutation. We have developed a non-radioactive protein truncation test that uses a biotinylated Lys-t-RNA to label the translation products and allows a chemiluminescent detection instead of the standard radioactive method. This generic protein truncation test kit was then used to develop a parameter-specific protein truncation test for adenomatous polyposis coli. The adenomatous polyposis coli gene was divided in 5 overlapping segments, and primers were optimized to produce distinct bands with very low background in the protein truncation test. The assay was tested on 20 familial adenomatous polyposis patient samples, where 18 mutations were found, demonstrating the efficiency of this method.
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PMID:Optimized non-radioactive protein truncation test for mutation analysis of the adenomatous polyposis coli (APC) gene. 980 61

The purpose of this study was to determine whether point mutations and loss of the p53 gene take place in ulcerative colitis which is histologically negative for dysplasia. DNA was extracted from 13 frozen rectal or colon biopsies and blood samples. Ulcerative colitis was classified histologically as active (10 cases) and inactive (3 cases). Exons 5-8 were amplified by PCR, treated with exonuclease and shrimp alkaline phosphatase and sequenced by the dideoxy chain termination method with the Sequenase Version 2.0 DNA sequencing kit. PCR products of intron 6 and exon 4 were digested with MspI and AccII, respectively, for RFLP analysis. No p53 gene mutation was detected in these cases. The number of informative patients for loss of heterozygosity (LOH) at the p53 intron 6 was high, 11 out of 12 (92%), whereas no LOH was observed. LOH affecting p53 exon 4 was not detected in lesions from 5 of 12 patients (42%). In ulcerative colitis, tumor progression is similar to that in sporadic colon cancer, and other oncogenes and tumor suppressor genes are likely to be mutated before the p53 gene.
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PMID:Infrequent p53 gene alterations in ulcerative colitis. 1046 83

There is strong evidence that tyrosine kinases are involved in the regulation of cellular growth and tumor progression. Over-expressions of tyrosine kinases have been documented in a number of neoplasms. To study the roles of tyrosine kinases in colon cancer, we developed a tyrosine-kinase-expression profile for each of the four different stages of colon carcinogenesis, using normal colon mucosa, adenomatous polyps, primary carcinoma and hepatic metastases collected from the same patient. We identified 30 tyrosine kinases expressed in these tissues: they include 10 non-receptor tyrosine kinases (yes, fyn, lyn, brk, abl, arg, jak1, jak3, tyk2 and itk), 17 receptor tyrosine kinases (erbB2, PDGF-Ralpha, PDGF-Rbeta, kit, c-fms, met, ron, FGF-R1, FGF-R2, FGF-R3, FGF-R4, cek5, tie-1, tkt, axl, sky and Ins-R), 2 dual kinases (mek and sek) and one possible novel kinase. Among these kinases, arg kinase appears to be expressed at a higher level in primary carcinoma and metastatic tumor than in adjacent normal mucosa or adenomatous polyp. This result was confirmed by extensive analysis of 50 additional matched sets of normal colon and colon-tumor specimens, using arg-specific primers and RT-PCR reactions. This study identifies a possible role for arg tyrosine kinase in colon carcinogenesis, especially in the transition from adenoma to carcinoma.
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PMID:Comparative tyrosine-kinase profiles in colorectal cancers: enhanced arg expression in carcinoma as compared with adenoma and normal mucosa. 1052 89

Using a cultured human colon cancer cell line (Col 2), a structurally diverse group of chemopreventive agents was evaluated for their potential to induce apoptosis. As a result, 1,4-phenylenebis(methylene)selenocyanate (p-xylylselenocyanate; p-XSC) was found to be active in this process. p-XSC, a synthetic organoselenium compound, has been shown to inhibit tobacco-specific 4-(methylnitrosoamino)-(3-pyridyl)-1-butanone-induced tumorigenesis in A/J mouse lung, rat tongue carcinogenesis and colon cancer. Known chemopreventive mechanisms include inhibition of DNA methylation, inhibition of thymidine kinase and reduction of oxidative DNA damage. In order to assess apoptosis induction, the cells were exposed to various concentrations of test substances for 48 hours. Enrichment of mono- and oligonucleosomes in the cytoplasm was monitored as an indication of apoptosis using an ELISA kit. As a result, p-XSC caused dose-dependent enrichment of fragmented nucleosomes. In further studies, p-XSC was found to induce DNA laddering in a dose-dependent manner, while apoptotic cells accumulated in a time-dependent manner up to 96 hours. The apoptotic peaks after treatment of p-XSC were also found as confirmed by the flow cytometric analysis of cell cycle distribution. In an additional study, however, p-XSC-mediated apoptosis was not shown to be dependent on p53 expression. Taken together, these results suggest that induction of apoptosis is one possible mechanism for the cancer chemopreventive activity mediated by p-XSC.
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PMID:Induction of apoptosis by 1,4-phenylenebis(methylene)selenocyanate in cultured human colon cancer cells. 1201 40


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