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)

A mouse monoclonal antibody V-715 was raised against fresh colon cancer tissues. Biochemical analysis elucidated that the antigen defined was adenosine deaminase binding protein (ADBP). In colon cancer cell lines, V-715 was positive in 8 out of 16 differentiated cancers and in 2 out of 8 poorly differentiated cancers. In frozen sections, ADBP was expressed in 17 out of 33 differentiated colon cancers, but none of 4 poorly differentiated colon cancers. In normal colon, the expression was observed in epithelium. In gastric cancers, ADBP was expressed in 10 out of 15 differentiated cancers, but weakly or only heterogenously expressed in 2 out of 8 poorly differentiated cancers. In normal gastric mucosa, ADBP was mainly detected in the foveolar epithelium, but was weakly or not expressed in the deep gastric glands. Carcinoid tumors and malignant lymphoma of the stomach did not express ADBP. These results suggest that ADBP may act as a marker of enterocytic differentiation in normal and neoplastic gastrointestinal cells, and might be exploitable in clinical and pathological diagnosis of gastrointestinal cancers.
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PMID:Distribution of adenosine deaminase binding protein in normal and malignant tissues of the gastrointestinal tract studied by monoclonal antibodies. 809 85

Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. At a protein levels low amount of A(1), A(2A), and A(2B) receptors were detected, whilst the A(3) was the most abundant subtype in both cancer tissues and cells, with a pharmacological profile typical of the A(3) subtype. All the receptors were coupled to stimulation/inhibition of adenylyl-cyclase in cancer cells, with the exception of A(1) subtype. Adenosine increased cell proliferation with an EC(50) of 3-12 microM in cancer cells. This effect was not essentially reduced by adenosine receptor antagonists. However dypiridamol, an adenosine transport inhibitor, increased the stimulatory effect induced by adenosine, suggesting an action at the cell surface. Addition of adenosine deaminase makes the A(3) agonist 2-chloro-N6-(3-iodobenzyl)-N-methyl-5'-carbamoyladenosine (Cl-IB-MECA) able to stimulate cell proliferation with an EC(50) of 0.5-0.9 nM in cancer cells, suggesting a tonic proliferative effect induced by endogenous adenosine. This effect was antagonized by 5-N-(4-methoxyphenyl-carbamoyl)amino-8-propyl-2(2furyl)-pyrazolo-[4,3e]-1,2,4-triazolo [1,5-c] pyrimidine (MRE 3008F20) 10 nM. Cl-IB-MECA-stimulated cell proliferation involved extracellular-signal-regulated-kinases (ERK1/2) pathway, as demonstrated by reduction of proliferation with 1,4-diamino-2,3-dicyano-1,4-bis-[2-amino-phenylthio]-butadiene (U0126) and by ERK1/2 phosphorylation. In conclusion this study indicates for the first time that in colon cancer cell lines endogenous adenosine, through the interaction with A(3) receptors, mediates a tonic proliferative effect.
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PMID:Adenosine receptors in colon carcinoma tissues and colon tumoral cell lines: focus on the A(3) adenosine subtype. 1734 28