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

Human intestinal intraepithelial lymphocytes (IEL) demonstrate target cell-restricted spontaneous cytotoxic (SC) activity that is due to CD2+CD3+CD8+CD16-CD56- effector cells; they kill epithelial cell (EC) tumours (such as DLD-1 colon cancer cells), but not natural killer (NK)-sensitive K-562 cells. The present study shows that the measured levels of SC activities by IEL correlated with those of autologous lamina propria lymphocytes (LPL), but not with those of peripheral blood lymphocytes (PBL). Also, the susceptibilities of DLD-1 cell clones to lysis by IEL and PBL effector cells did not correlate, suggesting different mechanisms of lysis. Antibody blocking experiments showed that the main surface molecules involved in lysis depended on the effector cell type: alpha E beta 7 (HML-1) on IEL and CD16 on PBL. No antibody-dependent cell-mediated cytotoxicity (ADCC) was demonstrated by IEL, even after stimulation with interferon-gamma (IFN-gamma). Few IEL expressed Fc receptors for IgG. This study describes further differences between the SC activities of IEL and PBL.
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PMID:Spontaneous cytotoxicity of intestinal intraepithelial lymphocytes: clues to the mechanism. 750 97

Human intraepithelial lymphocytes (IEL), predominantly CD8+ T-lymphocytes located between intestinal epithelial cells (EC), may represent the first-line immune defense against colon cancer. The mechanism by which IEL bind to the colon cancer line, DLD-1, was evaluated. A larger fraction of IEL than peripheral blood mononuclear cells bound to DLD-1 monolayers (25 +/- 16 versus 8 +/- 4% binding, P < 0.05). Binding increased when DLD-1 monolayers were incubated with interferon-gamma but not with tumor necrosis factor-alpha. Similar numbers of IEL adhered to EC tumors, HT-29 and 5637, and the non-EC tumor, A375, but fewer bound to nonmalignant smooth muscle (HISM) and fibroblast (KD) lines (P < 0.01). Binding of IEL to DLD-1 was reduced by monoclonal antibodies to HML-1 and CD11a (47 +/- 9 and 26 +/- 13% inhibition, respectively) and was completely eliminated by both combined (93 +/- 4% inhibition). Anti-HML-1 also inhibited the binding of IEL to other EC tumors but did not affect binding to non-EC tumors or fibroblasts. To conclude, the binding of IEL to EC tumors is mediated by HML-1 and CD11a [A. I. Roberts, S. M. O'Connell, and E. C. Ebert. Binding of intraepithelial lymphocytes to colon cancer cells is mediated by HML-1 and LFA-1 (abstract). Gastroenterology, 102: A685, 1992].
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PMID:Intestinal intraepithelial lymphocytes bind to colon cancer cells by HML-1 and CD11a. 845 30

Colon cancer is the fourth most common malignancy in both incidence and mortality in developed countries. Infectious agents are among the risk factors for colon cancer. Variations in human endogenous retrovirus (HERV) transcript and protein levels are associated with several types of cancers, but few studies address HERV expression in colon cancer. Fifty-eight patients with advanced-stage colon cancer were enrolled in this study. HERV-H, -K (HML-2), -P LTRs, Alu, and LINE-1 methylation levels and transcription of HERV-H, -K (HML-2), and -P env and HERV-K pol genes in normal adjacent and tumor tissues were investigated by pyrosequencing and RT-qPCR, respectively. Expression of the HERV-K (HML-2) Pol and Env proteins in selected tissues was examined by Western blotting. Associations between HERV transcript expression and methylation levels and between clinical characteristics and HERV expression were evaluated. Compared to adjacent normal tissues, LINE-1 was hypomethylated in tumor tissues (p < 0.05), whereas Alu, HERV-K (HML-2), and -H LTRs showed a decreasing trend in tumor tissue compared to normal tissue, though without a significant difference. The transcription levels of HERV env and pol genes were similar. However, the HERV-K (HML-2) Pol protein was more highly expressed (p < 0.01) in surrounding normal tissues, but the HERV-K (HML-2) Env protein was only expressed in tumor tissues. Although HERV LTR methylation and gene expression did not show significant differences between tumor and normal tissues, HERV protein expression differed greatly. Pol protein expression in normal cells may induce reverse transcription and subsequent integration into the host genome, likely favoring cell transformation; in contrast, the Env protein in tumor tissue may contribute to cancer progression through cell-to-cell fusion.
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PMID:Human Endogenous Retroviruses Long Terminal Repeat Methylation, Transcription, and Protein Expression in Human Colon Cancer. 3319 57