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

We present a fully automated three-dimensional (3-D) segmentation algorithm to extract the colon lumen surface in CT colonography. Focusing on significant-size polyp detection, we target at an efficient algorithm that maximizes overall colon coverage, minimizes the extracolonic components, maintains local shape accuracy, and achieves high segmentation speed. Two-dimensional (2-D) image processing techniques are employed first, resulting in automatic seed placement and better colon coverage. This is followed by near-air threshold 3-D region-growing using an improved marching-cubes algorithm, which provides fast and accurate surface generation. The algorithm constructs a well-organized vertex-triangle structure that uniquely employs a hash table method, yielding an order of magnitude speed improvement. We segment two scans, prone and supine, independently and with the goal of improved colon coverage. Both segmentations would be available for subsequent polyp detection systems. Segmenting and analyzing both scans improves surface coverage by at least 6% over supine or prone alone. According to subjective evaluation, the average coverage is about 87.5% of the entire colon. Employing near-air threshold and elongation criteria, only 6% of the data sets include extracolonic components (EC) in the segmentation. The observed surface shape accuracy of the segmentation is adequate for significant-size (6 mm) polyp detection, which is also verified by the results of the prototype detection algorithm. The segmentation takes less than 5 minutes on an AMD 1-GHz single-processor PC, which includes reading the volume data and writing the surface results. The surface-based segmentation algorithm is practical for subsequent polyp detection algorithms in that it produces high coverage, has a low EC rate, maintains local shape accuracy, and has a computational efficiency that makes real-time polyp detection possible. A fully automatic or computer-aided polyp detection system using this technique is likely to benefit future colon cancer early screening.
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PMID:Automatic colon segmentation with dual scan CT colonography. 1564 34

Metastasis and drug resistance are major problems in cancer chemotherapy. The purpose of this work was to analyze the molecular mechanisms underlying the invasive potential of drug-resistant colon carcinoma cells. Cellular models included the parental HT-29 cell line and its drug-resistant derivatives selected after chronic treatment with either 5-fluorouracil, methotrexate, doxorubicin, or oxaliplatin. Drug-resistant invasive cells were compared with noninvasive cells using cDNA microarray, quantitative reverse transcription-PCR, flow cytometry, immunoblots, and ELISA. Functional and cellular signaling analyses were undertaken using pharmacologic inhibitors, function-blocking antibodies, and silencing by retrovirus-mediated RNA interference. 5-Fluorouracil- and methotrexate-resistant HT-29 cells expressing an invasive phenotype in collagen type I and a metastatic behavior in immunodeficient mice exhibited high expression of the chemokine receptor CXCR4. Macrophage migration-inhibitory factor (MIF) was identified as the critical autocrine CXCR4 ligand promoting invasion in drug-resistant colon carcinoma HT-29 cells. Silencing of CXCR4 and impairing the MIF-CXCR4 signaling pathways by ISO-1, pAb FL-115, AMD-3100, monoclonal antibody 12G5, and BIM-46187 abolished this aggressive phenotype. Induction of CXCR4 was associated with the upregulation of two genes encoding transcription factors previously shown to control CXCR4 expression (HIF-2alpha and ASCL2) and maintenance of intestinal stem cells (ASCL2). Enhanced CXCR4 expression was detected in liver metastases resected from patients with colon cancer treated by the standard FOLFOX regimen. Combination therapies targeting the CXCR4-MIF axis could potentially counteract the emergence of the invasive metastatic behavior in clonal derivatives of drug-resistant colon cancer cells.
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PMID:Autocrine induction of invasive and metastatic phenotypes by the MIF-CXCR4 axis in drug-resistant human colon cancer cells. 2046 May 42