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)

MMTV induces the mouse mammary tumor through the dysregulation of Notch, Wnt, or Fgf signaling pathway. Activation of Notch signaling pathway leads to transcriptional activation of Hes family genes through the interaction between Notch intracellular domain and RBPSUH (CSL). Hes family proteins are mammalian homologs of Drosophila Hairy and Enhancer of split. Hes family of transcriptional repressors with basic Helix-loop-helix (bHLH) and Orange domains are implicated in the cell fate determination of stem cells (or precursor cells) by suppressing the expression of tissue-specific transcriptional activators. Human HES1, HES4, HES6, and HES7 genes have been reported by other groups. Here, we identified and characterized human HES2, HES3 and HES5 genes by using bioinformatics. FLJ33803 (AK091122.1) was the representative human HES2 cDNA. HES2 gene, encoding a 173-aa protein, was located within human genome sequence AL031848.11. HES3 gene, encoding a 186-aa protein, was identified within human genome sequence AL031847.17. HES5 gene, encoding a 166-aa protein, was identified within human genome sequence AL139246.20. HES2 and HES3 genes were mapped to human chromosome 1p36.31, while HES5 gene to 1p36.32. HES2 mRNA was expressed in placenta, pancreatic cancer, colon cancer with RER, cervical cancer, and in head and neck tumors. HES5 mRNA was expressed in fetal heart, and brain tumors. Human HES family proteins were found consisting of bHLH, Orange, Proline-rich domains, and WRPW motif. Phylogenetic analyses revealed that HES family proteins were distantly related except a paralog pair of HES1 and HES4. HES family genes are pharmacogenomic targets in the field of regenerative medicine and oncology.
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PMID:Identification and characterization of human HES2, HES3, and HES5 genes in silico. 1525 53

Diet interventions and natural bioactive supplements have now been extensively studied to reduce risks of colon cancer, which is one of the major public health problem throughout the world. The objective of our investigation was to study the effects of probiotic, prebiotic, nutritional plant extract, and plant oil on selected biochemical and immunological parameters in rats with colon cancer induced by N,N dimethylhydrazine (DMH). Male and female Wistar albino rats were were fed by a high-fat (HF) diet (10% fat in the diet) and were divided into 9 groups: Control group; PRO group - HF diet supplemented with probiotic Lactobacillus plantarum to provide 3 x 109 c.f.u. of strain/1 ml of medium; PRE group - HF diet supplemented with inulin enriched with oligofructose (2% of HF diet); HES group - HF diet supplemented with plant extract of Aesculus hippocastanum L. (1% of HF diet); OIL group - HF diet comprised Linioleum virginale (2% of HF diet); and combination of probiotic microorganisms and bioactive compounds in the groups - PRO-PRE, PRO-HES, PRO-OIL, PRE-OIL. Carcinogenesis was initiated with subcutaneous injection of DMH (20 mg/kg) two times at week interval and dietary treatments were continued for the six weeks. Application of probiotic microorganisms and bioactive compounds in all treated groups significantly decreased the activities of bacterial enzymes (p<0.001), the fecal bile acids concentration (p<0.01; p<0.001) and significantly increased serum TNFalpha level (p<0.001) in comparison to the control rats. The number of coliforms was reduced in PRO, PRO-PRE, PRO-OIL and PRE-OIL groups and significantly higher count of lactobacilli (p<0.05) was observed in PRO-PRE, PRO-OIL and PRE-OIL groups in compare with the controls. In conclusion, the results of this study indicate that probiotic microorganisms and bioactive compounds could exert a preventive effect on colon carcinogenesis induced by DMH.
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PMID:The effect of probiotic microorganisms and bioactive compounds on chemically induced carcinogenesis in rats. 2056 96

Hypercoagulability and excessive platelet activation account for a significant percentage of mortality and morbidity in cancer patients. In order to test the hypothesis that preloading infusion (PLI) with 6% hydroxyethyl starch 200/0.5 (HES 200), or 6% hydroxyethyl starch 130/0.4 (HES 130) solution can attenuate the hypercoagulable state and inhibit excessive platelet activation of patients with colon cancer, we selected 35 colon cancer patients undergoing laparoscopic-assisted radical colectomy. They were received randomly a test of 15 ml/kg of either HES 200 (n=17), or HES 130 (n=18) over a 30-min period preoperatively. In addition, fifteen healthy volunteers were selected as normal control group. Coagulation function was assessed by thrombelastography (TEG), platelet glycoprotein IIb/IIIa and CD62P was analyzed by flow cytometry before PLI, the end of PLI, 1 h after PLI, and 1 h after the end of surgery. Results demonstrated that hypercoagulable state indicated by TEG and excessive platelet activation was found in patients with colon cancer. We found that preloading infusion with HES 200/0.5 can inhibit platelet activation, and the two solutions, especially HES 200/0.5, compromised TEG parameters that indicated hypercoagulability of patients with colon cancer during perioperative period.
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PMID:The effects of preloading infusion with hydroxyethyl starch 200/0.5 or 130/0.4 solution on hypercoagulability and excessive platelet activation of patients with colon cancer. 2061 71