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)

Traditional rectal cancer surgery has been burdened with a high rate of sexual and urinary dysfunctions due to intraoperative injury or the cutting of the sympathetic and/or parasympathetic nerves. The experience acquired in the last ten years with total mesorectal excisions has permitted the use of the "nerve-sparing" technique. The present study regards 239 patients from two surgical centres, most of whom underwent sphincter-saving radical surgery between 1994 and 1998 with the above mentioned technique for resectable colon cancer. Details regarding the technique were recorded in the last 58 patients, in order to examine the severity of the surgical damage. The subgroup with the longest follow-up, which included 36 patients, was diagnostically evaluated by a surgeon, psychologist, urologist and neurologist to analyze the risk of sexual and urinary dysfunctions. A complete nerve-sparing was performed in 86.3% of the cases. The parasympathetic nerve trunks were those most often damaged because of perineural tumor spreading. Partial to complete sexual impotence was observed in 44% of the patients and surprisingly, preoperative dysfunctions were detected by means of the multidisciplinary approach in one third of these patients. Therefore, only 30.5% of the patients presented with strictly postoperative sexual impotency, above all, those who had undergone high-dose preoperative chemoradiation for T3 or T4 middle to low rectal cancer. A prospective study was initiated to evaluate the genitourinary dysfunctions after rectal cancer surgery in all of the clinical phases by means of a multidisciplinary approach aimed at functional recovery and improved quality of life.
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PMID:Nerve-sparing surgery in rectal cancer: feasibility and functional results. 1084 Sep 33

MicroRNAs (miRNAs) from the gene cluster miR-143-145 are diminished in cells of colorectal tumor origin when compared with normal colon epithelia. Until now, no report has addressed the coordinate action of these miRNAs in colorectal cancer (CRC). In this study, we performed a comprehensive molecular and functional analysis of the miRNA cluster regulatory network. First, we evaluated proliferation, migration, anchorage-independent growth and chemoresistance in the colon tumor cell lines after miR-143 and miR-145 restoration. Then, we assessed the contribution of single genes targeted by miR-143 and miR-145 by reinforcing their expression and checking functional recovery. Restoring miR-143 and miR-145 in colon cancer cells decreases proliferation, migration and chemoresistance. We identified cluster of differentiation 44 (CD44), Kruppel-like factor 5 (KLF5), Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) and v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) as proteins targeted by miR-143 and miR-145. Their re-expression can partially revert a decrease in transformation properties caused by the overexpression of miR-143 and miR-145. In addition, we determined a set of mRNAs that are diminished after reinforcing miR-143 and miR-145 expression. The whole transcriptome analysis ascertained that downregulated transcripts are enriched in predicted target genes in a statistically significant manner. A number of additional genes, whose expression decreases as a direct or indirect consequence of miR-143 and miR-145, reveals a complex regulatory network that affects cell signaling pathways involved in transformation. In conclusion, we identified a coordinated program of gene repression by miR-143 and miR-145, in CRC, where either of the two miRNAs share a target transcript, or where the target transcripts share a common signaling pathway. Major mediators of the oncosuppression by miR-143 and miR-145 are genes belonging to the growth factor receptor-mitogen-activated protein kinase network and to the p53 signaling pathway.
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PMID:Analysis of the combined action of miR-143 and miR-145 on oncogenic pathways in colorectal cancer cells reveals a coordinate program of gene repression. 2312 94