Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Light, electron microscopy, polymerase chain reaction (PCR), and immunohistochemistry were used to reveal the proliferative, alterative processes of hepatic parenchymal cells, P 53, K-ras, B-raf, c-Kit, p 16, APC, immunoreactive proteins Ki-67, cytokeratins 9, 14, 20, EMA, c-erb B-2, CD-117, mutated p 53 and bcl-2 genes. P53, K-ras, B-raf, c-Kit, and p 16 gene mutations were detected in the liver of animals with experimental superinvasive opisthorchiasis (SO) and cholangiocellular carcinoma (CCC). Mutations of these genes were found in the plasma samples taken from SO patients. The CCC tissue from SO patients displayed expression of the following genes: p 53 (100.0%), p 53+B-raf (50.0%), K-ras+c-Kit (33.3%), K-ras+B-rafat more than 5 cm from the tumor in 2 cases. Following 2 years, target therapy (canglait, megamin, immunomodulators) leveled mutations in 91.25% of the patients with SO.
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PMID:[Molecular genetic approaches in parasitology (in case of opisthorchiasis)]. 1766 39

We hypothesized that in a comprehensive analysis of colorectal carcinomas (CRC) the three currently known major molecular mechanisms of carcinogenesis (i.e., chromosomal instability, microsatellite instability, and CpG island methylator phenotype, CIMP) would associate with the molecular features indicative of these pathways, allowing a molecular classification. A prospectively collected clinicopathologically well-characterized series of 130 CRCs was tested for chromosomal instability (DNA-flow cytometry and analysis of allelic imbalance with microsatellite markers 5q21, 8p21, 9q21, 17p13, and 18q21), microsatellite instability (Bethesda panel), CIMP (MethyLight), and mutations of K-ras, B-raf, APC, and p53. Morphology was reviewed, and nuclear beta-catenin translocation was assessed by immunohistochemistry. Based on the molecular features, sporadic high-degree microsatellite instable tumours, tumours of the hereditary non-polyposis coli carcinoma syndrome, and 'sporadic standard-type' CRC could be delineated (14, 4, and 55, respectively). However, overlap between classes was seen for 46 of the remaining tumours where widespread or occasional methylations (excluding MLH1) were observed, and the majority had chromosomal instability. Importantly, a group of 11 tumours was observed without either microsatellite or chromosomal instability, nor any methylation. Morphologically, these tumours were without any distinguishing features, all had tumour budding and 10 showed nuclear beta-catenin translocation. Overall, the data give an overview of the molecular classes in CRC that should be taken into account in studies on carcinogenesis and clinicopathological studies. Specifically, the absence of CIN, MSI, and CIMP in an 8.46% fraction of tumours delineates a group to be aware of.
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PMID:Chromosomally and microsatellite stable colorectal carcinomas without the CpG island methylator phenotype in a molecular classification. 1957 46

The pathogenesis of sporadic colorectal cancer involves distinct pathways, with characteristic genomic alterations. The first pathway, chromosome instability (CIN), is driven by APC mutations and is typified by Kras mutations, p53 mutation/loss of heterozygosity, and deletions at chromosome 18q. The second pathway is referred to as microsatellite instability (MSI), a genetic hallmark of the accumulated mutations that occur as a consequence of derangements in the mismatch repair genes. Finally, proximal colon cancers may involve methylation of a number of genes, which is frequently referred to as the CpG island methylator phenotype (CIMP), and are associated with B-raf mutations. The ability to stratify colorectal cancers by risk would be facilitated by the identification of polymorphisms that might be utilized as biomarkers. LIN28B is an RNA binding protein that is overexpressed in colon cancers. We find that LIN28B rs314277 is associated with significant recurrence of colorectal cancer in Stage II disease, which may have translational therapeutic implications.
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PMID:A LIN28B polymorphism predicts for colon cancer survival. 2305 30