Fwd: Frequent mutations of the CA simple sequence repeat in intron 1 of EGFR in mismatch repair-deficient colorectal cancers.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Feb 22, 2008 at 10:17 AM
Subject: Frequent mutations of the CA simple sequence repeat in intron 1 of EGFR in mismatch repair-deficient colorectal cancers.
To: mesothelioma77@gmail.com


[1]World J Gastroenterol. 2008 Feb 21; 14(7): 1053-9
Buisine MP, Wacrenier A, Mariette C, Leteurtre E, Escande F, Aissi S, Ketele A, Leclercq A, Porchet N, Lesuffleur T

AIM: To investigate the polymorphic simple sequence repeat in intron 1 of the epidermal growth factor receptor gene (EGFR) (CA-SSR I), which is known to affect the efficiency of gene transcription as a putative target of the mismatch repair (MMR) machinery in colorectal tumors. METHODS: The CA-SSR I genotype was analyzed in a total of 86 primary colorectal tumors, selected upon their microsatellite instability (MSI) status [42 with high frequency MSI (MSI-H) and 44 microsatellite stable (MSS)] and their respective normal tissue. The effect of the CA-SSR I genotype on the expression of the EGFR gene was evaluated in 18 specimens using quantitative real-time reverse transcription PCR and immunohistochemistry. RESULTS: Mutations in CA-SSR I were detected in 86% (36 of 42) of MSI-H colorectal tumors and 0% (0 of 44) of MSS tumors, indicating the EGFR gene as a novel putative specific target of the defective MMR system (P

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Source: http://www.hubmed.org/display.cgi?uids=18286687
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Fwd: Multiple gene methylation of nonsmall cell lung cancers evaluated with 3-dimensional microarray.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Feb 22, 2008 at 10:17 AM
Subject: Multiple gene methylation of nonsmall cell lung cancers evaluated with 3-dimensional microarray.
To: mesothelioma77@gmail.com

[1]Cancer. 2008 Feb 19;
Wang Y, Zhang D, Zheng W, Luo J, Bai Y, Lu Z

BACKGROUND: Aberrant DNA methylation of the CpG islands for cancer-related genes is among the earliest and most frequent alterations in cancer and may be useful for diagnosing cancer or evaluating recurrent disease. METHODS: In this study, a 3-dimensional (3-D), polyacrylamide gel-based DNA microarray coupled with linker-polymerase chain reaction (PCR) was developed to detect hypermethylation of CpG islands in multiple genes from a large group of different samples. The authors determined the frequency of aberrant promoter methylation of 15 genes in 28 resected primary nonsmall cell lung cancers (NSCLCs) and in 12 corresponding nonmalignant lung tissues. RESULTS: Methylation frequencies in the tumor samples were detected in 18% of samples for the breast cancer 1 gene BRCA1, in 43% of samples for the tissue inhibitor of metalloproteinase 3 gene TIMP-3, in 38% of samples for the cyclin-dependent kinase inhibitor 4A gene p16INK4a, in 54% of samples for the cadherin 13 gene CDH13, in 50% of samples for the death-associated protein kinase gene DAPK, in 11% of samples for the E-cadherin gene ECAD, in 25% of samples for the insulin-like growth factor binding protein 7 gene IGFBP7, in 18% of samples for the Ras association domain family 1 gene RASSF1, in 68% of samples for the adenomatous polyposis coli gene APC, in 7% of samples for the cyclin-dependent kinase inhibitor gene p15, in 18% of samples for the CD44 cell adhesion molecule gene, in 29% of samples for the human Mut-L homolog gene hMLH, in 32% of samples for the human telomerase reverse transcriptase gene hTERT, in 64% of samples for the calcitonin gene-related polypeptide alpha gene CALCA, and in 54% of samples for the estrogen receptor gene ER; however, methylation was not observed in the majority of corresponding nonmalignant tissues. Six samples in from 28 tumors had >6 genes methylated, and 1 sample had 13 genes methylated. Methylation of these genes was correlated with some clinicopathologic patient characteristics. CONCLUSIONS: This study demonstrated that a 3-D microarray could be used to detect DNA hypermethylation and provided a high-throughput platform for DNA hypermethylation analysis. Cancer 2008. (c) 2008 American Cancer Society.



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Source: http://www.hubmed.org/display.cgi?uids=18286531
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