کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10897634 | 1083891 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hypermethylation of the CpG dinucleotide in epidermal growth factor receptor codon 790: implications for a mutational hotspot leading to the T790M mutation in non-small-cell lung cancer
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Hypermethylation of the CpG dinucleotide in epidermal growth factor receptor codon 790: implications for a mutational hotspot leading to the T790M mutation in non-small-cell lung cancer Hypermethylation of the CpG dinucleotide in epidermal growth factor receptor codon 790: implications for a mutational hotspot leading to the T790M mutation in non-small-cell lung cancer](/preview/png/10897634.png)
چکیده انگلیسی
Nearly one half of all cases of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) for non-small-cell lung cancer (NSCLC) are due to the T790M mutation in EGFR exon 20. The T790M mutation is a CâT transition mutation at a CpG dinucleotide. DNA methylation of cytosine (5-methylcytosine (5-mC)) in CpG dinucleotides is a common DNA modification; CpG dinucleotides are considered to be mutational hotspots that cause genetic diseases and cancers through spontaneous deamination of 5-mC, resulting in CâT transition mutations. This study aimed to examine the methylation level of cytosine of EGFR codon 790 and investigate whether DNA methylation was involved in acquiring the T790M mutation. We examined 18 NSCLC tumor tissues, 7 normal lymph node tissues, and 4 NSCLC cell lines (PC9, HCC827, 11-18, and A549). 5-mC was checked by bisulfite sequencing and quantified by pyrosequencing. We found that all tissue samples and cell lines had 5-mC in EGFR codon 790. The 5-mC range was 58.4-90.8%. Our results imply that hypermethylation of the CpG dinucleotide in EGFR codon 790 leads to the CâT transition mutation, causing resistance to EGFR-TKI treatment.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Genetics - Volume 208, Issue 5, May 2015, Pages 271-278
Journal: Cancer Genetics - Volume 208, Issue 5, May 2015, Pages 271-278
نویسندگان
Akiko Fujii, Taishi Harada, Eiji Iwama, Keiichi Ota, Kazuto Furuyama, Kayo Ijichi, Tatsuro Okamoto, Isamu Okamoto, Koichi Takayama, Yoichi Nakanishi,