کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2152280 | 1090058 | 2007 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IGFBP3 Promoter Methylation in Colorectal Cancer: Relationship with Microsatellite Instability, CpG Island Methylator Phenotype, p53
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کلمات کلیدی
MSI-HCIMPIGFBP3CTNNB1CDKN2ATP53RUNX3CDKN1APMRSOCS1Neurog1IGF2MSIMSI-LTGFCACNA1GMSSTMATGFBR2CRABP1CpG island methylator phenotype - phenotype methylparate جزیره CpGBax - باکسβ-catenin - بتا-کاتنینMicrosatellite instability - بی ثباتی ریزماهواره ایmicrosatellite instability-high - بی ثباتی ریزماهواره بالاtransforming growth factor - تبدیل فاکتور رشدtumor protein p53 - تومور پروتئین p53microsatellite stable - ریزماهواره پایدار استColon cancer - سرطان کولونsuppressor of cytokine signaling 1 - سرکوب کننده سیگنالینگ سیتوکین 1insulin-like growth factor 2 - فاکتور رشد مانند انسولین 2Methylation - متیلاسیونTissue microarray - میکروآرشی بافتNeurogenin 1 - نوروژنین 1polymerise chain reaction - واکنش زنجیره پلیمریزاسیونPCR - واکنش زنجیرهٔ پلیمرازBCL2-associated X protein - پروتئین X مرتبط با BCL2Insulin-like growth factor binding protein 3 - پروتئین اتصال دهنده فاکتور رشد مانند انسولین 3Calcium channel - کانال کلسیم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
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چکیده انگلیسی
Insulin-like growth factor binding protein 3 (IGFBP3), which is induced by wild-type p53, regulates IGF and interacts with the TGF-β pathway. IGFBP3 promoter methylation may occur in colorectal cancer with or without the CpG island methylator phenotype (CIMP), which is associated with microsatellite instability (MSI) and TGFBR2 mutation. We examined the relationship between IGFBP3 methylation, p53 expression, CIMP and MSI in 902 population-based colorectal cancers. Utilizing real-time PCR (MethyLight), we quantified promoter methylation in IGFBP3 and eight other CIMP-high-specific promoters (CACNA1G, CDKN2A, CRABP1, IGF2, MLH1, NEUROG1, RUNX3, and SOCS1). IGFBP3 methylation was far more frequent in non-MSI-high CIMP-high tumors (85% = 35/41) than in MSI-high CIMPhigh (49% = 44/90, P < .0001), MSI-high non-CIMP-high (17% = 6/36, P < .0001), non-MSI-high non-CIMP-high tumors (22% = 152/680, P < .0001). Among CIMPhigh tumors, the inverse relationship between MSI and IGFBP3 methylation persisted in p53-negative tumors (P < .0001), but not in p53-positive tumors. IGFBP3 methylation was associated inversely with TGFBR2 mutation in MSI-high non-CIMP-high tumors (P = .02). In conclusion, IGFBP3 methylation is inversely associated with MSI in CIMP-high colorectal cancers, this relationship is limited to p53-negative tumors. Our data suggest complex relationship between global genomic/epigenomic phenomena (such as MSI/ CIMP), single molecular events (e.g., IGFBP3 methylation, TP53 mutation, TGFBR2 mutation), the related pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neoplasia - Volume 9, Issue 12, December 2007, Pages 1091-1098
Journal: Neoplasia - Volume 9, Issue 12, December 2007, Pages 1091-1098
نویسندگان
Takako Kawasaki, Katsuhiko Nosho, Mutsuko Ohnishi, Yuko Suemoto, Gregory J. Kirkner, Charles S. Fuchs, Shuji Ogino,