کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10845633 | 1069796 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Eradication of gastric cancer is now both possible and practical
ترجمه فارسی عنوان
ریشه کن کردن سرطان معده در حال حاضر هر دو امکان و عملی است
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کلمات کلیدی
IARCCDH1MLH1hMLH1Activation-induced cytidine deaminaseVCPCDKN2ACpGMGMTH. pyloriRUNX3Klf5human MutL homolog 1MutL homolog 1 - MutL همولوگ 1International Agency for Research on Cancer - آژانس بین المللی تحقیقات سرطانOLGA - الگاNatural history - تاریخ طبیعیRisk - خطرGastrointestinal - دستگاه گوارشGastric cancer - سرطان معدهkruppel-like factor 5 - عامل خزش مانند 5Cancer screening - غربالگری سرطانconfidence interval - فاصله اطمینانRunt-related transcription factor 3 - فاکتور رونویسی مرتبط با روت 3cyclin-dependent kinase inhibitor 2A - مهارکننده 2A کیناز وابسته به سیکلینSurveillance - نظارتHelicobacter pylori - هلیکوباکتر پیلوریValosin-containing protein - پروتئین حاوی والوسینpepsinogen - پپسینوژنPrevention - پیشگیریPrimary prevention - پیشگیری اولیهsecondary prevention - پیشگیری ثانویه BRCA1 - ژن BRCA1breast cancer susceptibility gene 1 - ژن حساس به سرطان سینه 1cadherin-1 - کادرسین 1AID - کمکatrophic gastritis - گاستریت آتروفی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
In 1994, Helicobacter pylori was declared a human carcinogen. Evidence has now accumulated to show that at least 95% of gastric cancers are etiologically related to H. pylori. An extensive literature regarding atrophic gastritis and its effects on acid secretion, gastric microflora, and its tight association with gastric cancer has been rediscovered, confirmed, and expanded. Methods to stratify cancer risk based on endoscopic and histologic findings or serologic testing of pepsinogen levels and H. pylori testing have been developed producing practical primary and secondary gastric cancer prevention strategies. H. pylori eradication halts progressive mucosal damage. Cure of the infection in those with non-atrophic gastritis will essentially prevent subsequent development of gastric cancer. For all, the age-related progression in cancer risk is halted and likely reduced as eradication reduces or eliminates mucosal inflammation and reverses or reduces H. pylori-associated molecular events such aberrant activation-induced cytidine deaminase expression, double strand DNA breaks, impaired DNA mismatch repair and aberrant DNA methylation. Those who have developed atrophic gastritis/gastric atrophy however retain some residual risk for gastric cancer which is proportional to the extent and severity of atrophic gastritis. Primary and secondary cancer prevention starts with H. pylori eradication and cancer risk stratification to identify those at higher risk who should also be considered for secondary cancer prevention programs. Japan has embarked on population-wide H. pylori eradication coupled with surveillance targeted to those with significant remaining risk. We anticipate that countries with high gastric cancer burdens will follow their lead. We provide specific recommendations on instituting practical primary and secondary gastric cancer prevention programs as well identifying research needed to make elimination of gastric cancer both efficient and cost effective.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Seminars in Cancer Biology - Volume 23, Issue 6, Part B, December 2013, Pages 492-501
Journal: Seminars in Cancer Biology - Volume 23, Issue 6, Part B, December 2013, Pages 492-501
نویسندگان
Akiko Shiotani, Putao Cen, David Y. Graham,