Inhibition of tumor energy pathways for targeted esophagus cancer therapy
Inhibition of tumor energy pathways for targeted esophagus cancer therapy
نویسندگان: عباس شفایی , جلیل پیرایش اسلامیان
کلمات کلیدی: AMPK; Esophageal cancer; Gluconeogenesis; Metformin; Targeted therapy
نشریه: 23968 , 10 , 64 , 2015
| نویسنده ثبت کننده مقاله |
جلیل پیرایش اسلامیان |
| مرحله جاری مقاله |
تایید نهایی |
| دانشکده/مرکز مربوطه |
دانشکده پزشکی |
| کد مقاله |
71926 |
| عنوان فارسی مقاله |
Inhibition of tumor energy pathways for targeted esophagus cancer therapy |
| عنوان لاتین مقاله |
Inhibition of tumor energy pathways for targeted esophagus cancer therapy |
| ناشر |
4 |
| آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ |
خیر |
| عنوان نشریه (خارج از لیست فوق) |
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| نوع مقاله |
Review Article |
| نحوه ایندکس شدن مقاله |
ایندکس شده سطح یک – ISI - Web of Science |
| آدرس لینک مقاله/ همایش در شبکه اینترنت |
|
| nterest in targeting cancer metabolism has been renewed in recent years with the discovery that many cancer related pathways have a profound effect on metabolism and that many tumors become dependent on specific metabolic processes. Accelerated glucose uptake during anaerobic glycolysis and loss of regulation between glycolytic metabolism and respiration, are the major metabolic changes found in malignant cells. The non-metabolizable glucose analog, 2-deoxy-D-glucose inhibits glucose synthesis and adenosine triphosphate production. The adenosine monophosphate-activated protein kinase (AMPK) is a key sensor of cellular energy and AMPK is a potential target for cancer prevention and/or treatment. Metformin is an activator of AMPK which inhibits protein synthesis and gluconeogenesis during cellular stress. This article reviews the status of clinical and laboratory researches exploring targeted therapies via metabolic pathways for treatment of esophageal cancer. |
| نام فایل |
تاریخ درج فایل |
اندازه فایل |
دانلود |
| -Inhibition of tumor energy pathways for targeted esophagus cancer therapy.pdf | 1399/02/02 | 377227 | دانلود |