Rapamycin Extends Maximal Lifespan in Cancer-Prone Mice

被引：207

作者：

Anisimov, Vladimir N. ^{[1
]}

Zabezhinski, Mark A. ^{[1
]}

Popovich, Irina G. ^{[1
]}

Piskunova, Tatiana S. ^{[1
]}

Semenchenko, Anna V. ^{[1
]}

Tyndyk, Margarita L. ^{[1
]}

Yurova, Maria N. ^{[1
]}

Antoch, Marina P. ^{[3
]}

Blagosklonny, Mikhail V. ^{[2
]}

机构：

[1] NN Petrov Res Inst Oncol, Dept Carcinogenesis & Oncogerontol, St Petersburg 197758, Russia

[2] Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY 14263 USA

[3] Roswell Pk Canc Inst, Dept Mol & Cellular Biol, Buffalo, NY 14263 USA

来源：

AMERICAN JOURNAL OF PATHOLOGY | 2010年 / 176卷 / 05期

关键词：

TRANSGENIC MOUSE MODEL; FATAL NEOPLASTIC DISEASES; CALORIE RESTRICTION; DELAYED OCCURRENCE; MAMMALIAN TARGET; TOR; GROWTH; PROGRESSION; ONSET; MTOR;

D O I：

10.2353/ajpath.2010.091050

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

Aging is associated with obesity and cancer. Calorie restriction both slows down aging and delays cancer. Evidence has emerged that the nutrient-sensing mammalian target of rapamycin (mTOR) pathway is involved in cellular and organismal aging. Here we show that the mTOR inhibitor rapamycin prevents age-related weight gain, decreases rate of aging, increases lifespan, and suppresses carcinogenesis in transgenic HER-2/neu cancer-prone mice. Rapamycin dramatically delayed tumor onset as well as decreased the number of tumors per animal and tumor size. We suggest that, by slowing down organismal aging, rapamycin delays cancer. (Am J Pathol 2010, 176:2092-2097; DOI: 10.2353/ajpath.2010.091050)

引用

页码：2092 / 2097

页数：6

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