Paradoxical down-regulation of p16INK4a mRNA with advancing age in Acute Myeloid Leukemia

被引:13
作者
de Jonge, Hendrik J. M. [2 ]
Woolthuis, Carolien M. [1 ]
de Bont, Eveline S. J. M. [2 ]
Huls, Gerwin [1 ]
机构
[1] Univ Groningen, Dept Hematol, Univ Med Ctr Groningen, NL-9713 GZ Groningen, Netherlands
[2] Univ Groningen, Div Pediat Hematol Oncol, Univ Med Ctr Groningen, Dept Pediat,Beatrix Childrens Hosp, NL-9713 GZ Groningen, Netherlands
来源
AGING-US | 2009年 / 1卷 / 11期
关键词
p16(INK4a); aging; Acute Myeloid Leukemia; senescence; HEMATOPOIETIC STEM-CELLS; SELF-RENEWAL; TUMOR-SUPPRESSOR; HEART-FAILURE; EXPRESSION; SENESCENCE; CANCER; GROWTH; BMI-1; OLDER;
D O I
10.18632/aging.100096
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Aging is generally considered to be the consequence of stem cell attrition caused by the activity of tumor suppressor pathways that censor potentially malignant clones by eliciting apoptosis or senescence. An important effector of aging is the cyclin-dependent kinase inhibitor p16(INK4a), which is also a known suppressor of cancer. The expression of p16(INK4a) is very low or absent in young organisms but increases with advancing age. We recently showed that, unlike healthy cells, acute myeloid leukemia (AML) derived blasts show a down-regulation of p16(INK4a) mRNA with increasing age. Based on this observation we hypothesize that suppression of defense mechanisms which protect older cells against cellular and DNA damage might facilitate oncogenesis in older individuals.
引用
收藏
页码:949 / 953
页数:5
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