Inactivation of p14ARF as a key event for the progression of adult T cell leukemia/lymphoma

被引：14

作者：

Kohno, Tomoko ^{[1
]}

Yamada, Yasuaki ^{[2
]}

Tawara, Masayuki ^{[3
]}

Takasaki, Yumi ^{[3
]}

Kamihira, Shimeru ^{[2
]}

Tomonaga, Masao ^{[3
]}

Matsuyama, Toshifumi ^{[1
]}

机构：

[1] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Div Cytokine Signaling, Nagasaki 8528523, Japan

[2] Nagasaki Univ, Grad Sch Biomed Sci, Dept Lab Med, Nagasaki 8528523, Japan

[3] Nagasaki Univ, Grad Sch Biomed Sci, Dept Hematol, Nagasaki 8528523, Japan

来源：

LEUKEMIA RESEARCH | 2007年 / 31卷 / 12期

关键词：

ATLL; p14(ARF); p53; Pokemon; prognosis; CYCLE CONTROL GENES; TUMOR-SUPPRESSOR; LEUKEMIA-LYMPHOMA; INK4A LOCUS; METHYLATION; PROTEIN; P53; EXPRESSION; P19(ARF); PRODUCT;

D O I：

10.1016/j.leukres.2006.12.007

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The INK4a/ARF locus encodes two different proteins, p16(INK4a) and p14(ARF), which are crucial for two tumor suppressor pathways. We found that p14(ARF) mRNA expression was suppressed in 13 of 37 cases, among which 9 cases showed the inactivation of both of p14(ARF) and p16(INK4a), and 4 cases showed the inactivation of p14(ARF) alone. The inactivation of p14(ARF) and the mutation of p53 are mutually exclusive. The patients with the p14(ARF) inactivation had shorter survival, similar to that of patients with the p53 mutation. These results indicate that the inactivation of p14(ARF) plays a key role in the progression of ATLL. (C) 2006 Elsevier Ltd. All rights reserved.

引用

页码：1625 / 1632

页数：8

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