Requirement for cyclin D3 in lymphocyte development and T cell leukemias

被引：278

作者：

Sicinska, E

Aifantis, L

Le Cam, L

Swat, W

Borowski, C

Yu, QY

Ferrando, AA

Levin, SD

Geng, Y

von Boehmer, H

Sicinski, P ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA

[5] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

[6] Univ Chicago, Dept Med, Chicago, IL 60637 USA

[7] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[8] Univ Washington, Dept Immunol, Seattle, WA 98195 USA

来源：

CANCER CELL | 2003年 / 4卷 / 06期

关键词：

D O I：

10.1016/S1535-6108(03)00301-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The D-type cyclins (cyclins D1, D2, and D3) are components of the core cell cycle machinery in mammalian cells. Cyclin D3 gene is rearranged and the protein is overexpressed in several human lymphoid malignancies. In order to determine the function of cyclin D3 in development and oncogenesis, we generated and analyzed cyclin D3-deficient mice. We found that cyclin D3(-/-) animals fail to undergo normal expansion of immature T lymphocytes and show greatly reduced susceptibility to T cell malignancies triggered by specific oncogenic pathways. The requirement for cyclin D3 also operates in human malignancies, as knock-down of cyclin D3 inhibited proliferation of acute lymphoblastic leukemias deriving from immature T lymphocytes. These studies point to cyclin D3 as a potential target for therapeutic intervention in specific human malignancies.

引用

页码：451 / 461

页数：11

共 62 条

[1] THYMIC TUMORIGENESIS INDUCED BY OVEREXPRESSION OF P56LCK
ABRAHAM, KM
LEVIN, SD
MARTH, JD
FORBUSH, KA
PERLMUTTER, RM
[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (09) : 3977 - 3981
[2] A critical role for the cytoplasmic tail of pTα in T lymphocyte development
Aifantis, I
Borowski, C
Gounari, F
Lacorazza, HD
Nikolich-Zugich, J
von Boehmer, H
[J]. NATURE IMMUNOLOGY, 2002, 3 (05) : 483 - 488
[3] Separation of Notch1 promoted lineage commitment and expansion/transformation in developing T cells
Allman, D
Karnell, FG
Punt, JA
Bakkour, S
Xu, LW
Myung, P
Koretzky, GA
Pui, JC
Aster, JC
Pear, WS
[J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (01) : 99 - 106
[4] Essential roles for ankyrin repeat and transactivation domains in induction of T-cell leukemia by Notch1
Aster, JC
Xu, LW
Karnell, FG
Patriub, V
Pui, JC
Pear, WS
[J]. MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (20) : 7505 - 7515
[5] Cyclin D3: requirement for G1/S transition and high abundance in quiescent tissues suggest a dual role in proliferation and differentiation
Bartkova, J
Lukas, J
Strauss, M
Bartek, J
[J]. ONCOGENE, 1998, 17 (08) : 1027 - 1037
[6] BARTKOVA J, 1995, ONCOGENE, V10, P775
[7] BATES S, 1994, ONCOGENE, V9, P71
[8] Constitutive activation of NF-κB and T-cell leukemia/lymphoma in Notch3 transgenic mice
Bellavia, D
Campese, AF
Alesse, E
Vacca, A
Felli, MP
Balestri, A
Stoppacciaro, A
Tiveron, C
Tatangelo, L
Giovarelli, M
Gaetano, C
Ruco, L
Hoffman, ES
Hayday, AC
Lendahl, U
Frati, L
Gulino, A
Screpanti, I
[J]. EMBO JOURNAL, 2000, 19 (13) : 3337 - 3348
[9] Combined expression of pTα and Notch3 in T cell leukemia identifies the requirement of preTCR for leukemogenesis
Bellavia, D
Campese, AF
Checquolo, S
Balestri, A
Biondi, A
Cazzaniga, G
Lendahl, U
Fehling, HJ
Hayday, AC
Frati, L
von Boehmer, H
Gulino, A
Screpanti, I
[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (06) : 3788 - 3793
[10] Büschges R, 1999, BRAIN PATHOL, V9, P435

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