A mechanism of cyclin D1 action encoded in the patterns of gene expression in human cancer

被引：337

作者：

Lamb, J

Ramaswamy, S

Ford, HL

Contreras, B

Martinez, RV

Kittrell, FS

Zahnow, CA

Patterson, N

Golub, TR

Ewen, ME

机构：

[1] Harvard Univ, Sch Med, Dept Med Oncol, Boston, MA 02115 USA

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

[3] Harvard Univ, Sch Med, Dept Canc Biol, Boston, MA 02115 USA

[4] Harvard Univ, Sch Med, Dept Biochem, Boston, MA 02115 USA

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

[6] Harvard Univ, Sch Med, Dept Pediat Oncol, Boston, MA 02115 USA

[7] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA

[8] MIT, Whitehead Inst, Ctr Genome Res, Cambridge, MA 02139 USA

[9] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA

[10] Sidney Kimmel Comprehens Canc Ctr, Dept Oncol, Baltimore, MD 21231 USA

来源：

CELL | 2003年 / 114卷 / 03期

关键词：

D O I：

10.1016/S0092-8674(03)00570-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Here we describe how patterns of gene expression in human tumors have been deconvoluted to reveal a mechanism of action for the cyclin D1 oncogene. Computational analysis of the expression patterns of thousands of genes across hundreds of tumor specimens suggested that a transcription factor, C/EBPbeta/Nf-II6, participates in the consequences of cyclin Di overexpression. Functional analyses confirmed the involvement of C/EBPbeta in the regulation of genes affected by cyclin D1 and established this protein as an indispensable effector of a potentially important facet of cyclin D1 biology. This work demonstrates that tumor gene expression databases can be used to study the function of a human oncogene in situ.

引用

页码：323 / 334

页数：12

共 48 条

[31] LYMPHOPROLIFERATIVE DISORDER AND IMBALANCED T-HELPER RESPONSE IN C/EBP-BETA-DEFICIENT MICE [J].