Nuclear factor I/B is an oncogene in small cell lung cancer

被引：144

作者：

Dooley, Alison L. ^{[1
]}

Winslow, Monte M. ^{[1
]}

Chiang, Derek Y. ^{[2
,3
]}

Banerji, Shantanu ^{[2
,3
]}

Stransky, Nicolas ^{[2
]}

Dayton, Talya L. ^{[1
]}

Snyder, Eric L. ^{[1
]}

Senna, Stephanie ^{[1
]}

Whittaker, Charles A. ^{[1
]}

Bronson, Roderick T. ^{[4
]}

Crowley, Denise ^{[1
]}

Barretina, Jordi ^{[2
,3
]}

Garraway, Levi ^{[2
,3
]}

Meyerson, Matthew ^{[2
,3
]}

Jacks, Tyler ^{[1
,5
]}

机构：

[1] MIT, Dept Biol, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA

[2] Canc Program, Broad Inst, Cambridge, MA 02142 USA

[3] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Dept Med Oncol, Boston, MA 02115 USA

[4] Tufts Univ, Sch Med & Vet Med, Dept Pathol, North Grafton, MA 01536 USA

[5] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA

来源：

GENES & DEVELOPMENT | 2011年 / 25卷 / 14期

关键词：

small cell lung cancer; mouse model; Nuclear factor I/B; CONDITIONAL MOUSE MODEL; MYELOID-LEUKEMIA GENOME; COPY-NUMBER ALTERATIONS; RETINOBLASTOMA GENE; SOMATIC INACTIVATION; TOBACCO EXPOSURE; BREAST-CANCER; LIVER-CANCER; EXPRESSION; CARCINOMA;

D O I：

10.1101/gad.2046711

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed after it has metastasized. Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels. Using a genetically engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung, we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear factor I/B (Nfib), in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation.

引用

页码：1470 / 1475

页数：6

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