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Emerging Roles of DMP1 in Lung Cancer

Departments of ¹ Pathology and ² Cancer Biology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina

Requests for reprints: Kazushi Inoue, Wake Forest University Health Sciences Medical Center Boulevard, Winston-Salem, NC 27157-0001. Phone: 336-716-5863; Fax: 336-716-6757; E-mail: kinoue{at}wfubmc.edu.

Key Words: Dmp1 • K-ras • p19^Arf • p14^ARF • p16^Ink4a • p53 • non–small cell lung cancer (NSCLC) • loss of heterozygosity • deletion • promoter hypermethylation • haploid insufficiency

The Ras-activated transcription factor DMP1 can stimulate Arf transcription to promote p53-dependent cell arrest. One recent study deepens the pathophysiologic significance of this pathway in cancer, first, by identifying DMP1 losses in human lung cancers that lack ARF/p53 mutations, and second, by demonstrating that Dmp1 deletions in the mouse are sufficient to promote K-ras–induced lung tumorigenesis via mechanisms consistent with a disruption of Arf/p53 suppressor function. These findings prompt further investigations of the prognostic value of DMP1 alterations in human cancers and the oncogenic events that can cooperate with DMP1 inactivation to drive tumorigenesis. [Cancer Res 2008;68(12):4487–90]