The molecular genetics underlying basal cell carcinoma pathogenesis and links to targeted therapeutics

被引：55

作者：

Iwasaki, Julie K.

Srivastava, Divya ^{[2
]}

Moy, Ronald L. ^{[3
,4
]}

Lin, Henry J. ^{[3
,5
,6
]}

Kouba, David J. ^{[1
,7
]}

机构：

[1] Henry Ford Hlth Syst, Dept Dermatol, Div Mohs Microg Surg, Detroit, MI 48202 USA

[2] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA

[3] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA

[4] W Los Angeles Vet Affairs Med Ctr, Los Angeles, CA USA

[5] Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90509 USA

[6] Harbor UCLA Med Ctr, Div Med Genet, Torrance, CA 90509 USA

[7] Toledo Clin Dermasurg & Laser Ctr, Toledo, OH USA

来源：

JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY | 2012年 / 66卷 / 05期

关键词：

carcinoma; basal cell; sonic hedgehog; HEDGEHOG SIGNALING PATHWAY; NONMELANOMA SKIN-CANCER; HUMAN HOMOLOG; N-MYC; EXPRESSION; MUTATIONS; INHIBITION; PROLIFERATION; ACTIVATION; PREVENTS;

D O I：

10.1016/j.jaad.2010.06.054

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100227 [皮肤病学];

摘要：

Mutations in the sonic hedgehog signaling pathway play a key role in the development of basal cell carcinomas. Specifically, mutations in the PTCH1 (also known as PTCH or PTC1) and SMO genes cause tumor formation through constitutive activation of the pathway. Misregulation of the pathway has also been implicated in the nevoid basal cell carcinoma syndrome and other tumors. Understanding the function of the sonic hedgehog pathway has led to novel strategies for treatment. In this review we highlight the role of the pathway in the pathogenesis of basal cell carcinoma and review potential targeted therapies. (J Am Acad Dermatol 2012;66:e167-78.)

引用

页码：E167 / E178

页数：12

共 49 条

[1]

Expression of the PTCH1 tumor suppressor gene is regulated by alternative promoters and a single functional Gli-binding site [J].