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U19/Eaf2 knockout causes lung adenocarcinoma, B-cell lymphoma, hepatocellular carcinoma and prostatic intraepithelial neoplasia
Xiao, W.2,3; Zhang, Q.2; Habermacher, G.2; Yang, X.4,5; Zhang, A-y1,2; Cai, X.2; Hahn, J.2; Liu, J.1; Pins, M.4,5; Doglio, L.6; Dhir, R.7; Gingrich, J.1; Wang, Z.1,2,5,6; Wang, Z, Univ Pittsburgh, Dept Urol, Shadyside Med Ctr, Inst Canc,Sch Med, Suite G40,5200 Ctr Ave, Pittsburgh, PA 15232 USA
2008-03-06
Source PublicationONCOGENE
ISSN0950-9232
Volume27Issue:11Pages:1536-1544
AbstractUpregulated gene 19 (U19)/ELL-associated factor 2 (Eaf2) is a potential human tumor suppressor that exhibits frequent allelic loss and downregulation in high-grade prostate cancer. U19/Eaf2, along with its homolog Eaf1, has been reported to regulate transcriptional elongation via interaction with the eleven-nineteen lysine-rich leukemia (ELL) family of proteins. To further explore the tumor-suppressive effects of U19/Eaf2, we constructed and characterized a murine U19/Eaf2-knockout model. Homozygous or heterozygous deletion of U19/Eaf2 resulted in high rates of lung adenocarcinoma, B-cell lymphoma, hepato cellular carcinoma and prostate intraepithelial neoplasia. Within the mouse prostate, U19/Eaf2 defficiency enhanced cell proliferation and increased epithelial cell size. The knockout mice also exhibited cardiac cell hypertrophy. These data indicate a role for U19/Eaf2 in growth suppression and cell size control as well as argue for U19/Eaf2 as a novel tumor suppressor in multiple mouse tissues. The U19/Eaf2 knockout mouse also provides a unique animal model for three important cancers: lung adenocarcinoma, B-cell lymphoma and hepatocellular carcinoma.; Upregulated gene 19 (U19)/ELL-associated factor 2 (Eaf2) is a potential human tumor suppressor that exhibits frequent allelic loss and downregulation in high-grade prostate cancer. U19/Eaf2, along with its homolog Eaf1, has been reported to regulate transcriptional elongation via interaction with the eleven-nineteen lysine-rich leukemia (ELL) family of proteins. To further explore the tumor-suppressive effects of U19/Eaf2, we constructed and characterized a murine U19/Eaf2-knockout model. Homozygous or heterozygous deletion of U19/Eaf2 resulted in high rates of lung adenocarcinoma, B-cell lymphoma, hepato cellular carcinoma and prostate intraepithelial neoplasia. Within the mouse prostate, U19/Eaf2 defficiency enhanced cell proliferation and increased epithelial cell size. The knockout mice also exhibited cardiac cell hypertrophy. These data indicate a role for U19/Eaf2 in growth suppression and cell size control as well as argue for U19/Eaf2 as a novel tumor suppressor in multiple mouse tissues. The U19/Eaf2 knockout mouse also provides a unique animal model for three important cancers: lung adenocarcinoma, B-cell lymphoma and hepatocellular carcinoma.
SubtypeArticle
KeywordU19/eaf2 Lung Adenocarcinoma B-cell Lymphoma Hepatocellular Carcinoma Prostate Cancer Tumor Suppressor
Department[Zhang, A-y; Liu, J.; Gingrich, J.; Wang, Z.] Univ Pittsburgh, Dept Urol, Shadyside Med Ctr, Inst Canc,Sch Med, Pittsburgh, PA 15232 USA; [Xiao, W.; Zhang, Q.; Habermacher, G.; Zhang, A-y; Cai, X.; Hahn, J.; Wang, Z.] Northwestern Univ, Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA; [Xiao, W.] Chinese Acad Sci, Inst Hydrobiol, Wuhan, Peoples R China; [Yang, X.; Pins, M.] Northwestern Univ, Dept Pathol, Feinberg Sch Med, Chicago, IL 60611 USA; [Yang, X.; Pins, M.; Wang, Z.] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA; [Doglio, L.; Wang, Z.] Northwestern Univ, Feinberg Sch Med, Ctr Genet Med, Chicago, IL 60611 USA; [Dhir, R.] Univ Pittsburgh, Sch Med, Dept Pathol, Inst Canc, Pittsburgh, PA USA
Subject AreaBiochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
DOI10.1038/sj.onc.1210786
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Indexed BySCI
Language英语
WOS Research AreaBiochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
WOS SubjectBiochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
WOS IDWOS:000253815800005
WOS KeywordELONGATION-FACTOR ELL ; TUMOR-SUPPRESSOR ; VASCULAR TUMORS ; FACTOR-2 EAF2 ; CAJAL BODY ; GENE ; POLYMERASE ; MLL ; INACTIVATION ; EXPRESSION
Citation statistics
Cited Times:51[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/8228
Collection期刊论文
Corresponding AuthorWang, Z, Univ Pittsburgh, Dept Urol, Shadyside Med Ctr, Inst Canc,Sch Med, Suite G40,5200 Ctr Ave, Pittsburgh, PA 15232 USA
Affiliation1.Univ Pittsburgh, Dept Urol, Shadyside Med Ctr, Inst Canc,Sch Med, Pittsburgh, PA 15232 USA
2.Northwestern Univ, Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA
3.Chinese Acad Sci, Inst Hydrobiol, Wuhan, Peoples R China
4.Northwestern Univ, Dept Pathol, Feinberg Sch Med, Chicago, IL 60611 USA
5.Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA
6.Northwestern Univ, Feinberg Sch Med, Ctr Genet Med, Chicago, IL 60611 USA
7.Univ Pittsburgh, Sch Med, Dept Pathol, Inst Canc, Pittsburgh, PA USA
Recommended Citation
GB/T 7714
Xiao, W.,Zhang, Q.,Habermacher, G.,et al. U19/Eaf2 knockout causes lung adenocarcinoma, B-cell lymphoma, hepatocellular carcinoma and prostatic intraepithelial neoplasia[J]. ONCOGENE,2008,27(11):1536-1544.
APA Xiao, W..,Zhang, Q..,Habermacher, G..,Yang, X..,Zhang, A-y.,...&Wang, Z, Univ Pittsburgh, Dept Urol, Shadyside Med Ctr, Inst Canc,Sch Med, Suite G40,5200 Ctr Ave, Pittsburgh, PA 15232 USA.(2008).U19/Eaf2 knockout causes lung adenocarcinoma, B-cell lymphoma, hepatocellular carcinoma and prostatic intraepithelial neoplasia.ONCOGENE,27(11),1536-1544.
MLA Xiao, W.,et al."U19/Eaf2 knockout causes lung adenocarcinoma, B-cell lymphoma, hepatocellular carcinoma and prostatic intraepithelial neoplasia".ONCOGENE 27.11(2008):1536-1544.
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