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Identification of genes potentially involved in the acquisition of androgen‐independent and metastatic tumor growth in an autochthonous genetically engineered mouse prostate cancer model
Author(s) -
Morgenbesser Sharon D.,
McLaren Rajashree P.,
Richards Brenda,
Zhang Mindy,
Akmaev Viatcheslav R.,
Winter Scott F.,
Mineva Nora D.,
KaplanLefko Paula J.,
Foster Barbara A.,
Cook Brian P.,
Dufault Michael R.,
Cao Xiahong,
Wang Clarence J.,
Teicher Beverly A.,
Klinger Katherine W.,
Greenberg Norman M.,
Madden Stephen L.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20505
Subject(s) - prostate cancer , tramp , prostate , biology , microarray analysis techniques , cancer research , microarray , cancer , pca3 , tumor progression , metastasis , gene , adenocarcinoma , pathology , gene expression , medicine , genetics
BACKGROUND A major focus of prostate cancer research has been to identify genes that are deregulated during tumor progression, potentially providing diagnostic markers and therapeutic targets. METHODS We have employed serial analysis of gene expression (SAGE) and microarray hybridization to identify alterations that occur during malignant transformation in the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model. Many of these alterations were validated by real‐time PCR (rtPCR). RESULTS We identified several hundred mRNAs that were deregulated. Cluster analysis of microarray profiles with samples from various stages of the disease demonstrated that androgen‐independent (AI) primary tumors are similar to metastases; 180 transcripts have expression patterns suggesting an involvement in the genesis of late‐stage tumors, and our data support a role for phospholipase A2 group IIA in the acquisition of their highly aggressive characteristics. CONCLUSIONS Our analyses identified well‐characterized genes that were previously known to be involved in prostate cancer, validating our study, and also uncovered transcripts that had not previously been implicated in prostate cancer progression. Prostate 67:83–106, 2007. © 2006 Wiley‐Liss, Inc.