Overexpression of ETS-1 is associated with malignant biological features of prostate cancer

15Citations
Citations of this article
22Readers
Mendeley users who have this article in their library.

Abstract

E26 transformation-specific-1 (ETS-1), an ETS family transcription factor, has been reported to play an important role in a variety of physiological and pathological processes, but clinical implications of ETS-1 expression in prostate cancer (PCa), particularly high-risk cases, including response to androgen-deprivation therapy (ADT) have yet to be elucidated. We examined the expression of ETS-1 using immunohistochemical staining of paraffin-embedded prostate carcinoma tissue obtained by needle biopsy from 69 mostly advanced PCa patients. ETS-1 expression was compared with the clinicopathological characteristics of the 69 patients, including 25 who underwent ADT as a primary treatment. As a result, PCa patients with higher expression of ETS-1 were significantly more likely to be of high stage and high Gleason score (P0.05). There was no significant association between ETS-1 expression and the initial prostate-specific antigen (PSA) level. In the 25 patients treated by ADT, the staining score for ETS-1 was significantly associated with rapid development of castration-resistant disease within 24 months (P0.05), whereas the Gleason score and PSA level were not. In conclusion, increased ETS-1 expression was associated with a higher stage, higher Gleason score and shorter time to castration-resistant progression. These data suggest that immunostaining for ETS-1 could be a molecular marker for predicting a poor clinical outcome for PCa patients, particularly those with high-risk disease. © 2012 AJA, SIMM & SJTU. All rights reserved.

Cite

CITATION STYLE

APA

Li, B., Shimizu, Y., Kobayashi, T., Terada, N., Yoshimura, K., Kamba, T., … Ogawa, O. (2012). Overexpression of ETS-1 is associated with malignant biological features of prostate cancer. Asian Journal of Andrology, 14(6), 860–863. https://doi.org/10.1038/aja.2012.107

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free