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2015 Fiscal Year Final Research Report

Functional analysis of FOXA1 in castration resistant prostate cancer and development of nomogram

Research Project

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Project/Area Number 25462469
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Urology
Research InstitutionChiba University

Principal Investigator

Sakamoto Shinichi  千葉大学, 医学(系)研究科(研究院), 助教 (70422235)

Project Period (FY) 2013-04-01 – 2016-03-31
KeywordsCastration Resistance / Prostate Cancer / Androgen Receptor / Testosterone
Outline of Final Research Achievements

Through the immunohistochemical analysis, we have reported over expression of FOXA1 cause short time before acquire castration resistance. We have identified overexpression of aminoacid transporter; LAT1 in castration resistant prostate cancer and reporterd anti-androgen therapy incraese LAT1 expression, thus reported singificance of LAT1 in novel castration resistant mechanism(J Urol 2016). Through the analyisis of prostate cancer patients received hormonal therapy, we have identified testosterone 20ng/dL was the significant prognostic factor. Thus proposed testosterone 20ng/dL should be the ideal castration level in prostate cancer patients during hormonal therapy(J Urol 2015).

Free Research Field

前立腺癌

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Published: 2017-05-10  

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