5-Alpha-reductase inhibition and prostate cancer prevention
Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for normal and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving cellular growth and division. Therefore, an altered e...
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Veröffentlicht in: | Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 1994-03, Vol.3 (2), p.177 |
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creator | Brawley, O W Ford, L G Thompson, I Perlman, J A Kramer, B S |
description | Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for normal
and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving
cellular growth and division. Therefore, an altered endocrine state, such as suppression of dihydrotestosterone activity,
may have an impact on prostate cells inhibiting carcinogenic transformation. In vitro and in vivo preclinical observations
support this hypothesis. A placebo-controlled randomized trial using finasteride, an inhibitor of the enzyme that converts
testosterone to dihydrotestosterone, is planned. The endpoint of this trial will be reduction of prostate cancer incidence. |
format | Article |
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and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving
cellular growth and division. Therefore, an altered endocrine state, such as suppression of dihydrotestosterone activity,
may have an impact on prostate cells inhibiting carcinogenic transformation. In vitro and in vivo preclinical observations
support this hypothesis. A placebo-controlled randomized trial using finasteride, an inhibitor of the enzyme that converts
testosterone to dihydrotestosterone, is planned. The endpoint of this trial will be reduction of prostate cancer incidence.</description><identifier>ISSN: 1055-9965</identifier><identifier>EISSN: 1538-7755</identifier><identifier>PMID: 8049641</identifier><language>eng</language><publisher>United States: American Association for Cancer Research</publisher><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology ; 5-alpha Reductase Inhibitors ; Cell Transformation, Neoplastic - drug effects ; Cell Transformation, Neoplastic - pathology ; Dihydrotestosterone - metabolism ; Humans ; Male ; Neoplasms, Hormone-Dependent - mortality ; Neoplasms, Hormone-Dependent - pathology ; Neoplasms, Hormone-Dependent - prevention & control ; Prostate - pathology ; Prostatic Neoplasms - mortality ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms - prevention & control ; Risk Factors ; Survival Rate</subject><ispartof>Cancer epidemiology, biomarkers & prevention, 1994-03, Vol.3 (2), p.177</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8049641$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brawley, O W</creatorcontrib><creatorcontrib>Ford, L G</creatorcontrib><creatorcontrib>Thompson, I</creatorcontrib><creatorcontrib>Perlman, J A</creatorcontrib><creatorcontrib>Kramer, B S</creatorcontrib><title>5-Alpha-reductase inhibition and prostate cancer prevention</title><title>Cancer epidemiology, biomarkers & prevention</title><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><description>Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for normal
and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving
cellular growth and division. Therefore, an altered endocrine state, such as suppression of dihydrotestosterone activity,
may have an impact on prostate cells inhibiting carcinogenic transformation. In vitro and in vivo preclinical observations
support this hypothesis. A placebo-controlled randomized trial using finasteride, an inhibitor of the enzyme that converts
testosterone to dihydrotestosterone, is planned. The endpoint of this trial will be reduction of prostate cancer incidence.</description><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology</subject><subject>5-alpha Reductase Inhibitors</subject><subject>Cell Transformation, Neoplastic - drug effects</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Dihydrotestosterone - metabolism</subject><subject>Humans</subject><subject>Male</subject><subject>Neoplasms, Hormone-Dependent - mortality</subject><subject>Neoplasms, Hormone-Dependent - pathology</subject><subject>Neoplasms, Hormone-Dependent - prevention & control</subject><subject>Prostate - pathology</subject><subject>Prostatic Neoplasms - mortality</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Prostatic Neoplasms - prevention & control</subject><subject>Risk Factors</subject><subject>Survival Rate</subject><issn>1055-9965</issn><issn>1538-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotj0FLAzEQhYMotVZ_grAnb4Fs0tk0eCpFrVDwoucwSWZNpN0uyVbx37uyvbw3jw8e8y7YvAa14loDXI63AODGNHDNbkr5EkJoAzBjs5VYmmZZz9kj8PW-j8gzhZMfsFCVuphcGtKxq7ALVZ-PZcCBKo-dpzxm-qbuH9-yqxb3he7OvmAfz0_vmy3fvb28btY7HqXSA5cuGBLakSTnJASB3hPpUVqhpAFCRKVJBS2C1DVJbGUjpBRNACAR1ILdT739yR0o2D6nA-Zfex4x8oeJx_QZf1ImO72aqRBmH62y0tZaqz_GIVK7</recordid><startdate>19940301</startdate><enddate>19940301</enddate><creator>Brawley, O W</creator><creator>Ford, L G</creator><creator>Thompson, I</creator><creator>Perlman, J A</creator><creator>Kramer, B S</creator><general>American Association for Cancer Research</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19940301</creationdate><title>5-Alpha-reductase inhibition and prostate cancer prevention</title><author>Brawley, O W ; Ford, L G ; Thompson, I ; Perlman, J A ; Kramer, B S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h237t-2bd9e07be2ebb25d0accee7ccef03295eaaa37e3d70d271e2af2602206d55e0d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology</topic><topic>5-alpha Reductase Inhibitors</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Dihydrotestosterone - metabolism</topic><topic>Humans</topic><topic>Male</topic><topic>Neoplasms, Hormone-Dependent - mortality</topic><topic>Neoplasms, Hormone-Dependent - pathology</topic><topic>Neoplasms, Hormone-Dependent - prevention & control</topic><topic>Prostate - pathology</topic><topic>Prostatic Neoplasms - mortality</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Prostatic Neoplasms - prevention & control</topic><topic>Risk Factors</topic><topic>Survival Rate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brawley, O W</creatorcontrib><creatorcontrib>Ford, L G</creatorcontrib><creatorcontrib>Thompson, I</creatorcontrib><creatorcontrib>Perlman, J A</creatorcontrib><creatorcontrib>Kramer, B S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brawley, O W</au><au>Ford, L G</au><au>Thompson, I</au><au>Perlman, J A</au><au>Kramer, B S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>5-Alpha-reductase inhibition and prostate cancer prevention</atitle><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><date>1994-03-01</date><risdate>1994</risdate><volume>3</volume><issue>2</issue><spage>177</spage><pages>177-</pages><issn>1055-9965</issn><eissn>1538-7755</eissn><abstract>Studies of prostate biology support the concept that dihydrotestosterone is the principal androgen responsible for normal
and hyperplastic growth of the prostate gland. Cancer is a process of malignant transformation evolving over time, involving
cellular growth and division. Therefore, an altered endocrine state, such as suppression of dihydrotestosterone activity,
may have an impact on prostate cells inhibiting carcinogenic transformation. In vitro and in vivo preclinical observations
support this hypothesis. A placebo-controlled randomized trial using finasteride, an inhibitor of the enzyme that converts
testosterone to dihydrotestosterone, is planned. The endpoint of this trial will be reduction of prostate cancer incidence.</abstract><cop>United States</cop><pub>American Association for Cancer Research</pub><pmid>8049641</pmid></addata></record> |
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source | MEDLINE; American Association for Cancer Research; EZB Electronic Journals Library |
subjects | 3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology 5-alpha Reductase Inhibitors Cell Transformation, Neoplastic - drug effects Cell Transformation, Neoplastic - pathology Dihydrotestosterone - metabolism Humans Male Neoplasms, Hormone-Dependent - mortality Neoplasms, Hormone-Dependent - pathology Neoplasms, Hormone-Dependent - prevention & control Prostate - pathology Prostatic Neoplasms - mortality Prostatic Neoplasms - pathology Prostatic Neoplasms - prevention & control Risk Factors Survival Rate |
title | 5-Alpha-reductase inhibition and prostate cancer prevention |
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