Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17828
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dc.contributor.authorCheung, Ada S-
dc.contributor.authorYeap, Bu B-
dc.contributor.authorHoermann, Rudolf-
dc.contributor.authorHui, Jennie-
dc.contributor.authorBeilby, John P-
dc.contributor.authorGrossmann, Mathis-
dc.date2017-06-22-
dc.date.accessioned2018-05-31T00:02:51Z-
dc.date.available2018-05-31T00:02:51Z-
dc.date.issued2017-10-
dc.identifier.citationClinical Endocrinology 2017; 87(4): 381-385en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17828-
dc.description.abstractRecent evidence suggests that androgens either directly or via aromatisation to oestradiol may regulate telomere length, hence providing a mechanism whereby reproductive steroids are linked to biological ageing in men. Using men with prostate cancer initiating androgen deprivation therapy (ADT), we tested the hypothesis that severe sex steroid deprivation would accelerate telomere shortening. We conducted a secondary analysis of a 2-year prospective controlled study among 65 men with nonmetastatic prostate cancer newly commencing adjuvant ADT (n=40) and age- and radiotherapy-matched prostate cancer controls (n=25). We measured leucocyte telomere length (LTL) expressed as telomeric/single copy control gene (T/S) ratio at baseline, 6, 12 and 24 months. Generalized linear models determined the mean adjusted difference (MAD) (95% confidence interval) between groups during follow-up. Compared to controls over 24 months, men receiving ADT had no change in LTL, MAD for T/S ratio (0.105 [-0.004; 0.213], P=.235). Using men with prostate cancer receiving ADT as a model we found no evidence that prolonged and profound sex steroid deprivation is associated with accelerated telomere shortening. Larger studies will be required to confirm or refute these findings.en_US
dc.language.isoeng-
dc.subjectandrogensen_US
dc.subjectoestradiolen_US
dc.subjecttelomeresen_US
dc.subjecttestosteroneen_US
dc.titleEffects of androgen deprivation therapy on telomere length.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleClinical Endocrinologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationSchool of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australiaen_US
dc.identifier.affiliationDepartment of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, Western Australia, Australiaen_US
dc.identifier.affiliationPathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australiaen_US
dc.identifier.doi10.1111/cen.13382en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0001-5257-5525en_US
dc.identifier.orcid0000-0002-7612-5892en_US
dc.identifier.orcid0000-0001-8261-3457en_US
dc.identifier.pubmedid28543303-
dc.type.austinJournal Article-
local.name.researcherCheung, Ada S
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptEndocrinology-
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