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<art><ui>1897-4287-10-S2-A11</ui><ji>1897-4287</ji><fm>
<dochead>Meeting abstract</dochead>
<bibl>
<title>
<p>Association of tamoxifen use and reduced risk of contralateral breast cancer for BRCA1 and BRCA2 mutation carriers</p>
</title>
<aug>
<au ca="yes" id="A1"><snm>Phillips</snm><fnm>KA</fnm><insr iid="I1"/><insr iid="I2"/></au>
<au id="A2"><snm>Milne</snm><fnm>RL</fnm><insr iid="I2"/></au>
<au id="A3"><snm>Rookus</snm><fnm>MA</fnm><insr iid="I3"/></au>
<au id="A4"><snm>Goldgar</snm><fnm>D</fnm><insr iid="I4"/></au>
<au id="A5"><snm>Friedlander</snm><fnm>M</fnm><insr iid="I5"/></au>
<au id="A6"><snm>McLachlan</snm><fnm>SA</fnm><insr iid="I6"/></au>
<au id="A7"><snm>Buys</snm><fnm>S</fnm><insr iid="I7"/></au>
<au id="A8"><snm>Antoniou</snm><fnm>AC</fnm><insr iid="I8"/></au>
<au id="A9"><snm>Birch</snm><fnm>K</fnm><insr iid="I1"/></au>
<au id="A10"><snm>Terry</snm><fnm>MB</fnm><insr iid="I9"/></au>
<au id="A11"><snm>Easton</snm><fnm>DF</fnm><insr iid="I8"/></au>
<au id="A12"><snm>Weideman</snm><fnm>P</fnm><insr iid="I1"/></au>
<au id="A13"><snm>Daly</snm><fnm>M</fnm><insr iid="I10"/></au>
<au id="A14"><snm>Andrieu</snm><fnm>N</fnm><insr iid="I11"/></au>
<au id="A15"><snm>John</snm><fnm>EM</fnm><insr iid="I12"/></au>
<au id="A16"><snm>Hooning</snm><fnm>MJ</fnm><insr iid="I13"/></au>
<au id="A17"><snm>Andrulis</snm><fnm>IL</fnm><insr iid="I14"/></au>
<au id="A18"><snm>Caldes</snm><fnm>T</fnm><insr iid="I15"/></au>
<au id="A19"><snm>Olsson</snm><fnm>H</fnm><insr iid="I16"/></au>
<au id="A20"><snm>Hopper</snm><fnm>JL</fnm><insr iid="I2"/></au>
</aug>
<insg>
<ins id="I1"><p>Peter MacCallum Cancer Centre, Melbourne, Australia</p></ins>
<ins id="I2"><p>University of Melbourne, Melbourne, Australia</p></ins>
<ins id="I3"><p>Netherlands Cancer Institute, Amsterdam, Netherlands</p></ins>
<ins id="I4"><p>University of Utah, Salt Lake City, USA</p></ins>
<ins id="I5"><p>Prince of Wales Hospital, Randwick, Australia</p></ins>
<ins id="I6"><p>St Vincent&#8217;s Hospital, Melbourne, Australia</p></ins>
<ins id="I7"><p>Huntsman Cancer Institute, Salt Lake City, USA</p></ins>
<ins id="I8"><p>University of Cambridge, Cambridge, UK</p></ins>
<ins id="I9"><p>Columbia University, New York, USA</p></ins>
<ins id="I10"><p>Fox Chase Cancer Center, Philadelphia, USA</p></ins>
<ins id="I11"><p>Institut Curie, Paris, France</p></ins>
<ins id="I12"><p>Northern California Cancer Center, Fremont, USA</p></ins>
<ins id="I13"><p>Erasmus University Medical Center Daniel den Hoed Cancer Center, Rotterdam, Netherlands</p></ins>
<ins id="I14"><p>Ontario Cancer Genetics Network, Cancer Care Ontario, Toronto, Canada</p></ins>
<ins id="I15"><p>Hospital Clinico San Carlos, Madrid, Spain</p></ins>
<ins id="I16"><p>Lund University Hospital, Lund, Sweden</p></ins>
</insg>
<source>Hereditary Cancer in Clinical Practice</source>


<supplement><title><p>Familial Aspects of Cancer 2011 Research and Practice</p></title><editor>Rodney Scott</editor><note>Meeting abstracts</note></supplement><conference><title><p>Familial Aspects of Cancer 2011 Research and Practice: A combined meeting of kConFab, Australian Breast Cancer Family Study, Australian Colorectal Cancer Family Study, Australian Ovarian Cancer Study, Family Cancer Clinics of Australia and New Zealand and kConFab</p></title><location>Kingscliff, Australia</location><date-range>23-26 August 2011</date-range></conference><issn>1897-4287</issn>
<pubdate>2012</pubdate>
<volume>10</volume>
<issue>Suppl 2</issue>
<fpage>A11</fpage>
<url>http://www.hccpjournal.com/content/10/S2/A11</url>
<xrefbib><pubid idtype="doi">10.1186/1897-4287-10-S2-A11</pubid></xrefbib>
</bibl>
<history><pub><date><day>12</day><month>4</month><year>2012</year></date></pub></history>
<cpyrt><year>2012</year><collab>Phillips et al; licensee BioMed Central Ltd.</collab><note>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</note></cpyrt>
</fm><bdy>
<sec>
<st>
<p>Background</p>
</st>
<p>The efficacy of tamoxifen as a breast cancer (BC) prevention strategy for <it>BRCA1</it> and <it>BRCA2</it> mutation carriers is uncertain.</p>
</sec>
<sec>
<st>
<p>Patients and methods</p>
</st>
<p>Female <it>BRCA1</it> and <it>BRCA2</it> mutation carriers, with a personal history of BC since 1970, enrolled in any of the BC family studies, kConFab (Kathleen Cuningham Foundation Consortium for Research into Familial Breast Cancer), IBCCS (International BRCA1 and BRCA2 Carrier Cohort Study), or BCFR (Breast Cancer Family Registry) were eligible. Those with bilateral disease at first BC diagnosis, tamoxifen use prior to their first BC diagnosis, or another invasive cancer with were excluded. Data were self-reported at entry into the cohort and at follow-up. Hazard ratios (HRs) for development of contralateral BC associated with tamoxifen use after first BC diagnosis were estimated using Cox proportional hazards, modeling time from diagnosis of first primary BC, adjusting for year of birth (continuous), age at diagnosis (continuous), country and bilateral oophorectomy (yes/no, time-varying). Data were censored at contralateral mastectomy, death or loss to follow-up.</p>
</sec>
<sec>
<st>
<p>Results</p>
</st>
<p>Of 1642 <it>BRCA1</it> and 919 <it>BRCA2</it> mutation carriers, 374 (23%) and 444 (48%), respectively, took tamoxifen after their first BC diagnosis. During 21,344 person-years of follow-up, 596 contralateral BCs were observed. Overall, the adjusted HR estimates were 0.31 (95% CI: 0.22-0.45) and 0.24 (95% CI 0.16-0.35) for <it>BRCA1</it> and <it>BRCA2</it> mutation carriers, respectively. After left-truncating the analysis at time of recruitment, the adjusted HR estimates were 0.52 (95% CI: 0.26-1.04) and 0.39 (95% CI: 0.17-0.89) from studying 629 <it>BRCA1</it> and 412 <it>BRCA2</it> mutation carriers, respectively, with 4,869 person-years of follow-up.</p>
</sec>
<sec>
<st>
<p>Conclusions</p>
</st>
<p>Although biased estimates due to non-random use of tamoxifen cannot be excluded, these results are consistent with tamoxifen reducing BC risk for both <it>BRCA1</it> and <it>BRCA2</it> mutation carriers.</p>
</sec>
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