https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51129 Tue 22 Aug 2023 15:52:11 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55712 Tue 18 Jun 2024 12:50:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51169 Thu 24 Aug 2023 14:09:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5128 T and N2792S, 8375A>G) to be associated with an allele dose–dependent increase in risk of familial breast cancer in a German population. We extended the analysis of AKAP9 M463I, which is in strong linkage disequilibrium with AKAP9 N2792S, to 9523 breast cancer patients and 13 770 healthy control subjects from seven independent European and Australian breast cancer studies. All statistical tests were two-sided. The collaborative analysis confirmed the association of M463I with increased breast cancer risk. Among all breast cancer patients, the combined adjusted odds ratio (OR) of breast cancer for individuals homozygous for the rare allele TT (frequency = 0.19) compared with GG homozygotes was 1.17 (95% confidence interval [CI] = 1.08 to 1.27, P = .0003), and the OR for TT homozygotes plus GT heterozygotes compared with GG homozygotes was 1.10 (95% CI = 1.04 to 1.17, P = .001). Among the combined subset of 2795 familial breast cancer patients, the respective ORs were 1.27 (95% CI = 1.12 to 1.45, P = .0003) and 1.16 (95% CI = 1.06 to 1.27, P = .001).]]> Sat 24 Mar 2018 07:48:55 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54842 Fri 15 Mar 2024 14:38:56 AEDT ]]>