https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19936 Wed 27 Jul 2022 14:01:52 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18999 Wed 27 Jul 2022 13:53:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34087 Wed 17 Nov 2021 16:20:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24832 Wed 15 Dec 2021 16:10:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:31424 Wed 15 Dec 2021 16:08:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14178 Wed 11 Apr 2018 11:03:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7054 Wed 11 Apr 2018 09:50:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27801 Wed 04 Apr 2018 17:04:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23843 0.999) or in the number of variants predicted to be pathogenic by various in silico tools (Condel, Polyphen2, SIFT, and CADD) in the cases compared to the controls. In addition, there was no difference in the incidence of classic Lynch syndrome cancers in RINT1 rare variant-carrying families compared to RINT1 wild-type families. This study had 90 % power to detect an odds ratio of at least 2.06, and the results do not provide any support for RINT1 being a moderate-penetrance breast cancer susceptibility gene, although larger studies will be required to exclude more modest effects. This study emphasizes the need for caution before designating a cancer predisposition role for any gene based on very rare truncating variants and in silico-predicted missense variants.]]> Wed 02 Mar 2022 14:25:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:165 Thu 25 Jul 2013 09:09:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25887 Thu 21 Jul 2022 15:37:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41461 TP53 vary depending on the subtype, such that ER-negative tumours have a high rate, and in ER-positive tumours they are less common. Previous studies have implicated the intronic polymorphism in TP53 (rs17878362; or PIN3) with an increased risk of developing breast cancer, although little has been discerned on its prevalence in different subtypes. In this study, we investigated the prevalence of the PIN3 genotype in the blood of cohorts with ER-positive and the ER-negative subtype TNBC, and assessed its association with outcome. Methods: We genotyped 656 TNBC and 648 ER-positive breast cancer patients, along with 436 controls, and compared the prevalence of polymorphism rs17878362 in these cohorts. Results: We found there to be no differences in the prevalence of the PIN3 genotype between the ER-positive and TNBC cohorts. Furthermore, no statistically significant difference was observed in the outcome of patients in either cohort with respect to their PIN3 genotype. Conclusions: Taken together, our results do not support an association of the PIN3 genotype with increased breast cancer risk, either in ER-positive or ER-negative patients.]]> Thu 01 Sep 2022 11:19:24 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7415 Sat 24 Mar 2018 08:40:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7576 Sat 24 Mar 2018 08:37:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:8213 Sat 24 Mar 2018 08:36:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:7641 Sat 24 Mar 2018 08:36:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:9541 Sat 24 Mar 2018 08:35:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12510 Sat 24 Mar 2018 08:18:42 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21321 n = 4,798) and at the 12-month landmark (n = 4,682) were used for this report. Cohorts of patients with vasomotor symptoms, AMC symptoms, neither, or both were defined at both 3 and 12 months from randomization. Landmark analyses were performed for disease-free survival (DFS) and for breast cancer free interval (BCFI), using regression analysis to estimate hazard ratios (HR) and 95 % confidence intervals (CI). Median follow-up was 7.0 years. Reporting of AMC symptoms was associated with better outcome for both the 3- and 12-month landmark analyses [e.g., 12-month landmark, HR (95 % CI) for DFS = 0.65 (0.49-0.87), and for BCFI = 0.70 (0.49-0.99)]. By contrast, reporting of vasomotor symptoms was less clearly associated with DFS [12-month DFS HR (95 % CI) = 0.82 (0.70-0.96)] and BCFI (12-month DFS HR (95 % CI) = 0.97 (0.80-1.18). Interaction tests indicated no effect of treatment group on associations between symptoms and outcomes. While reporting of AMC symptoms was clearly associated with better DFS and BCFI, the association between vasomotor symptoms and outcome was less clear, especially with respect to breast cancer-related events.]]> Sat 24 Mar 2018 07:52:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5401 Sat 24 Mar 2018 07:43:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4920 Sat 24 Mar 2018 07:21:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38208 p = 0.02) and consumed more fruit (≥ 2 serves/day; 57.4% to 66.4%; p = 0.01) in the recent survivorship period, but were less likely to be classified in the healthy weight range (p < 0.01). The proportion of non-drinkers and non-smokers slightly increased over the survivorship period. Whole-vegetable intake did not significantly change; however, the intake of non-starchy vegetables significantly increased from pre-diagnosis (LS mean = 89.1g/day) to post-diagnosis, 6 to ≤ 9 years (LS mean = 137.1g/day), and 9 to ≤ 12 years (LS mean = 120.8g/day). There were no significant changes in the total intake of fibre, carotenoids, calcium, fat, saturated fat, vitamin C, or vitamin E observed, except for increased total energy intake (p = 0.012). Conclusion: Before diagnosis, BCSs had similar adherence to health behaviours compared to cancer-free women. Initial positive changes to health behaviours were observed post BC diagnosis, except healthy body weight, but maintenance of such changes over the long-term was poor. BCSs may benefit from additional advice and support to make healthy lifestyle choices throughout survivorship.]]> Mon 29 Jan 2024 17:55:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48509 2 with filgrastim support every 3 weeks for 3 cycles (HDEC) or standard dose epirubicin 75 mg/m² and cyclophosphamide 750 mg/m² every 3 weeks for 6 cycles (SDEC). Primary outcomes were time to progression, overall survival and quality of life. Results: In 118 patients allocated HDEC 90% of the planned dose was delivered, compared to 96% in the 117 participants allocated SDEC. There were no significant differences in the time to disease progression (5.7 vs. 5.8 months, P = 0.19) or overall survival (14.5 vs. 16.5 months, P = 0.29) between HDEC and SDEC, respectively. Patients on HDEC reported worse quality of life during therapy, but scores improved after completion to approximate those reported by patients allocated SDEC. Objective tumour response was recorded in 33 (28%) on HDEC and 42 patients (36%) on SDEC. HDEC produced more haematologic toxicity. Conclusion: For women with metastatic breast cancer, disease progression, survival or quality of life were no better with high-dose intensity compared to standard dose EC chemotherapy. Australian Clinical Trials Registry registration number ACTRN12605000478617.]]> Mon 20 Mar 2023 16:24:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41881 Mon 15 Aug 2022 14:09:04 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44148 Mon 10 Oct 2022 09:17:25 AEDT ]]>