Westmead Hospital Westmead
Westmead Hospital Westmead
Wong G.,Childrens Hospital at Westmead |
Wong G.,University of Sydney |
Wong G.,Westmead Hospital Westmead |
Lim W.H.,University of Western Australia |
And 11 more authors.
BMC Cancer | Year: 2015
Background: There is increasing evidence that vitamin D deficiency is a risk factor for cancer, however it remains uncertain whether vitamin D deficiency also predisposes to death from cancer. The aim of the study was to determine the association between serum 25-hydroxy-vitamin D (25 (OH) D) concentrations and cancer-specific mortality in a community-based cohort of older post-menopausal women. Methods: Cox proportional regression analyses were conducted to examine the association between serum 25 (OH) D concentrations and the risk of overall and site-specific cancer mortality in a cohort of elderly women. Results: Over a median follow-up time of 10years, a total of 84 cancer deaths were observed. Women with lower serum 25 (OH) D concentrations were at an increased risk of cancer death, but not for incident cancer. The excess risk for cancer death was observed with serum 25 (OH) D concentration less than 64nmol/L (the median value) [adjusted HR: 1.61 (95% CI: 1.02 - 2.54, p=0.04]. For every 30nmol/L reduction in serum 25 (OH) D concentrations, there was a 30% increase in the overall risk of cancer death [adjusted HR: 1.33; 95% CI: 1.03 - 1.72, p=0.02]. The excess risk appeared to be site-specific and greatest in those with haematological cancers [adjusted HR: 2.13: 95% CI: 1.0 - 4.55, p=0.05]. Conclusions: In elderly women, lower serum 25 (OH) D concentrations appear to be an independent risk factor for cancer-specific mortality, but not a risk factor for the development of cancer. © 2015 applies to the data made available in this article, unless otherwise stated.
Ramos E.M.,Massachusetts General Hospital |
Ramos E.M.,University of Porto |
Latourelle J.C.,Boston University |
Gillis T.,Massachusetts General Hospital |
And 41 more authors.
Neurogenetics | Year: 2013
Huntington's disease (HD) is a neurodegenerative disorder characterized by motor, cognitive, and behavioral disturbances. It is caused by the expansion of the HTT CAG repeat, which is the major determinant of age at onset (AO) of motor symptoms. Aberrant function of N-methyl-D-aspartate receptors and/or overexposure to dopamine has been suggested to cause significant neurotoxicity, contributing to HD pathogenesis. We used genetic association analysis in 1,628 HD patients to evaluate candidate polymorphisms in N-methyl-D-aspartate receptor subtype genes (GRIN2A rs4998386 and rs2650427, and GRIN2B rs1806201) and functional polymorphisms in genes in the dopamine pathway (DAT1 3′ UTR 40-bp variable number tandem repeat (VNTR), DRD4 exon 3 48-bp VNTR, DRD2 rs1800497, and COMT rs4608) as potential modifiers of the disease process. None of the seven polymorphisms tested was found to be associated with significant modification of motor AO, either in a dominant or additive model, after adjusting for ancestry. The results of this candidate-genetic study therefore do not provide strong evidence to support a modulatory role for these variations within glutamatergic and dopaminergic genes in the AO of HD motor manifestations. © 2013 The Author(s).
PubMed | Westmead Hospital Westmead
Type: Journal Article | Journal: Journal of medical radiation sciences | Year: 2015
Radiotherapy is an indispensible part of the management of all stages of breast cancer. In this article, the common indications for radiotherapy in the management of early breast cancer (stages 0, I, and II) are reviewed, including whole-breast radiotherapy as part of breast-conserving treatment for early invasive breast cancer and pre-invasive disease of ductal carcinoma in situ, post-mastectomy radiotherapy, locoregional radiotherapy, and partial breast irradiation. Key clinical studies that underpin our current practice are discussed briefly.