ORCID Profile
0000-0003-0374-1181
Current Organisation
University of South Australia
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Publisher: Elsevier BV
Date: 03-2007
DOI: 10.1016/J.JSBMB.2006.12.041
Abstract: The biologically active form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), regulates osteoblast proliferation and differentiation. Production of 1,25(OH)(2)D(3) is catalysed by the enzyme 25-hydroxyvitamin D(3)-1alpha-hydroxylase (CYP27B1). Though highly expressed in the kidney, the CYP27B1 gene is also expressed in non-renal tissues including bone. It is hypothesised that local production of 1,25(OH)(2)D(3) by osteoblasts plays an autocrine or paracrine role. The aim of this study was to investigate what factors regulate expression of the CYP27B1 gene in osteoblast cells. ROS 17/2.8 osteoblast cells were transiently transfected with plasmid constructs containing the 5'-flanking sequence of the human CYP27B1 gene fused to a luciferase reporter gene. Cells were treated with either parathyroid hormone (PTH), 1,25(OH)(2)D(3), transforming growth factor-beta (TGF-beta) or insulin-like growth factor-1 (IGF-1) and luciferase activity was measured 24h later. The results showed that 1,25(OH)(2)D(3) did not alter expression of the reporter construct, however treatment with PTH, IGF-1 and TGF-beta decreased expression by 18, 53 and 58% respectively. The repressive action of TGF-beta was isolated to the region between -531 and -305bp. These data suggest that expression of the 5'-flanking region for the CYP27B1 gene in osteoblast cells may be regulated differently to that previously described in kidney cells.
Publisher: Elsevier BV
Date: 08-2020
DOI: 10.1016/J.AMJSURG.2019.11.032
Abstract: Optimal management for papillary thyroid microcarcinoma (PTMC) remains controversial. The purpose of this study was to explore risk factors predictive of cervical lymph node metastasis in conventional PTMCs. Conventional PTMC patients (n = 2,404) undergoing surgery between 2010 and 2017 were grouped and analyzed according to the positivity of cervical lymph node. Central lymph node (CLN) metastases and lateral lymph node (LLN) metastases were observed in 915 (38.1%) and 184 (7.7%) cases, respectively. Multivariate analysis found that male (odds ratio [OR] = 1.974, p < 0.001), younger age (OR = 1.601, p < 0.001), tumor size (OR = 1.935, p < 0.001), extrathyroidal extension (ETE) (OR = 1.647, p < 0.001), multifocality (OR = 1.416, p < 0.001), and intrathyroidal spreading (OR = 3.355, p < 0.001) predicted increased CLN metastasis. In particular, younger age, multifocality, and intrathyroidal spreading were significantly associated with a high number of CLN metastases (n ≥ 5). The presence of CLN metastasis was strongly associated with LLN metastasis (OR = 5.426, p < 0.001). Male, younger age, tumor size, ETE, multifocality, and intrathyroidal spreading predict increased CLN metastasis in PTMCs. In patients with suspicious lateral lymphadenopathy, the presence of CLN metastasis is independently associated with LLN metastasis.
Publisher: Elsevier BV
Date: 10-2013
DOI: 10.1016/J.CCA.2013.07.024
Abstract: Vitamin D activity requires an adequate vitamin D status as indicated by the serum level of 25-hydroxyvitamin D and appropriate expression of genes coding for vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase, the enzyme which converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. Vitamin D deficiency contributes to the aetiology of osteomalacia and osteoporosis. The key element of osteomalacia, or rickets in children, is a delay in mineralization. It can be resolved by normalisation of plasma calcium and phosphate homeostasis independently of vitamin D activity. The well characterised endocrine pathway of vitamin D metabolism generates plasma 1,25-dihydroxyvitamin D and these endocrine activities are solely responsible for vitamin D regulating plasma calcium and phosphate homeostasis and protection against osteomalacia. In contrast, a large body of clinical data indicate that an adequate serum 25-hydroxyvitamin D level improves bone mineral density protecting against osteoporosis and reducing fracture risk. Recent research demonstrates that the three major bone cell types have the capability to metabolise 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D to activate the vitamin D receptor and modulate gene expression. Dietary calcium intake interacts with vitamin D metabolism at both the renal and bone tissue levels to direct either a catabolic action on bone through the endocrine system when calcium intake is inadequate or an anabolic action through a bone autocrine or paracrine system when calcium intake is sufficient.
Publisher: Springer Science and Business Media LLC
Date: 03-04-2017
DOI: 10.1038/ONC.2017.66
Abstract: Missense mutations in the TP53 tumor-suppressor gene inactivate its antitumorigenic properties and endow the incipient cells with newly acquired oncogenic properties that drive invasion and metastasis. Although the oncogenic effect of mutant p53 transcriptome has been widely acknowledged, the global influence of mutant p53 on cancer cell proteome remains to be fully elucidated. Here, we show that mutant p53 drives the release of invasive extracellular factors (the 'secretome') that facilitates the invasion of lung cancer cell lines. Proteomic characterization of the secretome from mutant p53-inducible H1299 human non-small cell lung cancer cell line discovered that the mutant p53 drives its oncogenic pathways through modulating the gene expression of numerous targets that are subsequently secreted from the cells. Of these genes, alpha-1 antitrypsin (A1AT) was identified as a critical effector of mutant p53 that drives invasion in vitro and in vivo, together with induction of epithelial-mesenchymal transition markers expression. Mutant p53 upregulated A1AT transcriptionally through the involvement with its family member p63. Conditioned medium containing secreted A1AT enhanced cell invasion, while an A1AT-blocking antibody attenuated the mutant p53-driven migration and invasion. Importantly, high A1AT expression correlated with increased tumor stage, elevated p53 staining and shorter overall survival in lung adenocarcinoma patients. Collectively, these findings suggest that A1AT is an indispensable target of mutant p53 with prognostic and therapeutic potential in mutant p53-expressing tumors.
Publisher: Wiley
Date: 08-2008
DOI: 10.1359/JBMR.080310
Publisher: Springer Science and Business Media LLC
Date: 13-05-2020
Publisher: Elsevier BV
Date: 04-2020
Publisher: Elsevier BV
Date: 07-2013
DOI: 10.1016/J.JSBMB.2012.11.016
Abstract: In osteoblast cultures, 1,25-dihydroxyvitamin D (1,25D) has been shown to play either catabolic or anabolic roles on differentiation and mineralisation. We have employed osteoblast-like cells extracted from neonatal mouse calvariae and cells derived from juvenile mouse long bones to compare the biological effects of 1,25D on differentiation and mineralisation in vitro. 1,25D exerts differential effects on osteoblast-like cells depending on their stage of maturation and possibly their skeletal origin. This article is part of a Special Issue entitled 'Vitamin D Workshop'.
Publisher: Elsevier BV
Date: 08-2012
DOI: 10.1016/J.CLINBIOCHEM.2012.02.020
Abstract: The endocrine action of plasma 1,25-dihydroxyvitamin D plays a key role in the regulation of plasma calcium and phosphate homeostasis with activities on the intestine, kidney and bone. A current, controversial question is whether vitamin D exerts direct actions on bone cells to regulate bone mineral homeostasis. Results from clinical, rodent model and in vitro studies on human bone cells provide an impressive body of data to support this proposal particularly at the level of serum 25-hydroxyvitamin D status. Each of the major bone cell types is capable of metabolising vitamin D to the active metabolite, 1,25-dihydroxyvitamin D. Thus under conditions when bone tissue synthesis of 1,25-dihydroxyvitamin D is optimal, vitamin D activity enhances bone mineral status. Dietary calcium and phosphate intakes are the critical environmental cues together with vitamin D status to determine whether 1,25-dihydroxyvitamin D exerts an anabolic or catabolic action on bone mineral status.
Publisher: Elsevier BV
Date: 07-2013
DOI: 10.1016/J.JSBMB.2012.08.008
Abstract: A current controversial question related to vitamin D supplementation is what level of serum 25-hydroxyvitamin D3 (25(OH)D3) is required to reduce the incidence of osteoporotic fractures. The reasoning behind vitamin D supplementation has been mostly derived from the role of vitamin D to promote intestinal calcium absorption and reduce bone resorption. While minimum 25(OH)D3 levels of 20nmol/L are required for sufficient intestinal calcium absorption to prevent osteomalacia, the mechanistic details of how higher 25(OH)D3 levels, well beyond that required for optimal calcium absorption, are able to prevent fractures and increase bone mineral density is unclear. Substantial evidence has arisen over the past decade that conversion of 25(OH)D3 to 1,25(OH)2D3via the 1-alpha hydroxylase (CYP27B1) enzyme in osteoblasts, osteocytes, chondrocytes and osteoclasts regulates processes such as cell proliferation, maturation and mineralization as well as bone resorption, which are all dependent on the presence the of the vitamin D receptor (VDR). We and others have also shown that increased vitamin D activity in mature osteoblasts by increasing levels of VDR or CYP27B1 leads to improved bone mineral volume using two separate transgenic mouse models. While questions remain regarding activities of vitamin D in bone to influence the anabolic and catabolic processes, the biological importance of vitamin D activity within the bone is unquestioned. However, a clearer understanding of the varied mechanisms by which vitamin D directly and indirectly influences mineral bone status are required to support evidence-based recommendations for vitamin D supplementation to reduce the risk of fractures. This article is part of a Special Issue entitled 'Vitamin D workshop'.
Publisher: Elsevier BV
Date: 07-2019
DOI: 10.1016/J.JACI.2019.01.053
Abstract: Mobile health can be used to generate innovative insights into optimizing treatment to improve allergic rhinitis (AR) control. A cross-sectional real-world observational study was undertaken in 22 countries to complement a pilot study and provide novel information on medication use, disease control, and work productivity in the everyday life of patients with AR. A mobile phone app (Allergy Diary, which is freely available on Google Play and Apple stores) was used to collect the data of daily visual analogue scale (VAS) scores for (1) overall allergic symptoms (2) nasal, ocular, and asthma symptoms (3) work and (4) medication use by using a treatment scroll list including all allergy medications (prescribed and over-the-counter) customized for 22 countries. The 4 most common intranasal medications containing intranasal corticosteroids and 8 oral H Nine thousand one hundred twenty-two users filled in 112,054 days of VASs in 2016 and 2017. Assessment of days was informative. Control of days with rhinitis differed between no (best control), single (good control for intranasal corticosteroid-treated days), or multiple (worst control) treatments. Users with the worst control increased the range of treatments being used. The same trend was found for asthma, eye symptoms, and work productivity. Differences between oral H This study confirms the usefulness of the Allergy Diary in accessing and assessing behavior in patients with AR. This observational study using a very simple assessment tool (VAS) on a mobile phone had the potential to answer questions previously thought infeasible.
Publisher: Elsevier BV
Date: 04-2018
DOI: 10.1016/J.JSBMB.2018.02.006
Abstract: The biologically active form of vitamin D
Publisher: IMR Press
Date: 2012
DOI: 10.2741/409
Abstract: Vitamin D status relates to two bone diseases, osteomalacia and osteoporosis which arise from distinct pathophysiogical pathways. They can occur in children as well as adults. Osteomalacia or rickets arises from a delay in mineralization and can be caused by severe vitamin D deficiency where the key to curing osteomalacia is the endocrine action of circulating 1,25-dihydroxyvitamin D to normalize the active intestinal transport of calcium and phosphate. Osteoporosis or sub-optimal bone mineral accretion during growth is a risk factor for fracture in children. Current evidence suggests serum 25-hydroxyvitamin D levels between 20 and 80 nmol/L are associated with decreased bone mineral content as a result, at least partly, of reduced vitamin D metabolism and activity within bone cells. The local synthesis of 1,25-dihydroxyvitamin D within bone is necessary to modulate bone resorption and promote bone formation. Thus an adequate vitamin D status is necessary for vitamin D activity within bone to establish a healthy skeleton.
Publisher: Elsevier BV
Date: 02-2011
DOI: 10.1016/J.BONE.2010.09.013
Abstract: Despite the therapeutic value of calcitonin in treating bone disease, a biological role of endogenous calcitonin is controversial. Having previously demonstrated that the CTR has a biological role in protecting against calcium stress using a global CTRKO mouse model, the purpose of this study was to determine whether the protection conferred by the CTR during induced hypercalcemia is mediated via CTR expression on osteoclasts. Mice were generated, in which the CTR was deleted specifically within osteoclasts (OCL-CTRKOs) and compared with mice in which the CTR was deleted globally (global CTRKOs). Significantly, peak serum calcium levels following induced hypercalcemia were >18% higher in global-CTRKOs and OCL-CTRKOs than controls (P<0.01) due to increased bone resorption (P<0.05). Peak serum calcium levels relative to controls were greater in global-CTRKO males than OCL-CTRKO males (P<0.001), which may, at least in part, be due to increased reabsorption of calcium in the kidney (P<0.01). Controls for all analyses were sex-matched littermates with normal CTR expression. In conclusion, the CTR protects against hypercalcemia predominantly via its inhibitory action on osteoclasts.
Publisher: Elsevier BV
Date: 11-2009
DOI: 10.1016/J.MCE.2009.06.001
Abstract: Synthesis of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is catalysed by the enzyme 25-hydroxyvitamin D(3)-1alpha-hydroxylase (CYP27B1). Regulation of CYP27B1 gene expression is poorly understood, particularly in non-renal tissues including bone where 1,25(OH)(2)D(3) is hypothesised to serve autocrine aracrine roles. Transient transfection of ROS 17/2.8 osteoblast-like cells with reporter gene constructs containing deletions of the 5'-flanking region of the human CYP27B1 gene revealed a proximal promoter, enhancer region and strong upstream repressive region. Putative CCAAT and GC boxes, as well as Ets protein binding sites were shown to contribute to promoter and enhancer activities respectively in common with kidney and prostate cells. Inhibition of basal expression was largely attributed to a palindrome 5'-GTCTCAGAC-3' (-1015/-1007bp) that contains two putative canonical Smad binding elements. We conclude that repression of CYP27B1 gene expression may be a common event but the novel inhibitory elements we have identified may be unique to osteoblasts.
Publisher: Elsevier BV
Date: 07-2010
DOI: 10.1016/J.JSBMB.2010.03.021
Abstract: Although the regulation of renal 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1) is reasonably well understood, the same cannot be said about the regulation of bone CYP27B1 expression. We have compared the regulation of kidney and bone CYP27B1 expression with modulation of dietary vitamin D and calcium levels. Vitamin D-deplete and vitamin D-replete female Sprague-Dawley rats were fed either 1% Ca (HC) or 0.1% Ca (LC) diets from 6 months of age. At 9 months of age, animals were killed for mRNA analyses from kidney and bone by real-time RT-PCR. Additionally, primary bone cells were cultured from pCYP27B1-Luc reporter mice in pro-osteogenic media over 15 days and analysed for mRNA for CYP27B1 and other osteogenic markers. In vivo expression of bone CYP27B1 mRNA was independent of changes to kidney CYP27B1 levels with both serum 1,25D and PTH as negative determinants of bone CYP27B1 mRNA levels. Bone cells in pro-mineralising conditions significantly increased CYP27B1 promoter activity over 15 days (P<0.001) which preceded marked increases in alkaline phosphatase, osteocalcin and vitamin D receptor mRNA expression and mineral deposition. These findings confirm that the regulation of bone CYP27B1 is unique from that in the kidney, and may play an important role in bone formation.
Publisher: Elsevier BV
Date: 12-2011
DOI: 10.1016/J.MCE.2011.05.024
Abstract: The endocrine activity of 1,25-dihydroxyvitamin D (1,25(OH)(2)D(3)) contributes to maintaining plasma calcium and phosphate homeostasis through actions on the intestine, kidney and bone. A significant body of evidence has been published over the last 10 years indicating that all major bone cells have the capacity to metabolise 25-hydroxyvitamin D (25(OH)D(3)) to 1,25(OH)(2)D(3), which in turn exerts autocrine aracrine actions to regulate bone cell proliferation and maturation as well as bone mineralisation and resorption. In vivo and in vitro studies indicate that these autocrine aracrine activities of 1,25(OH)(2)D(3) in bone tissue contribute to maintaining bone mineral homeostasis and enhancing skeletal health.
Publisher: Bentham Science Publishers Ltd.
Date: 31-12-2013
DOI: 10.2174/138945011131400212
Abstract: The active form of vitamin D, 1,25-dihydroxyvitamin D3, carries out its erse range of biological activities by binding to the nuclear vitamin D receptor, present in almost every cell of the body. It is well established that adequate serum 25-hydroxyvitamin D levels correlate with a reduction in the incidence of osteoporosis however, the physiological basis for this relationship remains elusive. Although, the endocrine actions of vitamin D are thoroughly appreciated, the effect of vitamin D on bone tissue and bone cells is yet to be completely understood. There exists a wealth of literature that suggests the VDR within the three major bone cell types, osteoblasts, osteocytes and osteoclasts, is responsible for the regulation of bone homeostasis. The circumstances, under which the action of 1,25-dihydroxyvitamin D3 elicits an anabolic or catabolic role have not been elucidated. However, it would seem that vitamin D can evoke both of these effects and that this is partly mediated by calcium homeostasis. This raises the possibility that dietary calcium intake and vitamin D metabolism act concomitantly at the kidney, intestine and the bone in a coordinated response. Thus, to maintain adequate bone homeostasis and reduce the risk of metabolic bone disease via the diet, it is important to consider this duality of vitamin D action in relation to the overall calcium economy.
Publisher: American Chemical Society (ACS)
Date: 10-10-2016
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.MCE.2015.06.005
Abstract: While vitamin D supplementation is common, the anabolic mechanisms that improve bone status are poorly understood. Under standard mineralising conditions including media ionised calcium of 1.1 mM, 1,25-dihydroxyvitamin D3 (1,25D) enhanced differentiation and mineral deposition by the mature osteoblast re-osteocyte cell line, MLO-A5. This effect was markedly increased with a higher ionised calcium level (1.5 mM). Gene expression analyses revealed that 1,25D-induced mineral deposition was associated with induction of Enpp1 mRNA, coding for nucleotide pyrophosphatase phosphodiesterase 1 (NPP1) and NPP1 protein levels. Since MLO-A5 cells express abundant alkaline phosphatase that was not further modified by 1,25D treatment or exposure to increased calcium, this finding suggested that the NPP1 production of pyrophosphate (PPi) may provide alkaline phosphatase with substrate for the generation of inorganic phosphate (Pi). Consistent with this, co-treatment with Enpp1 siRNA or a NPP1 inhibitor, PPADS, abrogated 1,25D-induced mineral deposition. These data demonstrate that 1,25D stimulates osteoblast differentiation and mineral deposition, and interacts with the extracellular calcium concentration. 1,25D regulates Enpp1 expression, which presumably, in the context of adequate tissue non-specific alkaline phosphatase activity, provides Pi to stimulate mineralisation. Our findings suggest a mechanism by which vitamin D with adequate dietary calcium can improve bone mineral status.
Publisher: Elsevier BV
Date: 11-2016
DOI: 10.1016/J.JSBMB.2016.03.004
Abstract: Clinical and animal data indicate that serum 25-hydroxyvitamin D
Publisher: Bioscientifica
Date: 08-2021
DOI: 10.1530/EC-21-0217
Abstract: Multiple studies have reported the increased incidence of thyroid cancer in patients with primary hyperparathyroidism (PHPT). However, the underlying risk factors of concomitant thyroid cancer in patients with PHPT remain unknown. The primary aim of this study was to examine the records of patients with PHPT to identify characteristics that correlated with the presence of coexisting thyroid nodules, and which may have an implication for the prediction of thyroid cancer. Medical records of consecutive patients with PHPT ( n = 318) were reviewed from January 2010 to September 2020 in two tertiary medical centers in China. Patient clinicopathological and biological data were collected and analyzed. Of a total of 318 patients with PHPT, 105 (33.0%) patients had thyroid nodules and 26 (8.2%) patients were concomitant with thyroid cancer. A total of 38 thyroid nodules taken from 26 patients were pathologically assessed to be well-differentiated papillary thyroid carcinoma (PTC), with 81% being papillary thyroid microcarcinoma (PTMC). In 79% (30/38) of these cancers, thyroid nodules were considered suspicious following preoperative ultrasound. Multinomial logistic regression analysis revealed that female gender was associated with increased risk of thyroid nodules (OR = 2.13, 95% CI: 1.13–3.99, P = 0.019), while lower log-transformed parathyroid hormone levels were an independent predictor of thyroid cancer in patients with PHPT (OR = 0.50, 95% CI: 0.26–0.93, P = 0.028). In conclusion, we observed a relatively high prevalence of thyroid cancer in our cohort of Chinese patients with PHPT. Evaluation of thyroid nodules by preoperative ultrasound may be advisable in patients with PHPT, particularly for females and patients with modestly elevated serum parathyroid hormone levels.
Publisher: Elsevier BV
Date: 10-2014
DOI: 10.1016/J.JSBMB.2013.10.003
Abstract: Maintenance of an adequate vitamin D status, as indicated by the level of circulating 25-hydroxyvitamin D (25(OH)D), is associated with higher bone mass and decreased risk of fracture. However, the molecular actions of vitamin D hormone (1,25(OH)2D3) in bone are complex, and include stimulation of osteoclastogenesis via RANK-ligand up-regulation, as well as the inhibition of mineralisation. We hypothesise that these ergent data may be reconciled by autocrine actions of 1,25(OH)2D3 which effect skeletal maintenance, as opposed to endocrine 1,25(OH)2D3 which acts to maintain serum calcium homeostasis. We have previously described local metabolism of 1,25(OH)2D3 within osteoblasts, with effects on gene expression and cell function. The aim of the current study was to investigate potential autocrine actions of 1,25(OH)2D3 within cells that exhibit osteocyte-like properties. Late osteoblastic MLO-A5 cells were cultured in the presence of 25(OH)D for 9 days with gene expression analysed pre- and post-mineralisation. Gene expression analysis revealed maturation within this time frame to an osteocyte-like stage, evidenced by increased Dmp1 and Phex mRNA expression. Expression of Cyp27b1 in 25(OH)D treated MLO-A5 cells was associated with elevated media levels of 1,25(OH)2D3 (p<0.05), induction of Cyp24a1 (p<0.001) and elevated ratios of Opg:Rankl mRNA (p<0.01). Chronic 25(OH)D exposure also increased osteocalcin mRNA in MLO-A5 cells, which contrasted with the dose-dependent inhibition of osteocalcin mRNA observed with acute treatment in MLO-Y4 cells (p<0.01). Treatment of MLO-Y4 cells with 25(OH)D also inhibited Phex mRNA expression (p<0.05), whilst Enpp1 gene expression was induced (p<0.01). Overall, the current study demonstrates that osteocyte-like cells convert physiological levels of 25(OH)D to 1,25(OH)2D3, with changes in gene expression that are consistent with increased osteocyte maturation. Although the physiological role of local metabolism of 1,25(OH)2D3 within osteocytes requires further investigation, the abundance and erse functions of this cell type within bone underscore its potential importance. This article is part of a Special Issue entitled '16th Vitamin D Workshop'.
Publisher: Elsevier BV
Date: 05-2019
DOI: 10.1016/J.JSBMB.2019.01.005
Abstract: Active vitamin D (1,25(OH)2D) has been shown to regulate numerous cell processes in mammary cells. Degradation of 1,25(OH)2D is initiated by the mitochondrial enzyme, 25-hydroxyvitamin D 24-hydroxylase (CYP24 A1), and provides local control of 1,25(OH)2D bioactivity. Several reports of the association between elevated CYP24 A1 activity and breast cancer incidence, suggest that CYP24 A1 may be a target for therapeutic intervention. Whether CYP24 A1 activity within the mammary epithelium regulates 1,25(OH)2D levels and mammary gland development is yet to shown. We have used a conditional knockout of the Cyp24a1 gene specifically in the mammary epithelium to demonstrate reduced terminal end bud number, ductal outgrowth and branching during puberty and alveologenesis at early pregnancy, by inhibiting proliferation but not apoptosis in both basal and luminal MECs. In vitro study showed increased sensitivity of luminal MECs to lower levels of 1,25(OH)2D with the ablation of Cyp24a1 activity. In summary, Cyp24a1 within MECs plays an important role in modulating postnatal and pregnancy-associated mammary gland development which provides support for inhibiting CYP24 A1 as a potential approach to activating the vitamin D pathway in breast cancer prevention and therapy.
No related grants have been discovered for Andrew Turner.