ORCID Profile
0000-0002-6383-4163
Current Organisation
The University of Auckland
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Publisher: Bentham Science Publishers Ltd.
Date: 03-2013
Publisher: MDPI AG
Date: 18-12-2019
DOI: 10.3390/NU12010002
Abstract: Background: There is variable reporting on the benefits of a 200 μg/d selenium supplementation towards reducing prostate cancer impacts. The current analysis is to understand whether stratified groups receive supplementation benefits on prostate health. Methods: 572 men were supplemented with 200 µg/d selenium as selinized yeast for six months, and 481 completed the protocol. Selenium and prostate-specific antigen (PSA) levels were measured in serum at pre- and post-supplementation. Changes in selenium and PSA levels subsequent to supplementation were assessed with and without demographic, lifestyle, genetic and dietary stratifications. Results: The post-supplementation selenium (p = 0.002) and the gain in selenium (p 0.0001) by supplementation were significantly dependent on the baseline selenium level. Overall, there was no significant correlation between changes in PSA and changes in selenium levels by supplementation. However, stratified analyses showed a significant inverse correlation between changes in PSA and changes in selenium in men below the median age (p = 0.048), never-smokers (p = 0.031), men carrying the GPX1 rs1050450 T allele (CT, p = 0.022 and TT, p = 0.011), dietary intakes above the recommended daily intake (RDI) for zinc (p 0.05), and below the RDI for vitamin B12 (p 0.001). Conclusions: The current analysis shows the influence of life factors on prostate health benefits of supplemental selenium.
Publisher: Public Library of Science (PLoS)
Date: 24-05-2019
Publisher: PeerJ
Date: 02-07-2015
DOI: 10.7717/PEERJ.1080
Publisher: Elsevier BV
Date: 05-2006
Publisher: Royal Society of Chemistry (RSC)
Date: 2017
DOI: 10.1039/C7MB00203C
Abstract: Prostate cancer is one of the most significant male health concerns worldwide. Various researchers carrying out molecular diagnostics have indicated that genetic interactions with biological and behavioral factors play an important role in the overall risk and prognosis of this disease. These will be discussed in details with New Zealand perspective.
Publisher: Wiley
Date: 2004
DOI: 10.1002/EM.20029
Abstract: The incidence of colon cancer is high in many developed nations, especially New Zealand. Molecular understanding of the nature of colon cancer shows a disease whose well-characterized morphological progression is paralleled at the cellular level by increased numbers of gene or chromosome mutations, loss of heterozygosity, changed methylation patterns, and genomic instability. In the present study, we consider whether an imbalance of factors that affect DNA methylation patterns might explain at least part of the high colon cancer incidence in New Zealand. Folate is the major micronutrient whose intake impacts methylation, particularly through interaction with choline and methionine. Folate is generally somewhat deficient in the New Zealand diet, with the voluntary addition of folate to white flour not producing desired levels. Selenium affects methylation status in several ways and is recognized as being low in New Zealand soils and, therefore, diet. Zinc is also low in the diets of some New Zealand population groups, which can lead to hypomethylation. Several of the components of fruits and vegetables affect methylation patterns, and the average New Zealand intake, at two to three servings per day, is considerably below recommended amounts. Low dietary fiber, high tobacco use, and increasing rates of obesity are also likely New Zealand risk factors that may impact on methylation status. Dietary supplementation is not as common in New Zealand as in countries such as the United States, but may provide a way to raise the levels of nutrients and phytochemicals affecting methylation status, thereby enhancing colon cancer protection.
Publisher: MDPI AG
Date: 07-09-2012
DOI: 10.3390/NU4091247
Publisher: Elsevier BV
Date: 05-2012
DOI: 10.1016/J.MRFMMM.2011.12.011
Abstract: Selenium (Se) is an essential micronutrient for humans, acting as a component of the unusual amino acids, selenocysteine (Se-Cys) and selenomethionine (Se-Met). Where Se levels are low, the cell cannot synthesise selenoproteins, although some selenoproteins and some tissues are prioritised over others. Characterised functions of known selenoproteins, include selenium transport (selenoprotein P), antioxidant/redox properties (glutathione peroxidases (GPxs), thioredoxin reductases and selenoprotein P) and anti-inflammatory properties (selenoprotein S and GPx4). Various forms of Se are consumed as part of a normal diet, or as a dietary supplement. Supplementation of tissue culture media, animal or human diets with moderate levels of certain Se compounds may protect against the formation of DNA adducts, DNA or chromosome breakage, and chromosome gain or loss. Protective effects have also been shown on mitochondrial DNA, and on telomere length and function. Some of the effects of Se compounds on gene expression may relate to modulation of DNA methylation or inhibition of histone deacetylation. Despite a large number of positive effects of selenium and selenoproteins in various model systems, there have now been some human clinical trials that have shown adverse effects of Se supplementation, according to various endpoints. Too much Se is as harmful as too little, with animal models showing a "U"-shaped efficacy curve. Current recommended daily allowances differ among countries, but are generally based on the amount of Se necessary to saturate GPx enzymes. However, increasing evidence suggests that other enzymes may be more important than GPx for Se action, that optimal levels may depend upon the form of Se being ingested, and vary according to genotype. New paradigms, possibly involving nutrigenomic tools, will be necessary to optimise the forms and levels of Se desirable for maximum protection of genomic stability in all humans.
Publisher: Elsevier BV
Date: 05-2004
Publisher: Frontiers Media SA
Date: 2011
Publisher: Elsevier BV
Date: 08-2006
Abstract: The study provides data relating serum selenium concentration to activities of 2 key selenoenzymes, hemolysate thioredoxin reductase (TR) and glutathione peroxidase (GPx), measured by spectrophotometry, in a group of men at high risk for prostate cancer. This trial enrolled 43 patients with elevated prostate-specific antigen but negative biopsy for prostate cancer. Such in iduals have a high risk of developing prostate cancer in the succeeding 5 y. In the men with baseline serum selenium concentrations ranging from 0.74-1.62 micromol/L (59-128 microg/L), hemolysate TR (r = 0.359, P < 0.05) and GPx (r = 0.341, P < 0.05) activities increased with increasing serum selenium. Furthermore, after a run-in period of 1 mo, men participated in a randomized, double-blind, placebo-controlled selenium supplementation trial for 6 mo and received a placebo, or 200 or 400 microg of Se per day, in the form of a seleno yeast. This study is a subsidiary of an ongoing Phase III cancer chemoprevention trial and, as such, randomization groups have not yet been revealed. After 6 mo of being on trial and with an estimated 66% of the group being supplemented with seleno yeast, the TR activity of the group increased by 80% relative to baseline. In contrast, 6 mo of selenium supplementation did not affect GPx activity. This study presents, to our knowledge for the first time, both measurements of human hemolysate TR activity and its relation to serum selenium.
Publisher: MDPI AG
Date: 27-04-2016
DOI: 10.3390/NU8050249
Publisher: PeerJ
Date: 03-2016
DOI: 10.7717/PEERJ.1731
Abstract: Background. Prostate cancer makes up approximately 15% of all cancers diagnosed in men in developed nations and approximately 4% of cases in developing nations. Although it is clear that prostate cancer has a genetic component and single nucleotide polymorphisms (SNPs) can contribute to prostate cancer risk, detecting associations is difficult in multi-factorial diseases, as environmental and lifestyle factors also play a role. In this study, specific clinical characteristics, environmental factors and genetic risk factors were assessed for interaction with prostate cancer. Methods. A total of 489 prostate cancer cases and 427 healthy controls were genotyped for SNPs found on chromosome 8q24 and a genetic risk score was calculated. In addition the SNPs were tested for an association with a number of clinical and environmental factors. Results. Age and tobacco use were positively associated, whilst alcohol consumption was negatively associated with prostate cancer risk. The following SNPs found on chromosome 8q24 were statistically significantly associated with prostate cancer: rs10086908 , rs16901979 rs1447295 and rs4242382 . No association between Gleason score and smoking status, or between Gleason score and genotype were detected. Conclusion. A genetic risk score was calculated based on the 15 SNPs tested and found to be significantly associated with prostate cancer risk. Smoking significantly contributed to the risk of developing prostate cancer, and this risk was further increased by the presence of four SNPs in the 8q24 chromosomal region.
Publisher: Springer Science and Business Media LLC
Date: 07-01-2022
DOI: 10.1038/S41598-021-04116-8
Abstract: It is being debated whether prostate-specific antigen (PSA)-based screening effectively reduces prostate cancer mortality. Some of the uncertainty could be related to deficiencies in the age-based PSA cut-off thresholds used in screening. Current study considered 2779 men with prostate cancer and 1606 men without a cancer diagnosis, recruited for various studies in New Zealand, US, and Taiwan. Association of PSA with demographic, lifestyle, clinical characteristics (for cases), and the aldo–keto reductase 1C3 ( AKR1C3 ) rs12529 genetic polymorphisms were analysed using multiple linear regression and univariate modelling. Pooled multivariable analysis of cases showed that PSA was significantly associated with demographic, lifestyle, and clinical data with an interaction between ethnicity and age further modifying the association. Pooled multivariable analysis of controls data also showed that demographic and lifestyle are significantly associated with PSA level. Independent case and control analyses indicated that factors associated with PSA were specific for each cohort. Univariate analyses showed a significant age and PSA correlation among all cases and controls except for the US-European cases while genetic stratification in cases showed variability of correlation. Data suggests that unique PSA cut-off thresholds factorized with demographics, lifestyle and genetics may be more appropriate for prostate cancer screening.
Publisher: Springer Science and Business Media LLC
Date: 02-08-2016
Publisher: Springer Science and Business Media LLC
Date: 02-11-2015
Publisher: Bentham Science Publishers Ltd.
Date: 08-2012
Publisher: Elsevier BV
Date: 1991
Publisher: Public Library of Science (PLoS)
Date: 19-06-2018
Publisher: MDPI AG
Date: 10-12-2022
DOI: 10.3390/BIOMEDICINES10123206
Abstract: Introduction-With the high global prevalence of prostate cancer and associated mortalities, it is important to enhance current clinical practices for better prostate cancer outcomes. The current review is towards understanding the value of Zn towards this mission. Method-General information on Zn in biology and multiple aspects of Zn involvement in prostate health and disease were referred to in PubMed. Results-The most influential feature of Zn towards prostate health is its ability to retain sufficient citrate levels for a healthy prostate. Zn deficiencies were recorded in serum, hair, and prostate tissue of men with prostate cancer compared to non-cancer controls. Zn gut absorption, albumin binding, and storage compete with various factors. There are multiple associations of Zn cellular influx and efflux transporters, Zn finger proteins, matrix metalloproteinases, and Zn signaling with prostate cancer outcomes. Such Zn marker variations associated with prostate cancer recorded from biological matrices may improve algorithms for prostate cancer screening, prognosis, and management when coupled with standard clinical practices. Discussion-The influence of Zn in prostatic health and disease is multidimensional, therefore more personalized Zn requirements may be beneficial. Several opportunities exist to utilize and improve understanding of Zn associations with prostate health and disease.
Publisher: Korean Society of Cancer Prevention
Date: 30-09-2017
Publisher: S. Karger AG
Date: 2012
DOI: 10.1159/000346279
Abstract: b i Background: /i /b Prostate cancer is a leading public health burden worldwide, and in New Zealand it is the most commonly registered cancer and the third leading cause of cancer deaths among males. Genetic variability and its associations with diet, demographic and lifestyle factors could influence the risk of this disease. b i Methods: /i /b The single nucleotide polymorphisms (SNPs) within a group of antioxidant genes and related markers were tested between patient and control cohorts, adjusted for significant differences between basic lifestyle and demographic characteristics. b i Results: /i /b Increasing age, smoking and low serum selenium levels were significantly associated with an increased risk for prostate disease. Alcohol consumption increased the glutathione peroxidase (GPx) activity. A significant reduction in alcohol consumption was recorded with prostate disease. Three SNPs, namely i GPx1 /i rs1050450, i SEL15 /i rs5845 and i CAT /i rs1001179, were significantly associated with prostate disease risk. A cumulative risk of prostate cancer was noted with 6 risk alleles. A lower GPx activity was recorded with prostate disease compared to the controls. However, the i GPx1 /i rs1050450 allele T in association with prostate cancer recorded a significantly higher GPx activity compared to the controls. b i Conclusions: /i /b These data point to a possibility of identifying in iduals at risk of prostate cancer for better management purposes.
Publisher: Elsevier BV
Date: 10-2006
Publisher: American Association for Cancer Research (AACR)
Date: 03-2016
DOI: 10.1158/1538-7755.DISP15-C74
Abstract: Background: Androgen deprivation therapy (ADT) is an effective palliation treatment for men with advanced prostate cancer (PC). This is a common treatment received by the majority of PC survivors among New Zealand (NZ) Maori men due to their late presentation of the disease. However, ADT have well documented side effects that could alter the patient's quality of life (QoL). ADT involves suppression of androgens produced either by the testes or the adrenal gland or both. Adrenal androgen production involves conversion of androstenedione to testosterone by the aldo-keto reductase 1C3 (AKR1C3) enzyme. We have previously reported that the AKR1C3 rs12529 G allele is associated with a lower prostate specific antigen (PSA) level, which is a downstream product of androgens binding to the androgen receptor. The AKR1C3 rs12529 G allele frequency is 14.2% higher among Maori, Pacific and East Asian men compared to Caucasians in our study cohort. Therefore, the current assessment is to evaluate whether genetic stratification with the AKR1C3 rs12529 polymorphism could support decision making on ADT to minimize QoL effects. Methods: A patient cohort with confirmed clinical diagnoses of PC was recruited with written consent from 2006-2014 to Urology studies carried out at the Auckland Cancer Society Research Centre, University of Auckland, NZ. Recruitment was carried out at hospitals managed under three District Health Boards of Auckland, and private Urology clinics from Waikato District, in NZ. From May 2013, patients were invited to complete a questionnaire that contained options for selecting PC treatment type/s received and a QoL survey. The primary outcomes were the percentage scores under each QoL subscale assessed using the European Organisation for Research and Treatment of Cancer quality of life questionnaires (EORTC QLQ-C30 and PR25). Genotyping of these men for the AKR1C3 rs12529 single nucleotide polymorphism (SNP) was carried out using the Sequenom MassArray and iPlex system or the Applied Biosystem's Taqman SNP genotyping procedure. Age at diagnosis, Gleason score and alcohol consumption were confounding variables between ADT and no ADT groups, and were corrected for subsequent analysis. Analysis of QoL scores were carried out against ADT duration or in association with the AKR1C3 rs12529 SNP using the Generalised Linear Model. P-values & .05 were considered significant. Findings: A total of 206 patients provided valid completed questionnaires and 191 patients were linked to the AKR1C3 rs12529 SNP genotype data. 36.4% of this cohort has received ADT either as a monotherapy or as a combined androgen blockage. 85.3% of ADT composed of anti-androgens (AA) either as a monotherapy or in combination with the luteinizing hormone- releasing hormone agonists. Increase in QoL subscales (95% CI) for insomnia [39.7 (1.9-77.4), p& .05] and hormone treatment-related effects [36.1 (18.6-53.7), p& .005] were recorded with long-term ADT as compared to no ADT. Hormone treatment-related effects showed an increase with ADT when associated with the AKR1C3 rs12529 G allele [4.9 (95% CI (1.1-8.6) p& .02]. This increase among the rs12529 GG genotype (9.7) is therefore, equivalent to 59% of the mean hormone treatment-related symptom score of 16.5 (SD16.6) recorded in this study. Interpretation: As 85.3% ADT recipients have used AA the current study is best interpreted as QoL effects of AA. This study suggests a possibility for those stratified with the AKR1C3 rs12529 G allele to receive intermittent AA treatment to minimize QoL effects. If larger prospective studies can confirm these findings, PC survivors particularly those of Maori and Pacific ethnic groups may greatly benefit through optimal ADT options not only for their survival benefits, but also to better maintain their QoL. Citation Format: Nishi Karunasinghe, Yifei Zhu, DugYeo Han, Katja Lange, Alice Wang, Shoutun Zhu, Jonathan Masters, Megan Goudie, Justin Keogh, Benji Benjamin, Michael Holmes, Lynnette Ferguson. Can we minimize androgen deprivation therapy-related quality of life effects in Māori and Pacific prostate cancer survivors using a genetic stratification? [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved Nov 13-16, 2015 Atlanta, GA. Philadelphia (PA): AACR Cancer Epidemiol Biomarkers Prev 2016 (3 Suppl):Abstract nr C74.
Publisher: CRC Press
Date: 19-04-2013
DOI: 10.1201/B15369-17
Publisher: Springer Science and Business Media LLC
Date: 03-12-2011
Publisher: Bentham Science Publishers Ltd.
Date: 09-08-2017
DOI: 10.2174/1568009617666170330115722
Abstract: Aldo-keto reductase 1C3 (AKR1C3) is an important oxidoreductase with multiple substrates, that are involved in producing extra-testicular androgens. Its activity is influenced by environmental exposures, as well as by genetic variants. These genetic variants could therefore produce variable testosterone levels and subsequent androgen receptor (AR) activation. This could lead to differential downstream production of the prostate-specific antigen (PSA). As PSA level is used for clinical evaluation of the prostate, these variations could impact prostate cancer (PC) diagnosis, as well as PC management outcomes. This review brings together information with regards to key functions of this enzyme, its relevance in PC, its transcriptional regulation, clinical aspects associated with genetics, differential regulation in cancer and cancer progression, and the types of AKR1C3 inhibitors with future therapeutic value. Based on these discussions, hypotheses are forwarded for future applicability of this enzyme and its genetic variants in transformational medical practices in PC. Options for the use of personalised AKR1C3 inhibitor drugs for late stage PC are also discussed.
Publisher: Springer Science and Business Media LLC
Date: 21-07-2021
DOI: 10.1038/S41598-021-94090-Y
Abstract: Androgen deprivation therapy (ADT) for men with prostate cancer (PCa) results in accelerated bone loss and increased risk of bone fracture. The aim of the present study was to evaluate serum bone markers—sclerostin, Dickkopf-1 (DKK-1) and osteoprotegerin (OPG), in a cohort of 88 PCa patients without known bone metastases, managed with and without ADT, and to analyse their relationship with bone mineral density (BMD) and sex steroids. The cross-sectional analysis between acute-, chronic- and former-ADT groups and PCa controls showed that sclerostin and OPG levels significantly differed between them ( p = 0.029 and p = 0.032). Groups contributing to these significant changes were recorded. There were no significant differences in serum DKK-1 levels across the four groups ( p = 0.683). In the longitudinal analysis, significant % decreases within groups were seen for DKK-1 [chronic-ADT (− 10.06%, p = 0.0057), former-ADT (− 12.77%, p = 0.0239), and in PCa controls group (− 16.73, p = 0.0022) and OPG levels in chronic ADT (− 8.28%, p = 0.003) and PCa controls group (− 12.82%, p = 0.017)]. However, % changes in sclerostin, DKK-1, and OPG did not differ significantly over 6-months across the evaluated groups. Sclerostin levels showed significant positive correlations with BMD at baseline in the ADT group, while in PCa controls this correlation existed at both baseline and 6-month time points. Sclerostin correlated negatively with testosterone in former ADT users and in PCa controls. Possible prognostic features denoted by parallel increases in sclerostin and BMD are discussed.
Publisher: Informa UK Limited
Date: 04-2013
DOI: 10.1080/01635581.2013.760743
Abstract: Selenium (Se) supplementation was tested in a group of healthy men from Auckland, New Zealnd with selenized yeast (Selplex, 200 μg/day) as the supplementation mode. A set of biomarkers, including DNA damage levels and seleno-antioxidant enzyme levels, were evaluated at pre- and postsupplementation time points. Supplementation produced significant increases in serum Se levels, red blood cell (RBC) thioredoxin reductase (TR) activity and peroxide-induced DNA damage, when the mean baseline serum Se level was 110 ng/ml. Those with higher baseline serum Se levels gained less serum Se and showed a significant reduction of RBC glutathione peroxidase (GPx) activity by supplementation. The optimum benefits of supplementation on DNA stability are observed when the serum Se level reaches between >120 and <160 ng/ml. However, the most significant observation was that those with highest baseline DNA damage benefit the most from Se supplementation, whereas those having lower baseline DNA damage are disadvantaged. A dose of 200 μg/day selenized yeast was also shown to be a safer supplementation option compared to a similar dose of selenomethionine (SeMet). This study highlights the requirement for prestratification of a population by standing serum Se level and baseline DNA damage level, before any Se supplementation is carried out.
Publisher: SAGE Publications
Date: 2017
Abstract: Reduction in bone mineral density (BMD) is a common side effect of androgen deprivation therapy (ADT). We aimed to examine the cross-sectional and longitudinal variation in BMD and associated bone markers in patients with nonmetastatic prostate cancer (PCa) managed with and without ADT. Bone mineral density of the total body, lumbar spine, femoral neck, ultradistal forearm, and one-third distal radius was measured in 88 patients with PCa without bone metastases at baseline and at 6 months. Patients were categorized into 4 groups: (1) acute ADT (≤6 months), (2) chronic ADT ( months), (3) former ADT, and (4) no ADT (controls). Serum levels of bone metabolism markers, procollagen type I N-terminal propeptide (PINP) and C-terminal cross-linking telopeptide of type I collagen (CTX), were also measured. In the cross-sectional analysis, men receiving chronic ADT had significantly lower total body BMD as compared with former ADT users and men with no ADT. In longitudinal analysis, a significant reduction in ultradistal forearm BMD was observed in both acute and chronic ADT users after 6 months (4.08% and 2.7%, P = .012 and .026, respectively). A significant reduction in total body BMD was observed in acute ADT users (2.99%, P = .032). Former ADT users had a significant increase in both lumbar spine and femoral neck BMD (2.84% and 1.59%, P = .008 and .002, respectively). The changes in BMD were not significantly different between acute and chronic ADT users. In the cross-sectional analysis, higher levels of PINP and CTX were observed in acute and chronic ADT users than former ADT users or PCa controls. In longitudinal analysis, the level of serum PINP and CTX did not change significantly from baseline to 6 months in acute, chronic, and former ADT users, or PCa controls, and the percentage change did not differ among the 4 groups. Men on acute ADT had a similar rate of bone loss to men on chronic ADT. Reversibility in ADT-induced bone loss was observed in those who discontinued ADT. Serum levels of PINP and CTX were higher in acute and chronic ADT users and levels returned to the range of PCa controls when treatment was withdrawn.
Publisher: MDPI AG
Date: 08-01-2015
DOI: 10.3390/NU7010405
Publisher: Sri Lanka Journals Online (JOL)
Date: 30-03-1995
Publisher: Elsevier BV
Date: 08-2010
DOI: 10.1016/J.MRFMMM.2010.01.017
Abstract: The Signal Transducers and Activators of Transcription (STAT)-Janus kinase (JAK) pathway controls signal transduction between cell surface receptors and the nucleus. Two members of that pathway, STAT3 and JAK2, enhanced the risk of Crohn's disease (CD) in recent genome-wide association studies. We replicated these findings in a New Zealand Caucasian case-control cohort, by genotyping two single nucleotide polymorphisms (SNPs) in STAT3 (rs744166(G>A) and rs3816769(C>T)) and rs10758669(A>C) in JAK2, in 302 CD patients and 382 controls. For STAT3, there was a significant decrease in the frequency of the G allele of rs744166 and the C allele of rs3816769 in CD patients as compared with controls (OR=0.76, 95% CI=0.61-0.95, p=0.013 OR=0.71, 95% CI=0.56-0.89, p=0.003). For the JAK2 rs10758669 polymorphism, the homozygous C/C or heterozygous A/C genotypes increased the risk of having CD as compared with the homozygous A/A (OR=1.76, 95% CI=1.26-2.45 and OR=2.36, 95% CI=1.44-3.86, respectively, p=0.0003). Variant alleles in either gene significantly modified the likelihood of inflammatory disease in a colonic location, and of developing extra-intestinal manifestations. The JAK2 variant also strongly enhanced the risk of ileocolonic disease, with stricturing or ileal/stricturing behaviour, requiring a bowel resection. We further studied a subset of our control population, stratified for JAK2 rs10758669 and/or STAT3 rs3816769 genotype. Carrying either the JAK2 or STAT3 IBD risk allele was associated with significantly enhanced susceptibility to DNA damage, as estimated by comet assays in peripheral blood leukocytes, with or without a subsequent oxidative challenge. That is, both risk alleles enhance genomic instability. The JAK2 SNP is part of a haplotype previously associated with enhanced susceptibility to myeloproliferative neoplasms, but functional consequences of the STAT3 variant had not been previously demonstrated. It will be of interest to follow up CD patients carrying either JAK2 or STAT3 risk alleles for development of further secondary effects, including cancer.
Publisher: Baishideng Publishing Group Inc.
Date: 2014
Start Date: 2020
End Date: 2021
Funder: Health Research Council of New Zealand
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