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Quality of life effects of androgen deprivation therapy in a prostate cancer cohort in New Zealand: Can we minimize effects using a stratification based on the aldo-keto reductase family 1, member C3 rs12529 gene polymorphism?

Background: Androgen deprivation therapy (ADT) is an effective palliation treatment in men with advanced prostate cancer (PC). However, ADT has well documented side effects that could alter the patient’s health-related quality of life (HRQoL). The current study aims to test whether a genetic stratification could provide better knowledge for optimising ADT options to minimize HRQoL effects. Methods: A cohort of 206 PC survivors (75 treated with and 131 without ADT) was recruited with written consent to collect patient characteristics, clinical data and HRQoL data related to PC management. The primary outcomes were the percentage scores under each HRQoL subscale assessed using the European Organisation for Research and Treatment of Cancer Quality of Life questionnaires (QLQ-C30 and PR25) and the Depression Anxiety Stress Scales developed by the University of Melbourne, Australia. Genotyping of these men was carried out for the aldo-keto reductase family 1, member C3 (AKR1C3) rs12529 single nucleotide polymorphism (SNP). Analysis of HRQoL scores were carried out against ADT duration and in association with the AKR1C3 rs12529 SNP using the generalised linear model. P-values <0 · 05 were considered significant, and were further tested for restriction with Bonferroni correction. Results: Increase in hormone treatment-related effects were recorded with long-term ADT compared to no ADT. The C and G allele frequencies of the AKR1C3rs12529 SNP were 53·4 % and 46·6 % respectively. Hormone treatmentrelated symptoms showed an increase with ADT when associated with the AKR1C3 rs12529 G allele. Meanwhile, decreasing trends on cancer-specific symptoms and increased sexual interest were recorded with no ADT when associated with the AKR1C3 rs12529 G allele and reverse trends with the C allele. As higher incidence of cancerspecific symptoms relate to cancer retention it is possible that associated with the C allele there could be higher incidence of unresolved cancers under no ADT options

Benjamin Reed

Benjamin “Benji” Reed is the Director of Crew Mission Management at SpaceX. In this role he is helping spearhead the company’s development and certification efforts for the Crew Transportation System, including the Dragon spacecraft, Falcon 9 rocket, ground systems, and operations. Prior to this position Benji was a Mission Manager for Dragon cargo missions to the International Space Station, including the CRS-3 mission which carried the first science payloads in the Dragon trunk. Over the past 20 years, he has been a leader in various commercial aerospace and NASA programs, including hardware development serving the Hubble Space Telescope, ISS, and planetary science missions. He spent many years as the co-owner of a software and internet development firm and has also been a teacher. A native of Boulder, Colorado, Benjamin graduated from the University of Colorado with a degree in Mathematics, working at the Center for Astrophysics and Space Astronomy on programs including the Far Ultraviolet Spectrographic Explorer and the Cosmic Origins Spectrograph. He lives in Los Angeles, California with his wife and three children.https://commons.erau.edu/space-congress-bios-2018/1030/thumbnail.jp

Can we minimize androgen deprivation therapy-related quality of life effects in Maori and Pacific prostate cancer survivors using a genetic stratification?

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 &amp;lt;0.05 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&amp;lt;0.05] and hormone treatment-related effects [36.1 (18.6-53.7), p&amp;lt;0.005] 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&amp;lt;0.02]. 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;25(3 Suppl):Abstract nr C74.</jats:p

iPLA2-VIA is Required for Healthy Aging of Neurons, Muscle, and the Female Germline in Drosophila melanogaster

Neurodegenerative disease (ND) is a growing health burden worldwide, but its causes and treatments remain elusive. Although most cases of ND are sporadic, rare familial cases have been attributed to single genes, which can be investigated in animal models. We have generated a new mutation in the calcium-independent phospholipase A2 (iPLA2) VIA gene CG6718, the Drosophila melanogaster ortholog of human PLA2G6/PARK14, mutations in which cause a suite of NDs collectively called PLA2G6-associated neurodegeneration (PLAN). Our mutants display age-related loss of climbing ability, a symptom of neurodegeneration in flies. Although phospholipase activity commonly is presumed to underlie iPLA2VIA function, locomotor decline in our mutants is rescued by a transgene carrying a serine-to-alanine mutation in the catalytic residue, suggesting that important functional aspects are independent of phospholipase activity. Additionally, we find that iPLA2-VIA knockdown in either muscle or neurons phenocopies locomotor decline with age, demonstrating its necessity in both neuronal and non-neuronal tissues. Furthermore, RNA in situ hybridization shows high endogenous iPLA2-VIA mRNA expression in adult germ cells, and transgenic HA-tagged iPLA2-VIA colocalizes with mitochondria there. Mutant males are fertile with normal spermatogenesis, while fertility is reduced in mutant females. Mutant female germ cells display age-related mitochondrial aggregation, loss of mitochondrial potential, and elevated cell death. These results suggest that iPLA2-VIA is critical for mitochondrial integrity in the Drosophila female germline, which may provide a novel context to investigate its functions with parallels to PLAN