By F. Nafalem. Rutgers University. 2018.
In trials with crossover buy primaquine 15mg without a prescription, because of the potential for differential withdrawal prior to crossover and drug carryover effects biasing subsequent results primaquine 15mg amex, outcomes for the first intervention were recorded if available primaquine 15 mg with visa. Validity Assessment We assessed the internal validity (quality) of trials based on the predefined criteria (see www. These criteria are based on the US Preventive Services Task Force and the National Health Service Centre for Reviews and Dissemination (United Kingdom) 12, 13 criteria. We rated the internal validity of each trial based on the methods used for randomization, allocation concealment, and blinding; the similarity of compared groups at baseline; maintenance of comparable groups; adequate reporting of dropouts, attrition, crossover, adherence, and contamination; loss to follow-up; and the use of intent-to-treat analysis. Trials that had a fatal flaw were rated poor quality; trials that met all criteria were rated good quality; the remainder were rated fair quality. As the fair-quality category is broad, studies with this rating vary in their strengths and weaknesses: The results of some fair-quality studies are likely to be valid, while others are only possibly valid. A poor-quality trial is not valid; the results are at least as likely to reflect flaws in the study design as a true difference between the compared drugs. A fatal flaw is reflected by failure to meet combinations of items of the quality assessment checklist. A particular randomized trial might receive 2 different ratings, 1 for effectiveness and another for adverse events. The criteria used to rate observational studies of adverse events reflect aspects of the study design that are particularly important for assessing adverse event rates. We rated observational studies as good quality for adverse event assessment if they adequately met 6 or Long-acting opioid analgesics 13 of 74 Final Update 6 Report Drug Effectiveness Review Project more of the 7 predefined criteria, fair quality if they met 3 to 5 criteria, and poor quality if they met 2 or fewer criteria. Included systematic reviews were also rated for quality. We rated the internal validity based a clear statement of the questions(s); reporting of inclusion criteria; methods used for identifying literature (the search strategy), validity assessment, and synthesis of evidence; and details provided about included studies. Again, these studies were categorized as good when all criteria were met. Two reviewers independently assigned quality ratings. Overall quality rating and quality rating scores were compared between reviewers. Grading the Strength of Evidence We graded strength of evidence based on the guidance established for the Evidence-based 20 Practice Center Program of the Agency for Healthcare Research and Quality. Developed to grade the overall strength of a body of evidence, this approach incorporates 4 key domains: risk of bias (includes study design and aggregate quality), consistency, directness, and precision of the evidence. It also considers other optional domains that may be relevant for some scenarios, such as a dose-response association, plausible confounding that would decrease the observed effect, strength of association (magnitude of effect), and publication bias. Table 2 describes the grades of evidence that can be assigned. Grades reflect the strength of the body of evidence to answer key questions on the comparative effectiveness, efficacy, and harms of different long-acting opioids and long-acting opioids compared with short-acting opioids. Grades do not refer to the general efficacy or effectiveness of pharmaceuticals. Two reviewers independently assessed each domain for each outcome and differences were resolved by consensus. Strength of evidence was graded for each key outcome measure and was limited to head- to-head comparisons except where a case could be made for assessing the strength of indirect evidence. Definitions of the grades of overall strength of evidence Grade Definition High confidence that the evidence reflects the true effect. Further research is very unlikely to High change our confidence in the estimate of effect. Moderate confidence that the evidence reflects the true effect. Further research may change our Moderate confidence in the estimate of the effect and may change the estimate. Low confidence that the evidence reflects the true effect. Further research is likely to change our Low confidence in the estimate of the effect and is likely to change the estimate. Insufficient Evidence either is unavailable or does not permit estimation of an effect. Data Synthesis We constructed evidence tables showing the study characteristics, quality ratings, and results for all included studies. We reviewed studies using a hierarchy of evidence approach, where the best evidence is the focus of our synthesis for each question, population, intervention, and outcome addressed. Studies that evaluated 1 long-acting opioid against another or a long-acting opioid Long-acting opioid analgesics 14 of 74 Final Update 6 Report Drug Effectiveness Review Project compared with a short-acting opioid provided direct evidence of comparative effectiveness and adverse event rates. Direct comparisons were preferred over indirect comparisons; similarly, effectiveness and long-term safety outcomes were preferred to efficacy and short-term tolerability outcomes. In theory, trials that compare long-acting opioids with other drug classes or with placebos can also provide evidence about effectiveness. This is known as an indirect comparison and can be difficult to interpret for a number of reasons, primarily heterogeneity of trial populations, interventions, and outcomes assessment.
WT1 vaccines prompt speciﬁc PlGF/VEGR1 signaling in CML purchase primaquine 15 mg visa. However primaquine 15 mg cheap, the response of BCR- immune responses in patients with hematologic malignancies ABL1–induced leukemia to dual treatment with imatinib and the without signiﬁcant side effects generic primaquine 15mg free shipping. When combined with imatinib, a JAK2 inhibitor TG101209 in the mouse retroviral CML model was WT1 peptide vaccine induced WT1-speciﬁc immune responses and disappointing, perhaps due to suppressive effects on normal hemato- was associated with achievement of CMR in a CML patient. Adding plerixafor to dasatinib combined PR1/WT1 peptide vaccine in myeloid neoplasms (www. Gambacorti-Passerini C, Antolini L, Mahon FX, et al. Multi- receptor in BM osteoblasts attenuates BCR-ABL1–induced CML- center independent assessment of outcomes in chronic my- like leukemia, but enhances MLL-AF9–induced AML in mouse eloid leukemia patients treated with imatinib. J Natl Cancer retroviral models, possibly through opposing effects of increased Inst. Current issues in chronic treatment of wild-type mice with CML-like leukemia caused a myeloid leukemia: monitoring, resistance, and functional 15-fold decrease in LSCs and reduced NSG engraftment by primary cure. Minimal residual disease and discontinu- manipulation of the CML stem cell niche is a novel strategy for ation of therapy in chronic myeloid leukemia: can we aim at a eradicating these cells. Conclusions and future directions: getting into the 5. Adherence is the critical clinic factor for achieving molecular responses in patients with From the foregoing summary, it is clear that we have no shortage of chronic myeloid leukemia who achieve complete cytogenetic innovative approaches to eliminating CML stem cells. J Natl and effective in our CML patients who are on TKI treatment, Compr Canc Netw. The price excellent quality of life and, as a corollary, that any proposed of drugs for chronic myeloid leukemia (CML) is a reﬂection of intervention must have very low toxicity and morbidity. The time is the unsustainable prices of cancer drugs: from the perspective ripe for clinical trials of these approaches because we now have of a large group of CML experts. Estimations of the increas- strategies that have the strongest existing evidence and best chance ing prevalence and plateau prevalence of chronic myeloid for success are indicated in Table 1. Because the depth of molecular leukemia in the era of tyrosine kinase inhibitor therapy. Early molecular cohorts of patients on the same TKI at the same point after initiation and cytogenetic response is predictive for long-term progres- of treatment. Given that CML is a relatively rare condition, this sion-free and overall survival in chronic myeloid leukemia poses a challenge, but the rising prevalence of the disease and the (CML). Assessment of BCR- motivate all stakeholders (patients, caregivers, payers) to participate ABL1 transcript levels at 3 months is the only requirement for in such studies. Outside of a clinical trial, should we advise our predicting outcome for patients with chronic myeloid leuke- CML patients to drink wine, consume ﬁsh oil, or take NSAIDs? That these are all reasonable suggestions is a measure of just how far 2012;30(3):232-238. Early switch to nilotinib does not overcome the adverse outcome for CML Acknowledgments patients failing to achieve early molecular response on ima- This work was supported in part by the National Institutes of Health tinib, despite excellent overall outcomes in the TIDEL II trial (Grants T32 CA009429 to W. Cancer stem cells: current status researchers whose work was not cited due to length considerations. Quintana E, Shackleton M, Sabel MS, Fullen DR, Johnson Conﬂict-of-interest disclosure: R. Efﬁcient tumour formation by single human ing from TEVA Pharmaceuticals and has consulted for Bristol melanoma cells. Myers Squibb, Deciphera Pharmaceuticals, and TEVA Pharmaceu- 14. Off-label growth need not be driven by rare cancer stem cells. MOZ-TIF2, but Correspondence not BCR-ABL, confers properties of leukemic stem cells to Richard A. Van Etten, MD, PhD, Chao Family Comprehensive committed murine hematopoietic progenitors. Cancer Center, University of California, Irvine, 839 Medical 2004;6(6):587-596. Sciences Court, Sprague Hall, Room 124, Irvine, CA 92697-4047; 16. Normal and leukemic Phone: 949-824-2655; Fax: 949-824-4023; e-mail: vanetten@ SCID-repopulating cells (SRC) coexist in the bone marrow uci. Lewis ID, McDiarmid LA, Samels LM, Bik To L, Hughes TP. Granulocyte- myeloid leukemia who maintain a complete molecular re- macrophage progenitors as candidate leukemic stem cells in sponse after stopping imatinib treatment have evidence of blast-crisis CML. Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S.
Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Jukema et al purchase primaquine 15 mg with amex, Men and women aged 40 to 80 Use of lipid-lowering drugs (including nicotinic acid) buy discount primaquine 15mg, dietary After a 6 week dietary lead-in buy discount primaquine 15mg on line, treatment 2005 years with established supplements or food additives after enrollment, history of for the first 6 weeks: cardiovascular disease, fasting hypersensitivity to statins; pregnancy, lactations or childbearing rosuva 10 mg (n=230) R, open-label, HDL-c <40 mg/dL at visit 1 and potential without reliable contraceptive use; active arterial disease or multicenter baseline, and triglycerides <=400 (unstable angina, MI, TIA, CVA, CABG or angioplasty) within 2 aorta 20 mg (n=231) mg/dL at visit 1. Kurabayashi, 2008 Patients with hypercholesterolemia Severe hypertension, type I diabetes, familial hypercholesterolemia, Atorvastatin 10 mg (continued treatment) Open label, multicenter who had received atorvastatin (10 occurrence of cerebrovascular disease or myocardial infarction within vs rosuvastatin 5 mg (switched treatment) mg) once daily for at least 4 weeks. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Jukema et al, % LDL-c reduction from baseline at 6, 12, and 18 weeks (p vs aorta): Occurrence of deaths, serious adverse events and withdrawals due to adverse 2005 rosuva 10/20/40: ─44. R, open-label, 1 death in rosuva group (sudden death), 1 in aorta (liver metastasis), neither multicenter % HDL-c increase from baseline at 6, 12, and 18 weeks: considered related to study treatment. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Jukema et al, Supported by 2005 AstraZeneca R, open-label, multicenter 461 patients randomized 18 week treatment period Kurabayashi, 2008 Japan Heart Open label, multicenter Foundation Statins Page 152 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Lloret R, et al 2006 Hispanic patients with low-density history of homozygous familial hypercholesterolemia or known type I, III, 6-week dietary lead-in phase, during which all (STARSHIP trial) lipoprotein (LDL) cholesterol levels or V hyperlipoproteinemia; active arterial disease (e. NS Milionis H, et al 2006 Men and women with dyslipidemia, Abnormal liver function tests; Impaired renal function;) Diabetes 6‑week dietary lead-in period, randomized to (ATOROS study) totla cholesterol>240mg/dL at week 4 mellitus; Raised thyroid-stimulating hormone (TSH) levels; any medical rosuvastatin 10 mg/day or atorvastatin 20 RCT, open-label, single and 2 and triglycerides <350mg/dL conditions that might preclude successful completion of the study. After 6 weeks on treatment the dose center of the statin was increased for 18 weeks if the Baseline LDL-c treatment goal was not achieved. Mean doses 120 patients randomized rosuva 205 (42) rosuva 12. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Lloret R, et al 2006 LDL-c change at 6 weeks rosuva10 vs. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Lloret R, et al 2006 AstraZeneca (STARSHIP trial) RCT (1:1:1:1), OL, MC, AC. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Olsson et al, 2002 Men and women age 18 and older Conventional exclusion criteria for lipid-modifying drugs under 5 or 10 mg rosuva or 10 mg aorta for 12 R, DB, MC with LDL-c level between 160 and development were applied weeks, then titrated up to 80 mg if NCEP <250 mg/dL and an EPAT score 28 ATP-II LDL-c goal not met, for a total of 52 412 patients or less. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Olsson et al, 2002 LDL-c reduction from baseline at 12 weeks: Adverse events considered to be treatment related occurred in 29% of rosuva R, DB, MC rosuva 5 mg: 46% (p<0. Of these 5 rosuva 5mg, rosuva 10mg, 140 aorta rosuva 5 mg: 86% 5 rosuva 10mg, and 8 aorta 10mg had adverse events considered treatment- 10mg) rosuva 10 mg: 89% related. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Olsson et al, 2002 Supported by a grant R, DB, MC from AstraZeneca 412 patients randomized (n=138 rosuva 5mg, 134 rosuva 10mg, 140 aorta 10mg) 52 weeks Statins Page 158 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Paoletti et al. Qu, 2009 Outpatients with primary Liver disease or transaminase levels >1. N=69 Statins Page 159 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Paoletti et al. No serious AEs considered by the investigator to be 502 patients randomized rosuva 10mg: 49% (p<0. Trigs reduction from baseline at 12 weeks: 4), abdominal pain (2 vs. No parva: 13% clinically significant ALT or CK elevations. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Paoletti et al. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Rawlings, 2009 Men with stale atherosclerosis and Unstable angina or revascularization within 3 months of study Atorvastatin 40 mg vs rosuvastatin 10 mg Multicenter (2 cardiology fasting LDL-C levels >=100 mg/dL enrollment, malignancy, chronic inflammatory disease, acute for 4 weeks clinics), double-blind off statin therapy. Presence of infection, history of myositis/myopathy, liver transaminases >2 times atherosclerosis determined by ULN, creatine phosphokinase greater than the ULN, and reluctance to >=50% stenosis in at least one discontinue statin therapy. Mean baseline LDL-C: 141 (SD 6) mg/dl N=30 Schneck et al, 2003 Men and women age 18 and older Pregnant or lactating women or women of childbearing potential not Atorva 10, 20, 40, or 80 mg qd or R, DB, MC with hypercholesterolemia and using a reliable form of contraception, as well as patients with a rosuvastatin 5, 10, 20, 40, or 80 mg qd for without active arterial disease history of heterozygous 6 weeks. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Rawlings, 2009 Percent change from baseline, atorvastatin vs rosuvastatin: Not reported Multicenter (2 cardiology LDL-C: -45. Withdrawals due to adverse events infrequent (1 patient each in 374 patients randomized 61. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Rawlings, 2009 NIH and Foundations Multicenter (2 cardiology clinics), double-blind Schneck et al, 2003 Supported by R, DB, MC AstraZeneca Pharmaceuticals 374 patients randomized (n=165 aorta, 209 rosuva) 6 weeks Statins Page 164 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Schuster et al. Patients aged >=18 years, with Pregnant and lactating women, women not using reliable 6 week dietary lead-in phase, then 2004 CHD or other atherosclerotic contraception, patients with a history of homozygous familial randomization to 5 arm trial system R,OL,MC,ITT disease, type 2 diabetes, a CHD hypercholesterolemia or known type III hyperlipoproteinemia, with (drug a for 8 weeks then drug b or c for risk >20% over 10 years, with LDL- active arterial disease (e. Statins Page 165 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Schuster et al. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Funding Source Schuster et al. Sponsored by Astra 2004 Zeneca R,OL,MC,ITT 5-arm trial that included statin switching (to rosuvastatin) at 8 weeks 3140 patients randomized 16 weeks of treatment Statins Page 167 of 395 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Inclusion Criteria/ Patient Clinical Trial Population Exclusion criteria Intervention Schwartz et al, 2004 Patients aged >18 years, with LDL- Pregnant women, patients currently taking concomitant drugs known After a 6 week dietary lead-in, treatment C levels >=160 and< 250 mg/dL, to affect the lipid profile or to present a potential safety concern, a for the first 12 weeks: R, DB, MC and trig levels <=400 mg/dL, and history of active arterial disease (e. Trials comparing LDL-c lowering/HDL-c raising abilities of 2 or more statins Clinical Trial Results (mean changes in lipoprotein levels) Harms/Comments Schwartz et al, 2004 Efficacy analysis for 382 patients: "Although adverse events were frequently reported in these high-risk patients, % LDL-C change from baseline they were generally mild and not attributed to trial medication.
Statistically significant discount primaquine 15 mg mastercard, but not considered clinically meaningful purchase 15mg primaquine otc, increases in systolic blood pressure and diastolic blood pressure were seen at various points throughout the study (mean increase in systolic blood pressure purchase 15 mg primaquine visa, 2. While a statistically significant increase in QTcB (7. Three percent withdrew due to cardiovascular events (2 due to palpitations or tachycardia – extent not reported, and 5 due to hypertension). Open-label extension studies of atomoxetine have reported on cardiovascular 257 285 adverse events in children or teens and in adults. One report involved 169 children and adolescents that continued on open or blinded atomoxetine (maximum dose of 2 mg/kg divided 257 into twice daily) for at least 1 year following 3 short-term, placebo-controlled trials. The timing of electrocardiogram measurements was not stated, but was presented by increasing dose. Linear regression suggested that there was no evidence of an increase in QTc with increasing 257 dosage of atomoxetine. An interim analysis of an open-label extension study in adults reported 285 no “clinically relevant changes in QTc” after a mean of 97 months of follow-up. Growth effects A non-systematic review, using estimation techniques, graphing, and qualitative synthesis, found that stimulants (amphetamines and methylphenidate) caused growth delays in both height and 246 weight but that these were attenuated over time. The qualitative analysis indicated that there may be a dose effect, that there are no important differences between amphetamines and methylphenidate, and that discontinuing treatment results in resumption of normal growth. Because this review was not systematic and pooled data from a wide variety of study designs, we suggest caution in interpreting these findings. A frequently cited nonsystematic review concluded that effects on weight and height associated with immediate-release methylphenidate vary across short-term clinical trials and 286 long-term observational studies and are mostly transient. We reached similar conclusions based on our analysis of a larger number of primarily long-term observational studies that 258, 259, compared immediate-release methylphenidate to immediate-release dextroamphetamine, 265 261, 265, 266 or unmedicated hyperactive control groups. Height and weight changes associated 254, 256, 260, 262, 263 with immediate-release methylphenidate and OROS were also observed in long- 262 term noncomparative studies. A noncomparative study of mixed amphetamine salts (Adderall ® XR ) found a low overall rate of withdrawal due to weight loss (4. Multiple noncomparative study findings provide inconclusive evidence regarding immediate-release methylphenidate effects on children’s height and weight. Analysis of 2- and 5-year data from open-label extensions of 13 trials of atomoxetine assessed the effect on height 249, 252 and weight. We did not analyze results from a poor-quality, comparative study of growth rebound in methylphenidate and immediate-release dextroamphetamine due to our concerns about how 267 possible additional biases may have affected the results. We cannot rule out the possibility of between-groups differences in baseline characteristics because no information/analysis was provided. We also cannot rule out the possibility that the results were confounded by time and other relevant factors. An additional study related to growth reported on tooth maturation in Attention deficit hyperactivity disorder 87 of 200 Final Update 4 Report Drug Effectiveness Review Project children taking immediate-release methylphenidate compared with an unexposed control group, 288 finding no difference (Table 14). Direct comparisons of long-term height and weight outcomes Interventions (mean dose) Age Duration Gender Study Sample size Population Height Weight Mean age=9 DEX 16. The only comparative evidence came from 2 studies of immediate-release 258, 265 dextroamphetamine and methylphenidate and 1 of methylphenidate and mixed 270 amphetamine salts. Results were mixed across the methylphenidate compared with immediate- release dextroamphetamine studies (Table 14). Both reported changes in height percentiles using Attention deficit hyperactivity disorder 88 of 200 Final Update 4 Report Drug Effectiveness Review Project the outdated Iowa City norms. Immediate-release dextroamphetamine and methylphenidate were 258 both associated with similar height increases at final follow-up (mean 6 years) in 1 study and immediate-release dextroamphetamine was associated with significantly greater height decreases 265 than methylphenidate after at least 2 years in the other. It is impossible to establish whether heterogeneity in group characteristics across studies may possibly contribute to the contradictory 265 findings, as 1 of the studies did not report mean age, dosage, or duration. The study of methylphenidate (any formulation) compared with mixed amphetamine salts (any formulation) did not find statistically significant differences in the z-score for height change over 3 years of 270 continuous treatment. Mixed amphetamine salts appeared to have a small negative impact at year 1, but this difference was not statistically significant. The authors found that the adjusted cumulative dose showed a statistically significant negative relationship to height (both drugs combined) (r = –0. In summary, studies of children taking immediate-release methylphenidate at various doses for 1-4 years showed inconsistent 289,255, 261, 266 suppression of growth in height as compared with children who were unmedicated, and those in noncomparative studies that reported varied analyses including differences between 254 256 260 expected and actual growth, change in percentile, percent of expected growth, and 263 proportion of patients with decreased growth rates. A study of children previously enrolled in a study of immediate-release methylphenidate were followed for 5 years, and a negative relationship between stimulant (any) dose and z-scores 269 for height was found. Further analysis indicated that the impact on height occurred after the dose reached ≥2. Extrapolation from the regression model indicates that a 13 year-old-boy receiving 2. This study is based on small numbers of patients (N=91 at baseline, N=68 at year 5) and many patients did not have height and weight data available for all years. A before-after study followed 407 children with ADHD taking methylphenidate OROS 280 40 mg daily for 12 months.
Early in 2008, Sue Clark brought a handful of epigenetics researchers from Australia together to form the Australian Epigenetics Alliance. The AEpiA has now grown to a membership of nearly 300, with members spanning not only Australasia, but the globe. Last year we hosted our seventh flagship conference, Epigenetics 2017 in Brisbane, QLD, and the WA team are already busy preparing for Epigenetics 2019 – watch this space!
Past Epigenetics meetings: