To validate this approach, we developed reagents for measurement of previously reported lung cancer diagnostic test comprising v-myc avian myelocytomatosis viral oncogene homolog, E2F transcription factor 1, and cyclin-dependent kinase inhibitor 1A genes measured relative to actin, beta. These reagents were subjected to analytical validation using synthetic templates as test articles and fitness for the purpose of testing using surgical benign and malignant FFPE samples according to recommended practices. Cardiovascular disease remains the leading cause of morbidity and mortality worldwide and whilst current drugs improve symptoms and reduce hospital admissions, the prevalence of cardiovascular disease is still increasing, highlighting the need for the identification of novel and efficacious therapies that can prevent cardiovascular disease. microRNAs are an abundant class of small, non-coding RNAs that target partially complementary sequences in the 3′ untranslated region of target mRNA, leading to mRNA cleavage and/or translational repression.Whilst miRNAs regulate a wide range of biological processes, recent Catharanthine sulfate studies have unveiled critical roles of miRNAs in cardiovascular disease. These studies highlight their potential as novel therapeutic targets. miRNA inhibitors or antimiRs have been shown to be efficient in silencing miRNAs in mice, and non-human primates, and the first miRNAtargeted drug, miravirsen, has advanced into clinical phase 2 trials for the treatment of hepatitis C virus infection. Although miRNA based therapies for cardiovascular disease have not yet reached clinical trials, a number of successful preclinical studies in animal models of heart failure, Albaspidin-AA cardiac hypertrophy and remodeling highlight the translational potential of targeting miRNAs in human heart failure. Most preclinical studies have focused on inhibiting individual miRNAs in the heart. However, more recent studies have demonstrated the therapeutic potential of targeting disease-implicated miRNAfamilies. Though a potential disadvantage of inhibiting an entire miRNA family is the increased risk of generating off-target effects. Thus it is important to assess whether the effects of silencing miRNA families can yield more therapeutic benefit in settings of cardiac stress than the targeting of individual miRNAs. We and others have previously shown that expression of miR34a is elevated in settings of cardiac stress and ageing, and that miR-34 family members, 34b and 34c, are also elevated in the mouse heart following a cardiac insult. Furthermore, expression of miR-34 family members was found to be elevated in cardiac tissue from patients with heart disease. We recently found that inhibition of the miR-34 family, but not miR-34a alone, displayed a therapeutic benefit in a chronic model of myocardial infarction remodeling; antimiR delivered 2 days after MI). Inhibition of the miR-34 family also improved cardiac function and attenuated LV remodeling in a mouse model with pre-existing pathological cardiac remodeling and dysfunction due to pressure overload by transverse aortic constriction, however the therapeutic impact of inhibiting miR-34a alone was not assessed in that study. More recently, it was shown that inhibition of miR-34a prevented cardiac contractile dysfunction, and reduced apoptosis and fibrosis following acute MI, but the first dose of the miRNA-based therapy was administered 3 hours after acute MI, before any chronic LV remodeling had occurred.