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Objectives: We aimed to investigate the association between weight change after smoking cessation and the risk of all-cause and cause-specific mortality among middle-aged male smokers. MethOds: We conducted a prospective cohort study using the National Health Insurance Service National Health Screening Cohort (NHIS-HealS) database. Male Participants (n= 102,403) without critical conditions aged between 40 and 79 at baseline who underwent biennial health examination were included in this study. Participants were categorized into continued smokers, recent quitters (within 4 years), long-term quitters (more than 4 years), and neversmokers based on the self-reported smoking status. Weight change was determined by the change of Body Mass Index (BMI) between the first (2002)(2003) and second (2004)(2005) health examination records. We followed patients from January 1, 2006 to December, 31, 2013. To assess the risk of all-cause, cancer, cardiovascular disease (CVD) mortality, and non-cancer, non-CVD mortality according to smoking cessation and weight change, we computed Hazard Ratio (HR) and 95% Confidence Interval (95% CI) using Cox proportional hazard models. Results: Severity of weight gain was more prevalent among recent quitters compared to long-term quitters. After adjusting for covariates and weight change, both recent quitters (HR:0.74; 95% CI: 0.63-0.87) and long-term quitters (HR:0.53; 95% CI:0.45-0.61) had decreased risk of all-cause mortality compared to continued smokers. Similarly, both recent and long-term quitters had decreased risk of cancer, CVD, non-cancer, and non-CVD death regardless of weight change following smoking cessation. Compared to continued smokers, non-smokers also had a lower risk of overall and cause-specific death. cOnclusiOns: Post-cessation weight change did not modify the protective association of smoking cessation with reduced risk of all-cause and cause-specific death. From a public health perspective, smoking cessation program may contribute to reducing risk of death in middle-aged male smokers despite the concern on weight change after quitting smoking.

BACKGROUND In recent years, there have been numerous molecular studies in the glioblastoma. With regard to glioblastoma showing primarily extensive subarachnoid spreading, however, the pathogenesis remains to be determined due to its low incidence. Present report is a rare case of glioblastoma with primitive neuroectodermal tumor (PNET)-like feature, showing extensive subarachnoid spread, as well as the distinguishing result of its molecular analysis using next generation sequencing (NGS). DESCRIPTION A 37-year-old male presented with a new onset, severe headache. Magnetic resonance imaging (MRI) test revealed a diffuse infiltrative mass in the right frontal lobe. The tumor was also spread broadly in subarachnoid space. The patient underwent craniotomy and tumorectomy. Microscopically, glioblastoma showed PNET-like feature. Tumor cells had high nuclear/cytoplasmic ratios, oval, slightly elongated or angulated hyperchromatic nuclei, markedly increased mitotic activity, and obvious apoptotic bodies. Immunohistochemical analysis showed partly positivity of GFAP. Also this tumor demonstrated CD56 and synaptophysin immunoreactivity. IDH-1 immunohistochemistry was negative, which initially led to the diagnosis of glioblastoma, IDH wild-type. However, IDH-1 (p.Arg132His) mutation was found in subsequent NGS test. Additionally, two frame shift genetic alteration was found including ATRX (p.Tyr2208fs) and TP53 (p.Pro301fs). Interestingly, also MYCN (2p24.3) amplification was identified by both NGS and fluorescence in situ hybridization (FISH) test. Estimated MYCN copy number was 18. Despite the post-operative therapy including temozolomide and radiotherapy was performed, the tumor aggressively progressed and the patient expired nine months after the first symptom onset. CONCLUSION Although there have been several previous reports of MYCN amplification in glioblastoma with PNET-like feature, this is the first case report which finding in IDH-mutant type. IDH-1 mutation and younger age are usually associated with a better prognosis in glioblastoma. However, this case may suggest that when MYCN amplification coexists in IDH-mutant type, the tumor behavior could be contrarily aggressive.

0 1 7 ) A 3 9 9 -A 8 1 1 A475 Objectives: To summarize prevalence rates globally for cardiovascular disease (CVD) in persons with type 2 diabetes (T2DM) published within the last 10 years (2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017). MethOds: We searched Medline, Embase, and proceedings of scientific meetings to identify published studies documenting the prevalence of CVD among people with T2DM. Search terms included stroke, myocardial infarction, angina, heart failure, ischemic heart disease, cardiovascular disease, coronary heart/artery disease (CAD), atherosclerosis, and cardiovascular death. No restrictions were placed on country of origin or publication language. Two reviewers independently searched for articles and abstracted data, with results adjudicated through consensus. Data were summarized descriptively. Risk of bias was explored by applying the checklist from the STROBE Initiative. Results: We analyzed data from 57 articles with 4,549,481 persons having T2DM. Overall, 51.8% were male, 47.0% obese, 63.6±6.9 years old, with T2DM duration of 10.4±3.7 years. CVD affected 32.2% overall (53 studies, N= 4,289,140); 29.1% had atherosclerosis in four studies (N= 1,153), 21.2% had CAD (42 articles, N= 3,833,200), 14.9% heart failure (14 studies, N= 601,154), 14.6% angina (4 studies, N= 354,743), 10.0% myocardial infarction (13 studies, N= 3,518,833), and 7.6% stroke (40 studies, N= 3,901,505). Males had higher rates than females for stroke (6.7% vs. 5.9%), myocardial infarction (11.9% vs. 9.8%), angina (21.1% vs. 17.4%), and CAD (18.7% vs. 14.3%). CVD was cause of death in 9.9% of all T2DM patients (representing 50.3% of all deaths), with CAD responsible for 6.3% (29.7% of all deaths) and cerebrovascular disease for 1.5% (11.0% of all deaths). Risk of death in T2DM doubled with CVD (OR= 2.09; CI95%:1.56-2.80) and nearly tripled with concomitant CAD (OR= 2.97;