PurposeAn epidemiologic study of childhood cancer would provide useful information on cancer etiology and development of management guidelines.Materials and MethodsData from the Korea National Cancer Incidence Database were used to examine the incidence and survival of cancer in patients aged 0-14 years. Patients were grouped according to the International Classification of Childhood Cancer, 3rd edition. Age-specific and age-standardized incidences per million and estimated annual percentage change (APC) were calculated by sex and age. Five-year relative survival was calculated for four periods from 1993 to 2011.ResultsThe study comprised 15,113 patients with malignant neoplasms. Age-standardized incidence rates for all cancers were 134.9 per million children in 1999-2011 and 144.0 and 124.9 per million for males and females, respectively (M/F ratio, 1.2; p < 0.05). The highest incidences were observed for ‘leukemias, myeloproliferative diseases, and myelodysplastic diseases’ (group I) (46.4), ‘central nervous system neoplasms’ (group III) (18.3), and ‘lymphomas and reticuloendothelial neoplasms’ (group II) (13.4). Age-standardized incidence increased from 117.9 in 1999 to 155.3 in 2011, with an APC of 2.4% (95% confidence interval, 2.1 to 2.7). There was a significant increase of APC in ‘neuroblastoma and other peripheral nervous cell tumors’ (group IV) (5.6%) and ‘other malignant epithelial neoplasms and malignant melanomas’ (group XI) (5.6%). The 5-year relative survival rate for all childhood cancers improved significantly from 56.2% (1993-1995) to 78.2% (2007-2011) (males, 56.7% to 77.7%; females, 55.5% to 78.8%).ConclusionThis study provides reliable information on incidence and survival trends for childhood cancer in Korea.

BackgroundLarge-scale epidemiologic analysis for hematologic malignancies will be helpful to understand the trends in incidence and survival.MethodsThe Korea Central Cancer Registry (KCCR) updated the nationwide analysis on the incidence and survival of myeloid malignancies, from the Korean National Cancer Incidence Database between 1999 and 2012. Myeloid malignancies were classified based on the International Classification of Diseases for Oncology 3rd edition (ICD-O-3).ResultsOverall 3,771 cases of myeloid diseases, which was 1.7% of all cancers, were identified in 2012. The highest incidence of myeloid malignancies was observed in age 70s and male predominance was noted (1.3:1). Acute myeloid leukemia (AML) was the most frequent subtype, followed by myeloproliferative neoplasms (MPN), myelodysplastic syndrome (MDS) and MDS/MPN: age-standardized incidence rates (ASR) in 2012 for each disease were 2.02, 1.95, 1.13, and 0.12 per 100,000 persons, respectively. The ASR for all myeloid malignancies was increased from 3.31 in 1999 to 5.70 in 2012 with the annual percentage change (APC) of 5.4 %. Five-year relative survival rate (RS) for myeloid malignancies has gradually improved for decades. RS changed from 26.3% to 34.8% in AML, specifically from 51.6% to 69.6% in acute promyelocytic leukemia (APL) and from 23.8% to 29.9% in non-APL AML, between 1996-2000 and 2008-2012. RS also increased from 81.8% to 87.1% in MPN, with a significant improvement in CML (from 74.5% to 85.5%), and from 27.3% to 31.7% in MDS/MPN between 2001-2005 and 2008-2012. However, there was no survival improvement in MDS during the study period (45.6% in 2001-2005 to 44.4% in 2008-2012).ConclusionThis report updated the nationwide statistical analysis on myeloid malignancies since 2008, showing increasing incidence and improving trends in survival.

PurposeBrain magnetic resonance imaging (MRI) findings and factors predictive of pathological brain lesions in boys with precocious puberty (PP) or early puberty (EP) were investigated.MethodsSixty-one boys with PP or EP who had brain MRI performed were included. PP was classified into the central or peripheral type. Brain MRI findings were categorized into group I (pathological brain lesion known to cause puberty; newly diagnosed [group Ia] or previously diagnosed [group Ib]); group II (brain lesion possibly related to puberty); and group III (incidental or normal findings). Medical history, height, weight, hormone test results, and bone age were reviewed.ResultsBrain lesions in groups I and II were detected in 17 of 23 boys (74%) with central PP, 9 of 30 boys (30%) with EP, and 7 of 8 boys (88%) with peripheral PP. All brain lesions in boys with peripheral PP were germ cell tumors (GCT), and 3 lesions developed later during follow-up. Group I showed earlier pubertal onset (P<0.01) and greater bone age advancement (P<0.05) than group III. Group III had lower birth weight and fewer neurological symptoms than "Ia and II" (all P<0.05).ConclusionEarlier onset of puberty, greater bone age advancement, and/or neurological symptoms suggested a greater chance of pathological brain lesions in boys with central PP or EP. All boys with peripheral PP, even those with normal initial MRI findings, should be evaluated for the emergence of GCT during follow-up.

Amentoflavone is a biflavonoid compound with antioxidant, anticancer, antibacterial, antiviral, anti-inflammatory, and UV-blocking activities that can be isolated from Torreya nucifera, Biophytum sensitivum, and Selaginella tamariscina. In this study, the molecular mechanism underlying amentoflavone's anti-inflammatory activity was investigated. Amentoflavone dose dependently suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW264.7 cells stimulated with the TLR4 ligand lipopolysaccharide (LPS; derived from Gram-negative bacteria). Amentoflavone suppressed the nuclear translocation of c-Fos, a subunit of activator protein (AP)-1, at 60 min after LPS stimulation and inhibited the activity of purified and immunoprecipitated extracellular signal-regulated kinase (ERK), which mediates c-Fos translocation. In agreement with these results, amentoflavone also suppressed the formation of a molecular complex including ERK and c-Fos. Therefore, our data strongly suggest that amentoflavone's immunopharmacological activities are due to its direct effect on ERK.

No abstract