Mothers' Difficulties and Expectations for Intervention of Bullying among Young Children in South Korea.

This study investigated the difficulties of mothers in coping with the bullying of their children and their expectations concerning bullying intervention for young children in South Korea. Twenty mothers with young children were interviewed. Interviews were transcribed in Korean. Nvivo 12 software was used to analyze the data. Four themes emerged: "mothers' coping strategies", "problems of interventions", "expectations of interventions", and "developmentally appropriate interventions for young children". Each theme was divided into categories and further into subcategories. Mothers used diverse strategies to intervene when their children were bullied and showed dissatisfaction with the current intervention system. Their expectations for interventions for young children were explained in terms of familial, school, and local/governmental levels. These results emphasized that intervention policies for bullying among young children should be urgently established, and intervention programs need to consider the developmental characteristics of young children.

Wnt5a is associated with cigarette smoke-related lung carcinogenesis via protein kinase C.

Wnt5a is overexpressed during the progression of human non-small cell lung cancer. However, the roles of Wnt5a during smoking-related lung carcinogenesis have not been clearly elucidated. We investigated the associations between Wnt5a and the early development of cigarette smoke related lung cancer using human bronchial epithelial (HBE) cells (NHBE, BEAS-2B, 1799, 1198 and 1170I) at different malignant stages established by exposure to cigarette smoke condensate (CSC). Abnormal up-regulation of Wnt5a mRNA and proteins was detected in CSC-exposed transformed 1198 and tumorigenic 1170I cells as compared with other non-CSC exposed HBE cells. Tumor tissues obtained from smokers showed higher Wnt5a expressions than matched normal tissues. In non-CSC exposed 1799 cells, treatment of recombinant Wnt5a caused the activations of PKC and Akt, and the blockage of Wnt5a and PKC significantly decreased the viabilities of CSC-transformed 1198 cells expressing high levels of Wnt5a. This reduced cell survival rate was associated with increased apoptosis via the down-regulation of Bcl2 and the induction of cleaved poly ADP-ribose polymerase. Moreover, CSC-treated 1799 cells showed induction of Wnt5a expression and enhanced colony-forming capacity. The CSC-induced colony forming efficiency was suppressed by the co-incubation with a PKC inhibitor. In conclusion, these results suggest that cigarette smoke induces Wnt5a-coupled PKC activity during lung carcinogenesis, which causes Akt activity and anti-apoptosis in lung cancer. Therefore, current study provides novel clues for the crucial role of Wnt5a in the smoking-related lung carcinogenesis.

Genomic copy number alterations associated with the early brain metastasis of non-small cell lung cancer.

Frequent early development of systemic metastasis leads to unfavourable clinical prognosis of non-small cell lung cancer (NSCLC). Although brain metastasis (BM) contributes significantly to morbidity and mortality of NSCLC, relevant driver mechanisms are largely unknown. To elucidate genetic alterations associated with early BM of NSCLC, we retrospectively collected 18 NSCLC cases with BM [12 adenocarcinomas (ADC) and 6 squamous cell carcinomas (SQCC)] whose surgical tissues of both primary and brain metastatic tumors were preserved as formaldehyde-fixed and paraffin-embedded (FFPE) pathological samples. When chromosomal copy number alterations (CNA) of those FFPE samples were analysed by the Molecular Inversion Probe (MIP) technology, the most frequent CNAs detected in primary lung ADCs were gains of 3q, 5p, 5q, 6p, 8q, 9p, 11p, 15q, 17q and losses of 10q and 22q whereas primary lung SQCCs revealed gains in 4q and 12q and loss in 9q. In particular, when comparative MIP was performed in primary 12 ADCs depending on the pattern of BM to uncover predetermining signatures that can predict the risk of BM, selectively amplified regions of primary lung ADCs (5q35, 10q23 and 17q23-24) were identified as significantly associated with the development of early BM within 3 months after first diagnosis of primary tumors. Those regions harbour several candidate genes including NeurL1B, ACTA2, FAS and ICAM2. Although more validation is needed, the genetic signatures elucidated in this study help to identify useful molecular markers defining an NSCLC patient subgroup at risk of early BM, guiding therapeutic decisions.