• Tuberculosis and Respiratory Diseases
• /
• v.49 no.4
• /
• pp.453-465
• /
• 2000

Background : Lung carcinogenesis is a multistage process involving alterations in multiple genes and diverse pathway. Mutational activation of oncogenes and inactivation of tumor suppressor genes, and subsequent increased genetic instability are the major genetic events. The p53 gene and FHIT gene as tumor suppressor genes contribute to the pathogenesis of lung cancer, evidenced by mutation, microsatellite instability(MI) and loss of heterozygosity(LOH). Methods : We analysed genetic mutations of p53 and FHIT gene in 29 surgical specimens of nonsmall cell lung cancer using PCR-single strand conformation polymorphism, DNA sequencing and RT-PCR. MI and LOH were analyzed in loci of D3S1285, D9S171, and TP53. Results : In 2 cases, point mutation of p53 gene was observed on exon 5. MI of 3 times and LOH of 14 times were observed in at least one locus. In terms of the location of microsatellite, D3S1285 as a marker of FH1T was observed in 5 cases out of 26 specimens; D9S171 as a marker of p16 in 5 out of 17; and TP53 as a marker of p53 in 7 out of 27. In view of histologic type, squamous cell carcinoma presented higher frequency of microsatellite alteration, compared to others. Mutation of FHIT gene was observed in 11 cases and 6 cases of those were point mutation as a silent substitution on exon 8. FHIT mRNA expression exhibited deletion on exon 6 to 9 in 4 cases among 15 specimens, presenting beta-actin normally. Conclusion : Our results show comparable frequency of genetic alteration in nonsmall cell lung cancer to previous studies of Western countries. Microsatellite analysis might have a role as a tumor marker especially in squamous cell carcinoma. Understanding molecular abnormalities involved in the pathogenesis could potentially lead to prevention, earlier diagnosis and the development of novel investigational approaches to the treatment of lung cancer.

• Korean Journal of Social Welfare
• /
• v.59 no.1
• /
• pp.301-327
• /
• 2007

The purpose of this study is to examine the timing and the risk factors associated with the adoption of legally-free foster children. The sample of the study was drawn from foster care files of Adoption and Foster Care Analysis and Reporting System(AFCARS) in 32 states between October 1998 (FY 1999) and September 2002(FY 2002). The timing post-TPR to adoption was examined by plotting the Kaplan-Meier cumulative hazard function for adoption and by plotting the KM hazard functions stratified by child's race and child's age at TPR. Cox proportional-hazards regression analysis was used to identify risk factors for adoption of legally-free foster children after TPR. The hazard of adoption was very low immediately after TPR but increased steadily starting at 3 months and then declined after 20 months. The cumulative hazard functions for White non-Hispanic children and Black non-Hispanic children crossed over at 13 months after TPR. Racial minority status, older age, and disability were negatively associated with the hazard of adoption. Physical abuse, sexual abuse had the lower hazard for adoption compared by neglect. Caretaker's inability to cope had the slightly lower hazard for adoption whereas inadequate housing showed the slightly greater hazard for adoption. Characteristics of foster care services turned into be powerful predictors of adoption. Specifically, legally-free children placed in pre-adoptive homes, those who shared the same racial/ethnic background with their foster caretakers, and those who were placed in two-parent families have a greater likelihood of adoption. The findings highlight the importance of foster care service provisions after TPR to facilitate adoption of legally-free foster children. Furthermore, a more substantial resources and targeted support for foster children who experience physical abuse and sexual abuse in need of adoption should be provided for moving the foster children into permanency.