Effects of cognitive-behavioral programs for criminal offenders

Cognitive-behavioral therapy (CBT) is among the more promising rehabilitative treatments for criminal offenders. Reviews of the comparative effectiveness of different treatment approaches have generally ranked it in the top tier with regard to effects on recidivism (e.g., Andrews et al., 1990; Lipsey & Wilson, 1998). It has a well-developed theoretical basis that explicitly targets “criminal thinking” as a contributing factor to deviant behavior (Beck, 1999; Walters, 1990; Yochelson & Samenow, 1976). And, it can be adapted to a range of juvenile and adult offenders, delivered in institutional or community settings by mental health specialists or paraprofessionals, and administered as part of a multifaceted program or as a stand-alone intervention. Meta-analysis has consistently indicated that CBT, on average, has significant positive effects on recidivism. However, there is also significant variation across studies in the size of those treatment effects. Identification of the moderator variables that describe the study characteristics associated with larger and smaller effects can further develop our understanding of the effectiveness of CBT with offenders. Of particular importance is the role such moderator analysis can play in ascertaining which variants of CBT are most effective. The objective of this systematic review is to examine the relationships of selected moderator variables to the effects of CBT on the recidivism of general offender populations

Influence of a nonfragile FHIT transgene on murine tumor susceptibility

FHIT, at a constitutively active chromosome fragile site, is often a target of chromosomal aberrations and deletion in a large fraction of human tumors. Inactivation of murine Fhit allelessignificantly increases susceptibility of mice to spontaneous and carcinogen-induced tumorigenesis. In this study, transgenic mice, carrying a human FHIT cDNA under control of the endogenous promoter, were produced to determine the effect of Fhit expression, from a nonfragile cDNA transgene outside the fragile region, on carcinogen-induced tumor susceptibility of wildtype and Fhit heterozygous mice. Mice received sufficient oral doses of N-nitrosomethybenzylamine (NMBA) to cause forestomach tumors in >80% of nontransgenic control mice. Although the level of expression of the FHIT transgene in the recombinant mouse strains was much lower than the level of endogenous Fhit expression, the tumor burden in NMBA-treated male transgenic mice was significantly reduced, while female transgenic mice were not protected. To determine if the difference in protection could be due to differences in epigenetic changes at the transgene loci in male versus female mice, we examined expression, hypermethylation and induced re-expression of FHIT transgenes in male and female mice or cells derived from them. The transgene was methylated in male and female mice and in cell lines established from male and female transgenic kidneys, the FHIT locus was both hypermethylated and deacetylated. It is likely that the FHIT transgene is more tightly silenced in female transgenic mice, leading to a lack of protection from tumor induction. Copyright © 2007 S. Karger AG