Making and sustaining change from psychotherapy: A mixed methods study.

This study explored both how changes are made and what encourages the maintenance of change after psychotherapy, from the perspective of a sample of former clients, using a mixed methods sequential design. Wampold & Imel's (2015) contextual model was used as a conceptual framework. Using secondary data analysis, quantitative analysis was used to explore the degree to which clients made and maintained progress from pretest to post test and 12 to 18 month follow-up. Fourteen interviews were used to hear from former clients about their impressions of what supported their efforts at change and how they maintained these gains post treatment. The findings of the quantitative strand demonstrated clinically meaningful change from pretest to follow-up, using a 1 x 3 repeated measures ANOVA. Qualitative themes emerged in response to questions asking about: what facilitates change, what participants do to maintain changes, and what characterized clinical relationships that did and did not go well.

Genomic instability and oncogene amplifications in colorectal adenomas predict recurrence and synchronous carcinoma.

Individual colorectal adenomas have different propensities to progress to invasive disease. In this study, we explored whether these differences could be explained by gene copy number alterations. We evaluated 18 adenomas of patients without synchronous or subsequent carcinoma (6.5 years follow-up), 23 adenomas of carcinoma patients, and 6 related carcinomas. All samples were measured for their DNA ploidy status. Centromere probes for chromosomes 17 and 18, as well as gene-specific probes for SMAD7, EGFR, NCOA3, TP53, MYC, and RAB20 were assessed by multicolor fluorescence in situ hybridization. An increased genomic instability index of CEP17, SMAD7, and EGFR, as well as TP53 deletions and MYC amplifications defined adenomas of patients with synchronous carcinoma (P<0.05). Diploid NCOA3 signal counts were associated with longer adenoma recurrence-free surveillance (P=0.042). In addition, NCOA3, MYC, EGFR, and RAB20 amplifications, as well as TP53 deletions correlated with increased DNA stem line values and/or aneuploidy in adenomas (P<0.05). Furthermore, aberrations of NCOA3, MYC, and RAB20 were associated with histopathologically defined high-risk adenomas (P<0.05). RAB20 amplifications were also correlated with high-grade dysplastic adenomas (P=0.002). We conclude that genomic instability in colorectal adenomas is reflected by EGFR, MYC, NCOA3, and RAB20 amplifications that do correlate with histomorphological features and are indicative for adenoma recurrence and the presence of synchronous carcinomas.

Prognostic and predictive value of 16p12.1 and 16q22.1 copy number changes in human breast cancer.

The present study investigated DNA copy number changes mapping to the p and q arms of chromosome 16 in breast cancer with the goal to determine their potential in identifying breast cancer patients with poor prognosis. We identified the minimal overlapping regions on chromosome 16 that are commonly deleted and amplified in breast tumors. Fluorescence in situ hybridization was used to screen a custom-made breast carcinoma tissue microarray representing all tumor grades, in order to detect DNA copy number changes mapping to 16p12.1 and 16q22.1. We generated 16q/16p ratios for each patient and examined the correlation between DNA copy number alterations and the patients' clinical and pathological parameters. We observed lower q/p ratios in grade I invasive carcinomas, compared with grade III carcinomas, which consistently showed high q/p ratios (P < 0.0091 and 0.0075). In addition, age adjusted for grade analysis revealed that tumors from younger patients (<45 yr) had significantly higher q/p ratios, suggesting that in younger individuals those tumors might be more aggressive (P < 0.0001). The finding that higher q/p ratios occur in younger patients offers a tool to identify high-risk individuals most likely to proceed to high grade.