Female Perspectives of Professional Identity and Success in the Counseling Field

The purpose of this study was to investigate the contextual and definitional qualities of professional identity as well as the perceptions of success as defined by female counseling professionals. The ideals and beliefs related to professional identity were examined in order to determine if they are upheld by females who practice as professional counselors, counseling doctoral students, and tenure-track counselor educators. Findings indicated 16 themes that addressed issues related to personal and professional congruence and the counseling philosophy; particularly with regard to a conflict with the professional success model as it intersected with personal and professional roles. The information gathered through a grounded theory approach was subsequently used to create an inventory to assess professional identity and success based on the perspectives of women in the field. This inventory was reviewed by experts and consensus coding team members prior to distribution. A quantitative analysis of the inventory was then conducted with male and female participants from the same professional demographic pool as the qualitative portion of the study. Discriminant, correlational, and regression analyses were performed in order to determine if the new inventory was compatible with the values and perspectives of female professionals and with a previously developed inventory developed to assess the counseling professional identity. Male professionals were included in quantitative procedures and analyses. Males were included in the analysis to determine if the data related to the responses of female counseling professionals were significantly different than those of their male counterparts. Significant statistical and practical differences for gender, status of development (student, faculty, and practitioner roles), family composition, and amount of income participants allocated to professional activities were found. Gender differences indicated significantly higher subscale scores for male professionals with regard to engagement and development and lower subscale scores for professional beliefs and orientation. Those who spent between 6-20% of their annual net income on professional activities were found to have significantly higher subscale scores across all dimensions of both instruments used. Implications for training and the counseling field are presented with the findings

Psychosocial Correlates of Insomnia Severity in Primary Care

Purpose: Insomnia is a substantive primary care issue that leads to adverse outcomes. These can be improved by addressing factors that accentuate insomnia severity. Accordingly, this study identifies correlates of insomnia severity and determines whether these relationships vary with sociodemographic attributes. Methods: This correlational cross-sectional study was conducted in a hospital-sponsored primary care clinic and 2 urban, academic family practice centers. Participants consisted of 236 patients 18 years old or older with clinically significant insomnia (Insomnia Severity Index scores of 7 or more). Surveys instruments included the Insomnia Severity Index, SF-8 (Medical Outcomes Study SF-8 global health status measure), CES-D (Center for Epidemiologic Studies-Depression Scale), DBAS (Dysfunctional Beliefs about Sleep scale), SE-S (Self-Efficacy for Sleep Scale), and a researcher-designed demographic survey. Analytic techniques included descriptive statistics to characterize the study sample, Pearson or Spearman Correlation Coefficients to examine individual associations with insomnia severity, and step-wise linear regression to identify net predictors. Results: Insomnia severity was significantly correlated with health status, depression, self-efficacy, and dysfunctional beliefs (P \u3c .001) but not with sociodemographic attributes. Linear regression demonstrated insomnia severity was best predicted by low self-efficacy and high depression scores. Discussion: These findings indicate that clinicians treating insomnia should not only manage comorbid depression but also facilitate self-efficacy for sleep-inducing behavioral change

Acceptability of Behavioral Treatments for Insomnia

Background: Behavioral treatments for insomnia are safe and efficacious but may not be embraced by patients in primary care. Understanding factors associated with acceptability can enhance successful use of these modalities. The objective of this study was to identify demographic and clinical/psychosocial correlates of behavioral insomnia treatment acceptability. Methods: This nonexperimental, inventory-based, cross-sectional study enrolled patients from a hospital-sponsored primary care clinic and 2 urban academic family practices. Participants (n = 236) were 18 years of age or older who had clinically significant insomnia (Insomnia Severity Index score \u3e= 8) and were recruited consecutively at these sites. A study coordinator obtained informed consent then distributed survey materials. Participants received a $10 honorarium. The main outcome measure was the Acceptability Insomnia Treatment Acceptability Scale-Behavioral subscale (ITAS-B). Results: Only acceptability of medications (r = 0.259) and dysfunctional beliefs (r = 0.234) scores had significant bivariate correlations with ITAS-B scores (P \u3c .001). Medication acceptability, dysfunctional beliefs, and self-efficacy accounted for 12.45% of ITAS-B variance in linear regression. Conclusions: Screening for dysfunctional beliefs about sleep may identify patients with interest in behavioral approaches. Improving self-efficacy for sleep may improve acceptance of behavioral insomnia therapies. Interest in behavioral and medication treatments are not mutually exclusive. However, the modest variance reported here suggests other factors impact acceptance of behavioral treatments

Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

Peer reviewedPublisher PD

Evaluation of polygenic risk scores for breast and ovarian cancer risk prediction in BRCA1 and BRCA2 mutation carriers

Background: Genome-wide association studies (GWAS) have identified 94 common single-nucleotide polymorphisms (SNPs) associated with breast cancer (BC) risk and 18 associated with ovarian cancer (OC) risk. Several of these are also associated with risk of BC or OC for women who carry a pathogenic mutation in the high-risk BC and OC genes BRCA1 or BRCA2. The combined effects of these variants on BC or OC risk for BRCA1 and BRCA2 mutation carriers have not yet been assessed while their clinical management could benefit from improved personalized risk estimates. Methods: We constructed polygenic risk scores (PRS) using BC and OC susceptibility SNPs identified through population-based GWAS: for BC (overall, estrogen receptor [ER]-positive, and ER-negative) and for OC. Using data from 15 252 female BRCA1 and 8211 BRCA2 carriers, the association of each PRS with BC or OC risk was evaluated using a weighted cohort approach, with time to diagnosis as the outcome and estimation of the hazard ratios (HRs) per standard deviation increase in the PRS. Results: The PRS for ER-negative BC displayed the strongest association with BC risk in BRCA1 carriers (HR = 1.27, 95% confidence interval [CI] = 1.23 to 1.31, P = 8.2 x 10(53)). In BRCA2 carriers, the strongest association with BC risk was seen for the overall BC PRS (HR = 1.22, 95% CI = 1.17 to 1.28, P = 7.2 x 10(-20)). The OC PRS was strongly associated with OC risk for both BRCA1 and BRCA2 carriers. These translate to differences in absolute risks (more than 10% in each case) between the top and bottom deciles of the PRS distribution; for example, the OC risk was 6% by age 80 years for BRCA2 carriers at the 10th percentile of the OC PRS compared with 19% risk for those at the 90th percentile of PRS. Conclusions: BC and OC PRS are predictive of cancer risk in BRCA1 and BRCA2 carriers. Incorporation of the PRS into risk prediction models has promise to better inform decisions on cancer risk management

Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.

Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression

BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

Common variants in LSP1, 2q35 and 8q24 and breast cancer risk for BRCA1 and BRCA2 mutation carriers

Genome-wide association studies of breast cancer have identified multiple single nucleotide polymorphisms (SNPs) that are associated with increased breast cancer risks in the general population. In a previous study, we demonstrated that the minor alleles at three of these SNPs, in FGFR2, TNRC9 and MAP3K1, also confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. Three additional SNPs rs3817198 at LSP1, rs13387042 at 2q35 and rs13281615 at 8q24 have since been reported to be associated with breast cancer in the general population, and in this study we evaluated their association with breast cancer risk in 9442 BRCA1 and 5665 BRCA2 mutation carriers from 33 study centres. The minor allele of rs3817198 was associated with increased breast cancer risk only for BRCA2 mutation carriers [hazard ratio (HR) = 1.16, 95% CI: 1.07–1.25, P-trend = 2.8 × 10−4]. The best fit for the association of SNP rs13387042 at 2q35 with breast cancer risk was a dominant model for both BRCA1 and BRCA2 mutation carriers (BRCA1: HR = 1.14, 95% CI: 1.04–1.25, P = 0.0047; BRCA2: HR = 1.18 95% CI: 1.04–1.33, P = 0.0079). SNP rs13281615 at 8q24 was not associated with breast cancer for either BRCA1 or BRCA2 mutation carriers, but the estimated association for BRCA2 mutation carriers (per-allele HR = 1.06, 95% CI: 0.98–1.14) was consistent with odds ratio estimates derived from population-based case–control studies. The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers. There was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not