The Management Development Program: A Competency-Based Model for Preparing Hospitality Leaders

As management educators increasingly focus their attention on instructional outcomes, competency-based education has emerged as an important component in graduate business education. The most sought after graduate students are not only knowledgeable in business fields but also demonstrate competence in critical managerial skills. This article focuses on the development, implementation, and assessment of a competency-based component of the Master of Management in Hospitality program at the School of Hotel Administration at Cornell University. This program component assesses and directs the development of graduate students’ skills in writing, presentational speaking, and leadership/group process skills. To the extent that it has proven effective in accomplishing its objectives, it may serve as a model for business educators interested in including competency-based education in their programs

Work group inclusion : test of a scale and model

We develop a theoretically based 10-item measure of work group inclusion comprised of two components (belongingness and uniqueness) and use this measure to empirically test the nomological network of work group inclusion developed by Shore et al. In Phase 1, we use two samples of full-time employees to develop and refine items as well as establish content validity. In Phase 2, we demonstrate convergent, discriminant, and incremental validity with both conceptually related and unrelated constructs. In Phase 3, we use data from an additional sample of employees and supervisors to test criterion-related validity and mediation by examining the multilevel relationships between inclusion and important antecedents and outcomes. Across the three phases of our study, the results demonstrate support not only for the factor structure, reliability, and validity of our work group inclusion measure but also for a theoretical model in which the construct of inclusion has important implications for individuals and organizations

Inclusive leadership : realizing positive outcomes through belongingness and being valued for uniqueness

We introduce a theoretically-grounded conceptualization of inclusive leadership and present a framework for understanding factors that contribute to and follow from inclusive leadership within work groups. We conceptualize inclusive leadership as a set of positive leader behaviors that facilitate group members perceiving belongingness in the work group while maintaining their uniqueness within the group as they fully contribute to group processes and outcomes. We propose that leader pro-diversity beliefs, humility, and cognitive complexity increase the propensity of inclusive leader behaviors. We identify five categories of inclusive leadership behaviors that facilitate group members' perceptions of inclusion, which in turn lead to member work group identification, psychological empowerment, and behavioral outcomes (creativity, job performance, and reduced turnover) in the pursuit of group goals. This framework provides theoretical grounding for the construct of inclusive leadership while advancing our understanding of how leaders can increase diverse work group effectiveness

Grooming Future Hospitality Leaders: A Competencies Model

Competency models can be useful tools for identifying and grooming future leaders. Rather than base leadership assessment on personality traits or other unrelated characteristics, competency models specify the actions and behavior needed for successful leaders. While some hotel companies have begun to identify leadership competencies, the hotel industry does not have an overall competency model. Starting with competency models from other industries and the assessments from a pilot study, the authors compiled a list of 99 competencies or skills (grouped into eight overarching factors comprising 28 dimensions) that might contribute to leadership success in the hospitality industry. Those competencies were rated on a five-point scale, ranging from not at all important to extremely important, in a survey of 137 industry leaders. The competency labeled “self-management” was the top dimension (of the 28)—composed of ethics and integrity, time management, flexibility and adaptability, and self-development. Second in importance was competency in strategic positioning, comprising awareness of customer needs, commitment to quality, managing stakeholders, and concern for the community. (However, concern for the community was rated least important compared to the other three dimensions in that category). Industry knowledge, leadership, and interpersonal skill were factors that, while important, were ranked lower by the respondents

PAR1- and PAR2-induced innate immune markers are negatively regulated by PI3K/Akt signaling pathway in oral keratinocytes

<p>Abstract</p> <p>Background</p> <p>Protease-Activated Receptors (PARs), members of G-protein-coupled receptors, are activated by proteolytic activity of various proteases. Activation of PAR1 and PAR2 triggers innate immune responses in human oral keratinocytes (HOKs), but the signaling pathways downstream of PAR activation in HOKs have not been clearly defined. In this study, we aimed to determine if PAR1- and PAR2-mediated signaling differs in the induction of innate immune markers CXCL3, CXCL5 and CCL20 via ERK, p38 and PI3K/Akt.</p> <p>Results</p> <p>Our data show the induction of innate immunity by PAR1 requires both p38 and ERK MAP kinases, while PAR2 prominently signals via p38. However, inhibition of PI3K enhances expression of innate immune markers predominantly via suppressing p38 phosphorylation signaled by PAR activation.</p> <p>Conclusion</p> <p>Our data indicate that proteases mediating PAR1 and PAR2 activation differentially signal via MAP kinase cascades. In addition, the production of chemokines induced by PAR1 and PAR2 is suppressed by PI3K/Akt, thus keeping the innate immune responses of HOK in balance. The results of our study provide a novel insight into signaling pathways involved in PAR activation.</p

Accuracy of Risk Estimates from the iPrevent Breast Cancer Risk Assessment and Management Tool.

BACKGROUND: iPrevent is an online breast cancer (BC) risk management decision support tool. It uses an internal switching algorithm, based on a woman's risk factor data, to estimate her absolute BC risk using either the International Breast Cancer Intervention Study (IBIS) version 7.02, or Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm version 3 models, and then provides tailored risk management information. This study assessed the accuracy of the 10-year risk estimates using prospective data. METHODS: iPrevent-assigned 10-year invasive BC risk was calculated for 15 732 women aged 20-70 years and without BC at recruitment to the Prospective Family Study Cohort. Calibration, the ratio of the expected (E) number of BCs to the observed (O) number and discriminatory accuracy were assessed. RESULTS: During the 10 years of follow-up, 619 women (3.9%) developed BC compared with 702 expected (E/O = 1.13; 95% confidence interval [CI] =1.05 to 1.23). For women younger than 50 years, 50 years and older, and BRCA1/2-mutation carriers and noncarriers, E/O was 1.04 (95% CI = 0.93 to 1.16), 1.24 (95% CI = 1.11 to 1.39), 1.13 (95% CI = 0.96 to 1.34), and 1.13 (95% CI = 1.04 to 1.24), respectively. The C-statistic was 0.70 (95% CI = 0.68 to 0.73) overall and 0.74 (95% CI = 0.71 to 0.77), 0.63 (95% CI = 0.59 to 0.66), 0.59 (95% CI = 0.53 to 0.64), and 0.65 (95% CI = 0.63 to 0.68), respectively, for the subgroups above. Applying the newer IBIS version 8.0b in the iPrevent switching algorithm improved calibration overall (E/O = 1.06, 95% CI = 0.98 to 1.15) and in all subgroups, without changing discriminatory accuracy. CONCLUSIONS: For 10-year BC risk, iPrevent had good discriminatory accuracy overall and was well calibrated for women aged younger than 50 years. Calibration may be improved in the future by incorporating IBIS version 8.0b

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

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN