Periodontal-Systemic Disease Education in U.S. and Canadian Dental Schools

Research has proliferated in recent years regarding the relationship of oral disease to systemic conditions. Specifically, periodontal disease has been studied as a potential risk factor for multiple conditions such as cardiovascular disease (CVD) and adverse pregnancy outcomes, while other research focuses on exposures or behaviors associated with oral disease. However, few articles have been published reporting how this information is integrated into schools of dentistry, both in the classroom and clinical curriculum. For our study, a thirty-three-item survey and cover letter were electronically mailed to academic deans at sixty-five accredited dental schools in the United States and Canada in the fall of 2007. The response rate was 77 percent. According to the responses to this survey, the primary topics covered in the didactic curriculum regarding periodontal oral-systemic disease are aging, CVD, diabetes, and tobacco use. Eighty-eight percent of the respondents reported that their students are knowledgeable about the role of inflammation and its impact on oral-systemic conditions. Forty-eight percent of the respondents said they provide formal training for their students in how to discuss or communicate aspects of periodontal oral-systemic disease with patients. Only seven schools reported teaching didactic content to dental students intermixed with other health professions students, and only two schools reported conducting joint projects. Only 9 percent of the respondents said they think nurses and physicians are knowledgeable about oral-systemic disease. The findings indicate that dental schools are confident about the knowledge of their students regarding oral-systemic content. However, much work is needed to educate dental students to work in a collaborative fashion with other health care providers to co-manage patients at risk for oral-systemic conditions

Hiring Criteria in Biology Departments of Academic Institutions

We surveyed faculty in the biology departments of US institutions of higher education to compare the experience and training valued by faculty at hiring institutions with the experience and training most graduate students receive. Our data show that associate, baccalaureate, and master\u27s institutions value teaching experience and skills more highly than research skills. In contrast, doctoral institutions place a higher value on the ability to publish research and obtain outside funding. These findings provide quantitative and qualitative insight into discrepancies between the values of those who train graduate students in biology and the expectations of the institutions likely to hire these individuals

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

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

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicity

BACKGROUND: There is a large body of evidence which suggests that bile acids increase the risk of colon cancer and act as tumor promoters, however, the mechanism(s) of bile acids mediated tumorigenesis is not clear. Previously we showed that deoxycholic acid (DCA), a tumorogenic bile acid, and ursodeoxycholic acid (UDCA), a putative chemopreventive agent, exhibited distinct biological effects, yet appeared to act on some of the same signaling molecules. The present study was carried out to determine whether there is overlap in signaling pathways activated by tumorogenic bile acid DCA and chemopreventive bile acid UDCA. METHODS: To determine whether there was an overlap in activation of signaling pathways by DCA and UDCA, we mutagenized HCT116 cells and then isolated cell lines resistant to UDCA induced growth arrest. These lines were then tested for their response to DCA induced apoptosis. RESULTS: We found that a majority of the cell lines resistant to UDCA-induced growth arrest were also resistant to DCA-induced apoptosis, implying an overlap in DCA and UDCA mediated signaling. Moreover, the cell lines which were the most resistant to DCA-induced apoptosis also exhibited a greater capacity for anchorage independent growth. CONCLUSION: We conclude that UDCA and DCA have overlapping signaling activities and that disregulation of these pathways can lead to a more advanced neoplastic phenotype