1999 Media Guide

1999 Men\u27s Track and Field Media Guide, George Fox College

Supplementary Table S1 from Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Supplementary Table S1 provides a summary of the whole-exome sequencing analysis for normal and tumor samples.</p

Supplementary Table S4 from Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Supplementary Table S4 provides information on the spectra of mutations seen in MEC tumors of varying histologic grades.</p

Supplementary Table S2 from Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Supplementary Table S2 provides a comprehensive list of somatic mutations identified via whole-exome sequencing in 18 MEC tumor samples.</p

Supplementary Figure S1 from Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Figure S1 contains representative images of cells with and without the MECT1-MAML2 translocation, as determined by fluorescence in situ hybridization.</p

Supplementary Table S3 from Whole-Exome Sequencing of Salivary Gland Mucoepidermoid Carcinoma

Supplementary Table S3 contains information on the clinical characteristics and mutational landscapes of MEC tumors of varying histologic grades.</p

Discovery tumor clinical characteristics.

<p>Discovery tumor clinical characteristics.</p

Expression Microarray Analysis Reveals Alternative Splicing of <i>LAMA3</i> and <i>DST</i> Genes in Head and Neck Squamous Cell Carcinoma

<div><p>Purpose</p><p>Prior studies have demonstrated tumor-specific alternative splicing events in various solid tumor types. The role of alternative splicing in the development and progression of head and neck squamous cell carcinoma (HNSCC) is unclear. Our study queried exon-level expression to implicate splice variants in HNSCC tumors.</p><p>Experimental Design</p><p>We performed a comparative genome-wide analysis of 44 HNSCC tumors and 25 uvulopalatopharyngoplasty (UPPP) tissue samples at an exon expression level. In our comparison we ranked genes based upon a novel score—the Maximum-Minimum Exon Score (MMES) – designed to predict the likelihood of an alternative splicing event occurring. We validated predicted alternative splicing events using quantitative RT-PCR on an independent cohort.</p><p>Results</p><p>After MMES scoring of 17,422 genes, the top 900 genes with the highest scores underwent additional manual inspection of expression patterns in a graphical analysis. The genes <i>LAMA3, DST, VEGFC, SDHA, RASIP1</i>, and <i>TP63</i> were selected for further validation studies because of a high frequency of alternative splicing suggested in our graphical analysis, and literature review showing their biological relevance and known splicing patterns. We confirmed <i>TP63</i> as having dominant expression of the short <i>DeltaNp63</i> isoform in HNSCC tumor samples, consistent with prior reports. Two of the six genes (<i>LAMA3</i> and <i>DST</i>) validated by quantitative RT-PCR for tumor-specific alternative splicing events (Student's t test, P<0.001).</p><p>Conclusion</p><p>Alternative splicing events of oncologically relevant proteins occur in HNSCC. The number of genes expressing tumor-specific splice variants needs further elucidation, as does the functional significance of selective isoform expression.</p></div

Probing requirements to bind a 42kDa cellular target and accumulate high molecular weight polyubiquitinated proteins.

(A) Chemical structures of candidate inhibitors. (B) Precleared ES2 cell lysate was incubated with compounds (20 μM) or vehicle (DMSO, 1:100) for 45 min and then with RA190B (5 μM) for 45 min at 4°C. Samples were subjected to SDS-PAGE, transfer to PVDF membrane, and after probing with HRP-streptavidin, binding was detected using chemiluminescence. (C) ES2 cells were treated with compounds (1 μM, 4 hr), lysed and the samples probed with ubiquitin or actin-specific antibody by Western blot.</p

Validation tumor clinical characteristics.

<p>Validation tumor clinical characteristics.</p