Association of Race/Ethnicity, Stage, and Survival in Oral Cavity Squamous Cell Carcinoma: A SEER Study.

OBJECTIVE: Survival differences in oral cancer between black and white patients have been reported, but the contributing factors, especially the role of stage, are incompletely understood. Furthermore, the outcomes for Hispanic and Asian patients have been scarcely examined. STUDY DESIGN: Retrospective, population-based national study. SETTING: Surveillance, Epidemiology, and End Results 18 Custom database (January 1, 2010, to December 31, 2014). SUBJECTS AND METHODS: In total, 7630 patients with primary squamous cell carcinoma in the oral cavity were classified as non-Hispanic white (white), non-Hispanic black (black), Hispanic, or Asian. Cox regression was used to obtain unadjusted and adjusted hazard ratios (HRs) of 5-year mortality for race/ethnicity with sequential adjustments for stage and other covariates. Logistic regression was used to examine the relationship between race/ethnicity and stage with adjusted odds ratios (aORs). RESULTS: The cohort consisted of 75.0% whites, 7.6% blacks, 9.1% Hispanics, and 8.3% Asians. Compared to whites, the unadjusted HR for all-cause mortality for blacks was 1.68 (P < .001), which attenuated to 1.15 (P = .039) after adjusting for stage and became insignificant after including insurance. The unadjusted HRs for all-cause mortality were not significant for Hispanics and Asians vs whites. Compared to whites, blacks and Hispanics were more likely to present at later stages (aORs of 2.63 and 1.42, P < .001, respectively). CONCLUSION: The greater mortality for blacks vs whites was largely attributable to the higher prevalence of later stages at presentation and being uninsured among blacks. There was no statistically significant difference in mortality for Hispanics vs whites or Asians vs whites.

An Unusual Presentation of B-Cell Lymphoma as a Large Isolated Epiglottic Mass: Case Report and Literature Review.

Extranodal presentation of B-cell lymphoma is uncommon. Isolated primary epiglottic B-cell lymphoma is even rarer. To our knowledge, there has been only one description of isolated B-cell lymphoma presenting as a large epiglottic mass. We report an unusual type of B-cell lymphoma of the epiglottis, as it could not be subtyped based on routine staining and hybridization. The lymphoma presented as a large isolated globular mass pedicled to the epiglottis, occupying most of the oropharynx, but did not have any ball-valving effect or increased respiratory efforts. Initial radiographic findings were nonspecific. The diagnosis of B-cell lymphoma was determined by transoral incisional biopsy under local anesthesia. The condition was treated successfully with chemoradiation. The current standard of treatment for high grade B-cell lymphoma is concurrent chemoradiotherapy, with excellent prognosis. Although rare, B-cell lymphoma should be considered when investigating pedunculated hypopharyngeal masses.

A novel dominant negative Smad2 mutation in a TGFbeta resistant human carcinoma cell line.

An important biological mechanism contributing to the transformed phenotype of cancer cells is the ability to escape normal growth regulatory signals. In epithelial cells, transforming growth factor beta (TGFbeta) inhibits cell cycle progression in the G1-phase. The abnormal ability of cancer cells to escape TGFbeta-induced cell cycle inhibition may lead to deregulated mitosis, providing a growth advantage to these clones. The effects of TGFbeta are mediated through type I and type II receptors, which are transmembrane proteins possessing cytoplasmic serine/threonine kinase domains for signal propagation. TGFbeta binds to the type II receptor which then phosphorylates the cytoplasmic domain of the type I receptor. The receptor complex recruits and phosphorylates the downstream signaling proteins, Smad2 and Smad3, which then associate with Smad4. The Smad complex translocates to the nucleus to regulate target gene expression resulting in cell cycle inhibition. We have identified a new Smad2 mutation in a TGFbeta-resistant human carcinoma line. The mutant Smad2 protein exhibits decreased association with the receptor complex, is not phosphorylated in response to TGFbeta, fails to associate with Smad4 and does not localize to the nucleus. Expression of the mutant Smad2 protein in a TGFbeta sensitive carcinoma line induces resistance to this growth inhibitory factor and deregulates TGFbeta-responsive gene expression. These results indicate that this novel Smad2 mutant protein has dominant negative activity in cultured cells.