The importance of quality of life (QOL) outcomes following treatments for head and neck tumors are now increasingly appreciated and measured to improve medical and surgical care for these patients. An understanding of the definitions in the setting of health care and the use of appropriate QOL instruments and measures are critical to obtain meaningful information that guides decision making in various aspects of patient health care. QOL outcomes following cranial base surgery is only recently being defined. In this article, we describe the current published data on QOL outcomes following cranial base surgery and provide preliminary prospective data on QOL outcomes and sinonasal morbidity in patients who underwent endonasal cranial base surgery for management of various skull base tumors at our institution. We used a disease-specific multidimensional instrument to measure QOL outcomes in these patients. Our results show that although sinonasal morbidity is increased, this is temporary, and the vast majority of patients have a very good QOL by 4 to 6 months after endonasal approach to the cranial base.

Purpose A key issue in cancer is apoptosis resistance. However, little is known about the transcription factors which contribute to cellular survival of head and neck squamous cell carcinoma (HNSCC). Experimental design Three batches (54, 64, and 38) of HNSCC specimens were used for cellular and molecular analyses in order to determine the major molecular signaling pathways for cellular survival in HNSCC. Animal models (cell culture and xenografts) were employed to verify the importance of apoptosis resistance in HNSCC. Results Inhibitor of differentiation (Id) family member, Id1, was significantly up-regulated in clinical HNSCC specimens and acted to protect keratinocytes from apoptosis. Transfection of HNSCC cells with Id1 in vitro induced the phosphorylation of Akt (p-Akt) via phosphoinositide kinase-3 (PI3K) and increased the expression of survivin via nuclear factor kappa B (NF-κB). Blockage of the both pathways by specific inhibitors (LY294002 and IκBαM, respectively) abrogated Id1-induced cell survival of keratinocytes. In vivo studies demonstrated that increased expression of Id1 allowed non-tumorigenic keratinocytes (Rhek-1A) to become tumorigenic in nude mice by increased expression of survival genes such as p-Akt and survivin. More importantly, short interfering RNA (siRNA) for Id1 significantly reduced HNSCC tumorvolume of HNSCC in xenograft studies. Analysis of clinical data verified the importance of the Id1 downstream molecule, survivin, in the prognosis of HNSCC patients. Conclusions The above data, taken together, suggest that Id1 and its downstream effectors are potential targets for treatment of HNSCC because of their contribution to apoptosis resistance.

The reverse flap provides complete remucosalization of the denuded donor septum, decreasing septal crusting within the first 1 to 2 postoperative weeks, and adds minimal morbidity.

NF-κB is activated during acute inflammatory states as well as in other injury response disease states. Several pathologic states in squamous tissue injury response are characterized by increased squamous proliferation. This study was performed to investigate the hypothesis that Pseudomonas aeruginosa LPS is able to activate a proliferative phenotype in squamous cells via NF-κB induction and that this NF-κB-mediated response may be abrogated with the classic anti-inflammatory agent indomethacin. EMSA, luciferase reporter gene experiments, Western blots, and cellular proliferation assays were performed in normal and transformed human keratinocytes after stimulation with P. aeruginosa LPS. EMSA and luciferase reporter gene assays showed a 3- to 5-fold induction of active NF-κB in human keratinocyte cell lines after stimulation with P. aeruginosa LPS. The stimulation correlated with significantly increased cellular proliferation. As one potential mechanism for this increase in proliferation, an NF-κB-specific activation of cyclin D1 was observed. Both the NF-κB induction and proliferation response were inhibited with indomethacin and in dominant negative stable transfection clones. P. aeruginosa LPS activates proliferation of human keratinocytes, potentially through the induction of NF-κB and cyclin D1. These findings suggest that bacterial components can contribute to proliferative disease states in squamous epithelium through NF-κB activation.