Molecular pathology of XXXX .

@entity135 @entity286 @entity5 @entity167 @entity957 @entity204 @entity213
@entity957 of the @entity135 ( @entity213 ) is the sixth most frequent @entity5 worldwide, comprising almost 50% of all @entity5 in some developing nations. In the United States, 30,000 new cases and 8,000 @entity204 are reported each year. Survival rates vary depending on @entity286 and @entity167 consumption, age, gender, ethnic background, and geographic area. This variability reflects the multifactorial pathogenesis of the disease. Early detection and diagnosis has increased survival but the overall 5 year rate of 50% is among the lowest of the major @entity5 . Differences between normal epithelium and @entity5 cells of the upper aerodigestive tract arise from specific alterations in genes controlling DNA repair, proliferation, immortalization, apoptosis, invasion, and angiogenesis. These proteins include both @entity5 suppressors and activating oncogenes which regulate a wide variety of intracellular signaling pathways. Included in these pathways are growth factor receptors, signal transducers, and transcription factors which regulate DNA damage response, cell cycle arrest, and programmed cell death. In @entity135 , alterations of three signaling pathways occur with sufficient frequency and produce such dramatic phenotypic changes as to be considered the critical transforming events of the disease. These changes include mutation of the p53 @entity5 suppressor, inactivation of the cyclin dependent kinase inhibitor p16, and overexpression of epidermal growth factor receptor (EGFR). This review will focus on the molecular changes which occur in these pathways and how they contribute to the pathogenesis of @entity213 .
