Impact of the anatomical location, alcoholism and smoking on the prevalence of advanced oral cancer in Brazil.

BACKGROUND: To evaluate the prevalence of oral cancer in Brazil according to the clinical stage, anatomical location, alcoholism and smoking. MATERIAL AND METHODS: Data referring to 31,217 cases of oral cancer, from 2000 to 2010, were obtained from the Integrator Module of the Hospital Registry of Cancer. Inconsistent data ("non-classified" cases) was eliminated and 21,160 cases were analyzed. The frequency distribution according to clinical stage, anatomical location, alcoholism and smoking was analyzed descriptively and through a binary logistic regression model (α<0.05). The clinical stage (dependent variable) was dichotomized in early stage (I and II) or advanced stage (III and IV). The year of diagnosis, anatomical location and deleterious habits (alcoholism and smoking) were considered independent variables. RESULTS: The most frequent characteristics were: oropharynx location (n=3856, 18.41%), clinical stage IV (n=11924, 56.09%) and combined use of alcohol and tobacco (n=19226; 61.59%). The year 2009 (p<0.01, PR = 1.162, CI-95%=1.053-1.283) and location at the base of tongue (p<0.01, PR = 2.485, CI-95% = 2.182-2.807) presented a higher prevalence ratio for advanced stage oral cancer. The combined use of alcohol and tobacco showed a higher prevalence rate for the advanced clinical stage of cancer (p<0.01, PR =1.449, CI-95%=1.382-1.520) if compared to individuals without habits, or just alcoholics. CONCLUSIONS: Higher prevalence of advanced stage of oral cancer is related to the localization at the base of the tongue and to the concomitant use of alcohol and tobacco. Therefore, it can be suggested that all these characteristics lead to a worse prognosis of oral cancer.

Effects of ammonia and lactate on growth, metabolism, and productivity of BHK cells.

The aim of the present work was to study the effect of ammonia and lactate on growth, metabolism, and productivity of BHK cells producing a recombinant fusion protein. Results show that cell growth was reduced with the increase in ammonia or lactate: k(1/2) of 1.1 mM and 3.5 mM for stirred and stationary cultures, respectively, for ammonia and of 28 mM for both stationary and stirred cultures for lactate, were obtained. The cell-specific consumption rates of both glucose (q(Glc)) and glutamine (q(Gln)) increased, whereas that of oxygen (q(O2)) decreased, with the increase in ammonia or lactate concentrations. The cell-specific production rates of lactate (q(Lac)) increased with an increase in ammonia concentration; similarly for the cell-specific production rates of ammonia (q(Amm)), which also increased with an increase in lactate concentration; on the other hand, both q(Lac) and q(Amm) markedly decreased when lactate or ammonia concentrations were increased, respectively; lactate was consumed at lactate concentrations above 30 mM and ammonia was consumed at ammonia concentrations above 5 mM. In vivo (31)P NMR experiments showed that ammonia and lactate affect the intracellular pH, leading to intracellular acidification, and decrease the content in phosphomonoesters, whereas the cell energy state was maintained. The effect of lactate on cell growth and q(Gln) is partially due to osmolarity, on q(Glc) and q(Amm) is entirely due to osmolarity, but on q(Lac) is mainly due to lactate effect per se. An increase in ammonia from 0 to 20 mM induced a 50% reduction in specific productivity, whereas an increase in lactate from 0 to 60 mM induced a 40% decrease.