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Our previous study showed high frequency of allelic loss at chromosome 2q37 region in oral cancer. This location contains several candidate tumor suppressor genes such as PPP1R7, ILKAP, DTYMK and ING5. We previously showed 3 members of inhibitor of growth (ING) family, ING1, ING3 and ING4 as tumor suppressor gene in head and neck cancer. As ING5 shows high homology with other members of ING genes including highly conserved carboxy-terminal plant homeodomain and nuclear localization signal, we first picked up ING5 and examined it as a possible tumor suppressor in oral cancer. For this aim, mutation and mRNA expression status of ING5 in paired normal and oral squamous cell carcinoma samples were examined by reverse transcription polymerase chain reaction (RT-PCR) and sequencing. Three missense mutations located within leucine zipper like (LZL) finger and novel conserved region (NCR) domains in ING5 protein were detected, probably abrogating its normal function. We also found 5 different alternative splicing variants of ING5. Then, we examined mRNA level of ING5 by quantitative real time reverse transcription polymerase chain reaction (qRT-PCR) analysis, which demonstrated decreased expression of ING5 mRNA in 61% of the primary tumors as compared to the matched normal samples. In conclusion, tumor-specific mutation and downregulation of ING5 mRNA suggested it as a tumor suppressor gene in oral squamous cell carcinoma.Oral and oropharyngeal squamous cell carcinoma is the 6th most frequently occurring cancer worldwide, with $400,000 new cases diagnosed each year. 1 Similar to other type of cancer, oral squamous cell carcinoma (OSCC) is the result of accumulation of multiple genetic events in the cell. Among these events, inactivation of tumor suppressor genes (TSG) is considered to be an important step in carcinogenesis. Thus, localization and identification of TSG are of great interest for a better comprehension of cancer and development of molecular diagnostics as well as therapies.TSG are referred as genetic elements with negative influence on cell proliferation and growth. 2 Inactivation of TSG causes cells to display one or more phenotypes of neoplastic growth. Knudson's definition of a classical TSG requires inactivation of both alleles of a candidate gene in tumors. 3 Inactivation of these classical TSG usually occurs through deletion of one of its allele and mutation in the rest of the allele. However, a new class of TSG with haploid insufficiency, in which one allele is lost and the remaining allele is haploinsufficient, has been described recently, and these hemizygous TSG show a tumor-prone phenotype when challenged with carcinogens. 4,5 One of the critical steps for the identification of TSG is loss of heterozygosity (LOH) analysis. By using LOH analysis, we recently showed high frequency of allelic loss on chromosomes 13q34, 7q31 and 12p13 in oral, and head and neck cancer. Our continuous effort for detailed analysis of these regions resulted in identification of various inhibitor of growth (ING) tumor s...

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In the present study, the expression levels of TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, and TRPM8 genes were evaluated in heart tissues after ischemia/reperfusion (IR). For this study, 30 albino male Wistar rats were equally divided into three groups as follows: Group 1: control group (n:10), Group II: ischemia group (ischemia for 60 min) (n:10) and Group III: IR (reperfusion 48 h after ischemia for 60 min and reperfusion for 48 h). The expression levels of the TRPM genes were analyzed by semi-quantitative reverse transcriptase-PCR. When compared to the ischemia control, the expression levels of TRPM2, TRPM4, and TRPM6 did not change, whereas that of TRPM7 increased. However, TRPM1, TRPM3, TRPM5, and TRPM8 were not expressed in heart tissue. Histopathological analysis of the myocardial tissues showed that the structures that were most damaged were those exposed to IR. The findings showed that there is a positive relationship between TRPM7 expression and myocardial IR injury.

The effect of occupational lead exposure on the liver function and on the blood biochemical parameters among the battery workers and the muffler repair workers was studied. The study included 22 battery and 38 muffler repair workers. Whole blood lead levels were determined by atomic absorption spectrophotometers. Total protein, albumin, globulin, cholesterol, triglyceride, total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), gamma glutamyltransferase (GGT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) levels were determined in the serum by spectrophotometry. The blood lead levels of the battery workers, muffler repair workers, and the controls were found to be 36.83 +/- 8.13 microg/dL, 26.99 +/- 9.42 microg/dL, and 14.81 +/- 3.01 microg/dL, respectively. Blood lead levels of the workers were significantly higher than those of controls (p < 0.001). The lead level of the battery workers was also significantly higher than that of muffler repair workers (p < 0.001). Although, statisticly significant, higher blood lead levels are not related to toxicity for battery and muffler repair workers. Total protein, globulin, cholesterol, LDH, and ALP levels were within normal levels, however, they were slightly higher than the control levels. Increased LDH among the workers seems to be related rather to other causes than to the liver injury.