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Background Cancer is often caused by disturbance in the regulation and /or execution of programmed cell death (PCD, including apoptosis and autophagy). Our aim was to investigate these two pathways simultaneously in the same samples to understand further the pathological roles of PCDs in colorectal cancer. Materials and methods Real time quantitative PCR (RT-qPCR) array was used to analyse the mRNA levels of 22 apoptosis and autophagy-related genes involved in pro- and anti-action of the pathways in 15 paired (tumour and non-cancerous part) colorectal samples using Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as the reference gene. Results GAPDH mRNA content was significantly higher (approximately 4·01 fold) in tumour tissue than that of paired non-cancerous part. The absolute mRNA levels for most of the 22 genes were higher in the tumour tissue also. However, after normalization with GAPDH Ct, the expressions of all the analysed genes were decreased in the tumour tissues, except for damage-regulated autophagy modulator (DRAM). The expression of most of the genes involved in the same pathway was closely correlated to each other in both tumour and non-cancerous tissues, and the correlation of tumour necrosis factor receptor (TNFR) and Akt to other genes in the same pathway was increased in tumour tissues. Conclusions The high level expression of GAPDH might reflect the metabolic state of cancer cells, and PCDs were down-regulated in the tumour tissues when metabolic state was taken into consideration. This relative suppression of PCDs in tumour tissue is supposed to be in favour of cancer cell survival. [ABSTRACT FROM AUTHOR]

Background. The aim of this study was to estimate the relationship of glutathione S-transferases (GST)P1, GSTA1, GSTM1, and GSTT1 gene polymorphisms to oral cancer risk. Methods. Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) was used to measure these 4 gene polymorphisms in 274 controls and 164 oral cancer patients. Results. Individuals with at least 1 varied G allele of GSTP1 had a 1.53-fold risk (95% confidence interval [CI] = 1.01–2.31) of developing oral cancer compared with patients with wild-type A/A homozygotes. Oral cancer patients with at least 1 varied T allele of GSTA1 gene had a 0.42-fold risk (95% CI = 0.18–0.95) of having a tumor size >2 cm compared with patients with C/C homozygotes. Conclusions. The varied G allele of GSTP1 may be considered as a factor contributing to increased susceptibility, whereas the T allele of GSTA1 could be a protective factor for tumor size progression in Taiwanese with oral cancer. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [ABSTRACT FROM AUTHOR]

Background. The aim of this study was to evaluate the relations of SDF-1 and its receptor, CXCR4, gene variants on oral cancer risk. Methods. PCR-RFLP was used to measure SDF-1-3′A and CXCR4 gene polymorphisms in 284 controls and 113 patients with oral cancer. Results. After being adjusted for age, individuals with A/G heterozygotes of SDF-1 had a higher risk of 1.86-fold to develop oral cancer when compared with those with G/G wild type homozygotes. Furthermore, patients with oral cancer with at least 1 mutant T allele of CXCR4 gene had a risk of 2.66-fold to progress to stage III or IV. Conclusions. SDF-1-3′A gene polymorphism may be considered as a factor of increased susceptibility to oral cancer, and at least 1 mutated T allele of CXCR4 gene is associated with the development of stage III or IV and the induction of lymph-node metastasis of oral cancer disease in Taiwanese. © 2009 Wiley Periodicals, Inc. Head Neck, 2009 [ABSTRACT FROM AUTHOR]