GST M1 and CYP1A1 gene polymorphism and daily fruit consumption in Turkish patients with non-small cell lung carcinomas

Background: In general, the metabolism of carcinogens involves two pathways. The oxidative pathway, which enhances carcinogenesis (phase I), and the protective pathway, in which carcinogens are conjugated with a series of substances such as glutathione to achieve detoxification (phase II). It has been suggested that an increased phase I enzyme activity (CYP1A1) and a decreased phase II enzyme activity (GST M1) could each individually cause an increase in the risk of cancer. Materials and Methods: In the present study we explored the association between genetic polymorphisms of CYP1A1 and GST M1 and non-small cell lung cancer (n = 55) and controls (n = 60) in Turkish subjects. We used PCR methods and enzyme restriction for determining polymorphism. A standard food questionnaire was used to determine daily fresh fruit consumption. Results and Conclusion: We found that CYP1A1 mutant variant (Ile/Val) was more highly expressed in Turkish patients and controls than in other Caucasian populations. Our findings were similar to Far Eastern populations (32.7% for patient group, 43.1% for controls). In spite of the similarity between the groups regarding GST M1 polymorphism, in the patient group, patients with GST M1 null genotype had a statistically significant positive history of exposure to carcinogens other than smoking, such as asbestos, petrochemicals and/or other chemicals (p = 0.01). The patients, who had CYP1A1 mutant variant, had increased risk of,adenocarcinoma (p = 0.046) of lung (8 out of 18 patients) and 6 of them also had GST M1 (-) gene variants together. The patients who consumed less fruit daily had a greater risk of epidermoid carcinoma of lung (p = 0.019). However this study showed that there were no differences between the patient and control groups regarding genetic polymorphism of genes

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field