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    • Previous work on a limited scale

    2018-11-13

    Previous work, on a limited scale compared to Yu et al.\'s, has also sought to explore the mutational spectrum of lung cancer tissues in Xuanwei. A small exploratory study among 40 never smoking females who had NSCLCs from Xuanwei had mutations detected in 35% of tumors (). mutations were observed in 15% of tumors, and and mutations were mutually exclusive. Most and point mutations were transversions and were also found in tumors from patients who used coal in their homes. The observed high mutation frequencies in Gefitinib manufacturer 18 and and low mutation frequency in exon 21 were strikingly divergent from those in other smoking and never smoking populations from Asia, suggesting a unique signature of lung cancer attributed to coal smoke. Overall, it appears that populations who have unique environmental exposures, such as burning coal indoors, may be susceptible to lung cancer attributed to unique underlying mechanisms of pathogenesis. Although household air pollution has been classified as a Group 1 human carcinogen, little is known about the underlying mechanism of tumorigenesis. Yu et al.\' findings are an important step in uncovering the mutation spectrum of air pollution-related lung cancers. The genes associated with lung cancer that were observed by Yu et al. provide mechanistic evidence as to what biological pathways are involved in the relationship between air pollution and lung cancer. Additionally, this research provides evidence for the pollution exposure-genomic variation relationship at a large scale, potentially providing a spring board for future research analyzing genomic variants in never smoking patients who are exposed to vast amounts of inhalable pollution. As with many genomic applications, however, researchers should replicate these findings in additional populations prior to considering translation to the clinic. Given that roughly 50% of all lung cancer cases reported in women and 15% of lung cancer cases reported in men throughout the world are not attributable to tobacco use (), understanding the underlying mechanism of lung carcinogenesis related to exposures other than tobacco may have a large impact on the global burden of disease. Funding
    Authors\' Contributions
    Acknowledgments
    Telomeres are the protective structure at both ends of each chromosome. Telomere length is widely considered a marker of biological aging. For convenience, telomere lengths in human population studies have been predominately measured in peripheral blood leukocytes. Although leukocyte telomere length (LTL) is generally inversely correlated with age, there is considerable inter-individual variation of LTL among people of the same ages (). An individual\'s LTL at any given age is determined by a combination of genetic, environmental, and lifestyle factors (). The inter-individual variation of LTL has been proposed to contribute to an individual\'s susceptibility to age-related diseases, including cancer. Since the first epidemiologic study linking short LTL with increase risks of several cancers in 2003 (), there have been numerous studies assessing the association of LTL with the risks of cancer (), but the results were inconsistent. The inconsistent results are often attributed to technical variations in LTL measurement methods, “reverse causation” limitation in retrospective case control studies, small sample size of cancer cases in prospective cohort studies, and heterogeneous populations. Furthermore, all the published studies relating LTL to cancer risks have used a single time measurement of LTL without consideration of longitudinal changes of LTL. In this issue of , , for the first time, reported a dynamic change of LTL in the context of cancer risks. This study included 792 Normative Aging Study participants with one to four LTL measurements during a follow-up of 12-years. The authors observed that age-related LTL attrition was accelerated among participants who ultimately developed cancer. Strikingly, this trend reversed when age-adjusted LTL was examined relative to time to diagnosis. This divergence of age-adjusted LTL attrition began seven years pre-diagnosis and culminated in significantly longer LTL 3–4years pre-diagnosis among cancer cases compared to cancer-free participants, resulting in a positive association between longer LTL measured within 4years of diagnosis and increased risks of prostate cancer and all cancers combined. This provocative observation provides important biological insight into the role of the telomeres in cancer etiology and adds another possible explanation to the prior inconsistencies in reporting the association of LTL with cancer risks.