Transcriptome alterations induced by cigarette smoke

Abstract

Cigarette smoke alters the transcriptome of multiple tissues; those directly exposed to toxic products and those exposed to circulating components and metabolic products of tobacco smoke. In most tissues and organs that have been studied, the smoking transcriptome is characterized by increased expression of antioxidant and xenobiotic genes as well as a wide spectrum of inflammation‐related genes, and potential oncogenic genes. Smoking is associated with an increased incidence of cancer in a number of organs both those directly exposed (lungs and airways) and those indirectly exposed (bladder, liver, pancreas). Individual transcriptomic responses vary, based to some degree on as yet to be clarified genetic factors, and likely how and what the individual has smoked. The complexity of individual responses to tobacco exposure and of smoking‐related cancers in various organs is beginning to be revealed in transcriptomic and whole genome sequencing studies, of both tumors and cytologically normal appearing cells that have been exposed to cigarette smoke or its products creating a genomic “field of injury.” The recent application of next generation sequencing to defining the transcriptome alterations induced by cigarette smoke holds the promise of discovering new approaches to personalized prevention and treatment of smoking‐related lung diseases in the future.

IL1RN and KRT13 Expression in Bladder Cancer: Association with Pathologic Characteristics and Smoking Status

“…Due to its reservoir function the exposure time is the longest in the urinary bladder. Metabolites of tobacco smoke may cause inflammatory reactions and lead to perturbation of cellular processes which may alter gene expression [8, 9]. We have previously reported on changes of different gene expressions in UCB tissue depending on smoking status in a microarray study [10].…”

Genetic similarities between tobacco use disorder and related comorbidities: an exploratory study

“…Regarding disorders that result from smoking, the most plausible theory is epigenomic changes due to carcinogenic compounds of tobacco [21]. For example, it was reported that smoking induced a down-regulation of the interferon IFIT1 involved in the progression and invasiveness of bladder cancer [22]. Therefore, genes are just one of the pathways linking TUD and related disorders.…”

The Promise and Problems of E-Cigarettes

“…Unfortunately, the need to classify asthma into distinct phenotypes implies that study populations must be even larger than ever, and more data on the incidence of various phenotypes in different populations are required to estimate sample size needs when designing a study. Furthermore, analytic approaches to classifying children with asthma into discrete phenotypes are not straightforward (10). In risk factor studies, the factors themselves cannot be used in the identification of phenotype clusters.…”

“…Nicotine, the main ingredient of e-cigarettes, is addictive (9) and has been implicated in a number of cancers (10). It crosses the placenta and alters fetal gene expression and tissue development in a variety of organs (11).…”