Smoking Tobacco Case Study

1544 Words 7 Pages
The detrimental health affects caused by smoking tobacco have long been known in our society. Tobacco smoke is composed of a complex, chemical mixture of roughly 60 known carcinogens (Alexandrov, et al., 2016). Smoking tobacco and exposure to other carcinogens increases human risk for cancer significantly by enhancing DNA mutation rates. Different carcinogens cause slightly different types of DNA damage in humans that eventually lead to cancer (Ehrenberg, 2016). These unique patterns of mutations that occur in different types of cancer tissue are what makes each carcinogenic mutation unique and leave behind their own mutational signature on the cancer genome. These signatures can be used as a physiological ‘receipt’ to assess the history of …show more content…
DNA damage can range from the formation of DNA adducts, base substitutions, insertions, and deletions (Alexandrov, et al., 2016), genomic structural rearrangements, chromosomal instability (Helleday, Eshtad, & Nik-Zainal, 2014), over activity of DNA repair mechanisms, damage to mitochondrial DNA and microRNA, excessive apoptosis, and damage to genes related to cellular respiration (Izzotti & Pulliero, 2015). The type and progression of damages to the genome that occur depend on the intensity of tobacco smoke exposure and the length of exposure, The human body has many defense mechanisms against damage to DNA (sweeping cells, detoxifying metabolic reacions, etc.), and the progression of carcinogenesis can only occur if the amount of mutations are able to overwhelm the body’s defense …show more content…
At a certain point of prolonged exposure, apoptosis is actually halted by the silencing of the Fragile Histidine Triad (FHIT), a gene associated with apoptosis functions. CS also starts to contribute to the loss of function of the let-7 microRNA family (Izzotti & Pulliero, 2015). MicroRNAs are sensitive to carcinogens (having about 5.4 times more adducts than nuclear DNA), and in relation to carcinogenesis, is an effector of p53 activities, which induce apoptosis and also work to silence the expression of the oncogene, K-ras, proven through p53 knockout mouse strain models. With microRNAs and other defense functionalities lost, cancer progression can continue and is further supported by proangiogenic genes, which are activated when microRNA are damaged and downregulated. Now with damaged defense mechanisms and a proangiogenic environment (increased carbon dioxide and monoxide, tissue hypoxia, etc.) activated by tobacco smoke exposure, cancer tissues can continue to progress very rapidly (Izzotti & Pulliero,

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