ABSTRACT
Tumorigenesis is the result of genetic alterations that drive the progressive transformation of normal cells into highly malignant derivatives. This process disrupts the normal functions of cells, tissues, and organs via the introduction of mutations, genome rearrangements, amplications, deletions, and epigenetic modulation of gene expression (Hanahan and Weinberg 2000; Kelloff and Sigman 2012). DNA damage, oxidative stress, mitotic stress, proapoptotic stress, and metabolic stress have been identied as stress phenotypes of cancer (Luo et al. 2009). Molecules such as DNA, RNA, microRNA (miRNA), and proteins, and genetic and posttranslational modications that participate in these stress responses in cells have been identied as cancer biomarkers and targets for preventive and therapeutic intervention (Bartsch et al. 2011; Kelloff and Sigman 2012). These biomarkers may be utilized for achieving an early diagnosis, prognosis, or classication of disease subtype; predicting the treatment response; and identifying potential targets for drug therapy (Leth-Larsen et al. 2010).
