Cancer is a genetic disease
The etiology of cancer has evolved over the past 50 years, with early theories in the late 20th century suggesting that tumor development could result from diverse causes including dysregulated cellular differentiation, infectious agents (viruses), and genetic mutations.
Although these rival hypotheses were not mutually exclusive, the prevailing theory, which has gained the broadest scientific support, is the concept that altered cellular genetics, or altered expression (epigenetics), is responsible for cancer formation. Supporting the hypothesis that gene mutations might be incriminated in cancer development were the experiments conducted by Bruce Ames. Through an in-vitro screening test using histidine auxotrophic mutant strains of Salmonella typhimurium, Ames was able to characterize the mutagenic potential of different chemical compounds (Ames et al., 1960, 1963). Derived from these seminal experiments, chemical agents identified as being mutagenic, i.e., having the capacity to alter the genetic code, were then correlated with their ability to act as carcinogens through the formation of cancer (Ames, 1979; Ames et al., 1973). The foundational correlations documented by Ames yielded the compelling inference that the carcinogenic potential of chemical agents was derived from their ability to damage genes and thus the DNA of cells. While the foundations of cancer development still are hinged on ‘altered’ genetic messaging, in the era of epigenetics, it is now well accepted that altered gene transcription, in the absence of mutated genes, is enough to drive cancer development (Flavahan et al., 2017).
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