Abstract
Nucleic acids are macromolecules comprised of chains of nucleotides. In the double helix formed by deoxyribonucleic acid (DNA), purines pair with pyrimidines and are joined together by hydrogen bonds. DNA serves as a template for the transcription of RNA; in a process called translation, RNA provides instructions for the synthesis of proteins. Cancer is a genetic disease. Most cancers are sporadic and result from genetic alterations in somatic cells. Some cancers are inherited, with genetic alterations in germline cells conferring an increased oncogenic risk. Oncogenesis is a complex, dynamic, and often multistep process which is likely dependent on the acquisition of several biological capabilities by somatic cells that result in their independence to external growth signals, insensitivity to external anti-growth signals, indefinite replication, evasion of apoptosis, sustained angiogenesis, activation of tissue invasion and metastasis, reprogramming of energy metabolism, and evasion of host immune response. Knowledge about oncogenic hallmarks has allowed for the establishment and expansion of many areas of personalized cancer care through detection or measurement of molecular biomarkers.
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Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646–74.
Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;100(1):57–70.
Hainaut P, Plymoth A. Targeting the hallmarks of cancer: towards a rational approach to next-generation cancer therapy. Curr Opin Oncol. 2013;25(1):50–1.
Fouad YA, Aanei C. Revisiting the hallmarks of cancer. Am J Cancer Res. 2017;7(5):1016–36.
Tomasetti C, Vogelstein B. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science. 2015;347(6217):78–81.
Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949–54.
Pratilas CA, Taylor BS, Ye Q, et al. (V600E)BRAF is associated with disabled feedback inhibition of RAF-MEK signaling and elevated transcriptional output of the pathway. Proc Natl Acad Sci U S A. 2009;106(11):4519–24.
Henke LE, Perkins SM, Pfeifer JD, et al. BRAF V600E mutational status in pediatric thyroid cancer. Pediatr Blood Cancer. 2014;61(7):1168–72.
Kurppa KJ, Caton J, Morgan PR, et al. High frequency of BRAF V600E mutations in ameloblastoma. J Pathol. 2014;232(5):492–8.
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Stewart, R.L., Koo, S.C., Furtado, L.V. (2018). Principles of Molecular Biology and Oncogenesis. In: Furtado, L., Husain, A. (eds) Precision Molecular Pathology of Neoplastic Pediatric Diseases . Molecular Pathology Library. Springer, Cham. https://doi.org/10.1007/978-3-319-89626-7_1
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DOI: https://doi.org/10.1007/978-3-319-89626-7_1
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