Principles of Molecular Biology and Oncogenesis

  • Rachel L. StewartEmail author
  • Selene C. Koo
  • Larissa V. Furtado
Part of the Molecular Pathology Library book series (MPLB)


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.


Deoxyribonucleic acid DNA RNA Nucleosomes Transcription Translation Oncogenes Tumor suppressor genes Oncogenesis 


  1. 1.
    Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646–74.CrossRefGoogle Scholar
  2. 2.
    Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000;100(1):57–70.CrossRefGoogle Scholar
  3. 3.
    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.CrossRefPubMedGoogle Scholar
  4. 4.
    Fouad YA, Aanei C. Revisiting the hallmarks of cancer. Am J Cancer Res. 2017;7(5):1016–36.PubMedPubMedCentralGoogle Scholar
  5. 5.
    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.CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949–54.CrossRefGoogle Scholar
  7. 7.
    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.CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Henke LE, Perkins SM, Pfeifer JD, et al. BRAF V600E mutational status in pediatric thyroid cancer. Pediatr Blood Cancer. 2014;61(7):1168–72.CrossRefPubMedGoogle Scholar
  9. 9.
    Kurppa KJ, Caton J, Morgan PR, et al. High frequency of BRAF V600E mutations in ameloblastoma. J Pathol. 2014;232(5):492–8.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Rachel L. Stewart
    • 1
    Email author
  • Selene C. Koo
    • 2
  • Larissa V. Furtado
    • 3
  1. 1.Department of Pathology and Laboratory MedicineUniversity of KentuckyLexingtonUSA
  2. 2.Department of Pathology and Laboratory MedicineNationwide Children’s HospitalColumbusUSA
  3. 3.Department of PathologyUniversity of Utah/ARUP LaboratoriesSalt Lake CityUSA

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