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Are Parallel Proliferation Pathways Redundant?

  1. Author:
    Nussinov,Ruth
    Tsai,Chung-Jung
    Jang,Hyunbum

  2. Author Address

    NCI, Computat Struct Biol Sect, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.Tel Aviv Univ, Sackler Sch Med, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel.
    1. Year: 2020
    2. Date: Jul
    3. Epub Date: 2020 04 25
  2. Journal: Trends in biochemical sciences
  3. ELSEVIER SCIENCE LONDON,
    1. 45
    2. 7
    3. Pages: 554-563
  5. Type of Article: Review
  6. ISSN: 0968-0004
  1. Abstract:

    Are the receptor tyrosine kinase (RTK) and JAK-STAT-driven proliferation pathways 'parallel' or 'redundant'? And what about those of K-Ras4B versus N-Ras? 'Parallel' proliferation pathways accomplish a similar drug resistance outcome. Thus, are they 'redundant'? In this paper, it is argued that there is a fundamental distinction between 'parallel' and 'redundant'. Cellular proliferation pathways are influenced by the genome sequence, 3D organization and chromatin accessibility, and determined by protein availability prior to cancer emergence. In the opinion presented, if they operate the same downstream protein families, they are redundant; if evolutionary-independent, they are parallel. Thus, RTK and JAK-STAT-driven proliferation pathways are parallel; those of Ras isoforms are redundant. Our Precision Medicine Call to map cancer proliferation pathways is vastly important since it can expedite effective therapeutics.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.tibs.2020.03.013
  3. PMID: 32345469
  4. View record in Web of Science®
  5. WOS: 000540873500004

Library Notes

  1. Fiscal Year: FY2019-2020
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