Open questions: The disrupted circuitry of the cancer cell

Journal Article · Fri Oct 24 00:00:00 EDT 2014 · BMC Biology

DOI:https://doi.org/10.1186/s12915-014-0088-y· OSTI ID:1244827

Wiley, H. S.

Every new decade of biology brings with it a change in outlook driven by new technologies and fresh perspectives. Such is the case for cancer and how we consider the disease. The advent of molecular biology led to the identification of altered signaling molecules and 'oncogenes' that were proposed to drive uncontrolled cell proliferation. The rise of cell biology and new imaging and culturing technologies led to the idea that disruptions in the extracellular environment prime cells for transformation. In the current genomics era, cancer is most commonly seen as a genetic disorder where an unstable genome gives rise to a variety of different cell variants that are selected for proliferation and survival. All of these views are partially correct, of course, and are simply different ways of saying that genetic alterations in cancer cells result in a loss of growth homeostasis. They also take the view that molecular changes 'drive' a cell to grow uncontrollably, rather than tip the balance from one normal state (quiescence) to another (proliferation). Underlying this oversimplification is a profound ignorance of what controls homeostatic cell growth in the first place and how specific mutations impact it.

• Research Organization: Pacific Northwest National Laboratory (PNNL), Richland, WA (United States)
• Sponsoring Organization: USDOE
• DOE Contract Number: AC05-76RL01830
• OSTI ID: 1244827
• Report Number(s): PNNL-SA-106172; 400412000
• Journal Information: BMC Biology, Vol. 12; ISSN 1741-7007
• Publisher: BioMed Central
• Country of Publication: United States
• Language: English

Related Subjects

receptors
cancer
modeling