Cancer: tilting at windmills?
One of the striking characteristics of cancer cells is their phenotypic diversity and ability to switch phenotypes in response to environmental fluctuations. Such phenotypic changes (e.g. from drug-sensitive to drug-resistant), which are critical for survival and proliferation, are widely believed to arise due to mutations in the cancer cell's genome. However, there is growing concern that such a deterministic view is not entirely consistent with multiple lines of evidence which indicate that cancer can arise in the absence of mutations and can even be reversed to normalcy despite the mutations. In this Commentary, we wish to present an alternate view that highlights how stochasticity in protein interaction networks (PINs) may play a key role in cancer initiation and progression. We highlight the potential role of intrinsically disordered proteins (IDPs) and submit that targeting IDPs can lead to new insights and treatment protocols for cancer.
Department of Urology, The Johns Hopkins University School of Medicine, 600 N Wolfe St, 105B Marburg, 21287, Baltimore, MD, USA. pkulkar4@jhmi.edu.
Prakash
P
Kulkarni
Takumi
T
Shiraishi
Rahul V
RV
Kulkarni
D000818:Animals; D006801:Humans; D064267:Intrinsically Disordered Proteins / Q000502:physiology; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D010641:Phenotype; D011487:Protein Conformation; D060066:Protein Interaction Maps; D013269:Stochastic Processes
D064267:Intrinsically Disordered Proteins