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      Viewing Cancer Through the Lens of Corruption: Using Behavioral Ecology to Understand Cancer

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      Frontiers in Ecology and Evolution
      Frontiers Media SA

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          Abstract

          All biological systems depend on signals for coordination: signals which pass information among agents that run the gamut from cells to organisms. However, their very importance makes signals vulnerable to subversion. How can a receiver know whether a signal is honest or deceptive? In other words, are signals necessarily a reliable indicator of agent quality or need? By drawing parallels to ecological phenomena ranging from begging by nestlings to social insects, we investigate the role of signal degradation in cancer. We thus think of cancer as a form of corruption, in which cells command huge resource investment through relatively cheap signals, just as relatively small bribes can leverage large profits. We discuss various mechanisms which prevent deceptive signaling in the natural world and within tissues. We show how cancers evolve ways to escape these controls and relate these back to evasion mechanisms in ecology. We next introduce two related concepts, co-option and collusion, and show how they play critical roles in ecology and cancer. Drawing on public policy, we propose new approaches to view treatment based on taxation, changing the incentive structure, and the recognition of corrupted signaling networks.

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            The biology, function, and biomedical applications of exosomes

            The study of extracellular vesicles (EVs) has the potential to identify unknown cellular and molecular mechanisms in intercellular communication and in organ homeostasis and disease. Exosomes, with an average diameter of ~100 nanometers, are a subset of EVs. The biogenesis of exosomes involves their origin in endosomes, and subsequent interactions with other intracellular vesicles and organelles generate the final content of the exosomes. Their diverse constituents include nucleic acids, proteins, lipids, amino acids, and metabolites, which can reflect their cell of origin. In various diseases, exosomes offer a window into altered cellular or tissue states, and their detection in biological fluids potentially offers a multicomponent diagnostic readout. The efficient exchange of cellular components through exosomes can inform their applied use in designing exosome-based therapeutics.
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              Understanding the Warburg effect: the metabolic requirements of cell proliferation.

              In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.
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                Author and article information

                Journal
                Frontiers in Ecology and Evolution
                Front. Ecol. Evol.
                Frontiers Media SA
                2296-701X
                July 8 2021
                July 8 2021
                : 9
                Article
                10.3389/fevo.2021.678533
                a8de4462-39f0-455d-af73-3b8125321f59
                © 2021

                Free to read

                https://creativecommons.org/licenses/by/4.0/

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