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      Cancer control through principles of systems science, complexity, and chaos theory: A model

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          Abstract

          Cancer is a significant medical and societal problem. This reality arises from the fact that an exponential and an unrestricted cellular growth destabilizes human body as a system. From this perspective, cancer is a manifestation of a system-in-failing.

          A model of normal and abnormal cell cycle oscillations has been developed incorporating systems science, complexity, and chaos theories. Using this model, cancer expresses a failing subsystem and is characterized by a positive exponential growth taking place in the outer edge of chaos. The overall survival of human body as a system is threatened. This model suggests, however, that cancer's exponential cellular growth and disorganized complexity could be controlled through the process of induction of differentiation of cancer stem cells into cells of low and basic functionality.

          This concept would imply reorientation of current treatment principles from cellular killing (cyto-toxic therapies) to cellular retraining (cyto-education).

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          Most cited references 25

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          Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells.

          Transformed, oncogenic precursors, possessing both defining neural-stem-cell properties and the ability to initiate intracerebral tumours, have been identified in human brain cancers. Here we report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, trigger a significant reduction in the stem-like, tumour-initiating precursors of human glioblastomas (GBMs). Transient in vitro exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most importantly, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality that occur in 100% of mice after intracerebral grafting of human GBM cells. We demonstrate that BMPs activate their cognate receptors (BMPRs) and trigger the Smad signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation, and increased expression of markers of neural differentiation, with no effect on cell viability. The concomitant reduction in clonogenic ability, in the size of the CD133+ population and in the growth kinetics of GBM cells indicates that BMP4 reduces the tumour-initiating cell pool of GBMs. These findings show that the BMP-BMPR signalling system--which controls the activity of normal brain stem cells--may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and the results also identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
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            Calorie restriction mimetics: an emerging research field.

             Sige Zou,  rafael,  Min Zhu (2006)
            When considering all possible aging interventions evaluated to date, it is clear that calorie restriction (CR) remains the most robust. Studies in numerous species have demonstrated that reduction of calories 30-50% below ad libitum levels of a nutritious diet can increase lifespan, reduce the incidence and delay the onset of age-related diseases, improve stress resistance, and decelerate functional decline. A current major focus of this research area is whether this nutritional intervention is relevant to human aging. Evidence emerging from studies in rhesus monkeys suggests that their response to CR parallels that observed in rodents. To assess CR effects in humans, clinical trials have been initiated. However, even if results from these studies could eventually substantiate CR as an effective pro-longevity strategy for humans, the utility of this intervention would be hampered because of the degree and length of restriction required. As an alternative strategy, new research has focused on the development of 'CR mimetics'. The objective of this strategy is to identify compounds that mimic CR effects by targeting metabolic and stress response pathways affected by CR, but without actually restricting caloric intake. For example, drugs that inhibit glycolysis (2-deoxyglucose), enhance insulin action (metformin), or affect stress signaling pathways (resveratrol), are being assessed as CR mimetics (CRM). Promising results have emerged from initial studies regarding physiological responses which resemble those observed in CR (e.g. reduced body temperature and plasma insulin) as well as protection against neurotoxicity (e.g. enhanced dopamine action and up-regulated neurotrophic factors). Ultimately, lifespan analyses in addition to expanded toxicity studies must be accomplished to fully assess the potential of any CRM. Nonetheless, this strategy clearly offers a very promising and expanding research endeavor.
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              The cancer stem cell hypothesis: a work in progress.

              There is a growing body of evidence that supports the idea that malignant tumors are initiated and maintained by a population of tumor cells that share similar biologic properties to normal adult stem cells. This model, the cancer stem cell (CSC) hypothesis, is based on the observation that tumors, like adult tissues, arise from cells that exhibit the ability to self-renew as well as give rise to differentiated tissue cells. Although the concept of the CSC is not entirely new, advances made over the past two decades in our understanding of normal stem cell biology in conjunction with the recent application of these concepts to experimentally define CSCs have resulted in the identification of CSCs in several human malignancies.
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                Author and article information

                Journal
                Int J Med Sci
                ijms
                International Journal of Medical Sciences
                Ivyspring International Publisher (Sydney )
                1449-1907
                2007
                5 June 2007
                : 4
                : 3
                : 164-173
                Affiliations
                Health Research International, 333 Westbrook Rd, St. Helena Island, SC 29920, USA
                Author notes
                Correspondence to: Ivo P. Janecka, MD, MBA, PhD, 333 Westbrook Rd, St. Helena Island, SC 29920, janecka@ 123456post.harvard.edu . Telephone: 843-838-3602

                Conflict of interest: The author has declared that no conflict of interest exists.

                Article
                ijmsv04p0164
                1891444
                17589568
                d8f95be2-49c9-41b0-9fba-1cf77647344f
                © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
                Categories
                Research Paper

                Medicine

                complexity, systems, melatonin, physical activity, chaos, cancer

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