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Author: Nathan A. Berger
Publisher:
ISBN: 9783319167343
Category :
Languages : en
Pages :
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Book Description
This volume provides a transdisciplinary and translational review of many of the leading murine models used to study the mechanisms, mediators and biomarkers linking energy balance to cancer. It provides a review of murine models that should be of interest to basic, clinical and applied research investigators as well as nutrition scientists and students that work in cancer prevention, cancer control and treatment. The worldwide obesity pandemic has been extensively studied by epidemiologic and observational studies and even, in some cases, by randomized controlled trials. However, the development and control of obesity, its comorbidities and its impact on cancer usually occurs over such long periods that it is difficult, if not impossible to conduct randomized controlled trials in humans to investigate environmental contributions to obesity, energy balance and their impact on cancer. In contrast, model organisms, especially mice and rats, provide valuable assets for performing these studies under rigorously controlled conditions and in sufficient numbers to provide statistically significant results. In this volume, many of the leading and new murine models used to study the mechanisms and mediators linking cancer with obesity, sleep, exercise, their modification by environment and how they may continue to be used to further elucidate these relations as well as to explore preclinical aspects of prevention and/or therapeutic intervention are considered. This volume provides an important compilation and analysis of major experimental systems and principles for further preclinical research with translational impact on energy balance and cancer.
Author: Nathan A. Berger
Publisher:
ISBN: 9783319167343
Category :
Languages : en
Pages :
Get Book Here
Book Description
This volume provides a transdisciplinary and translational review of many of the leading murine models used to study the mechanisms, mediators and biomarkers linking energy balance to cancer. It provides a review of murine models that should be of interest to basic, clinical and applied research investigators as well as nutrition scientists and students that work in cancer prevention, cancer control and treatment. The worldwide obesity pandemic has been extensively studied by epidemiologic and observational studies and even, in some cases, by randomized controlled trials. However, the development and control of obesity, its comorbidities and its impact on cancer usually occurs over such long periods that it is difficult, if not impossible to conduct randomized controlled trials in humans to investigate environmental contributions to obesity, energy balance and their impact on cancer. In contrast, model organisms, especially mice and rats, provide valuable assets for performing these studies under rigorously controlled conditions and in sufficient numbers to provide statistically significant results. In this volume, many of the leading and new murine models used to study the mechanisms and mediators linking cancer with obesity, sleep, exercise, their modification by environment and how they may continue to be used to further elucidate these relations as well as to explore preclinical aspects of prevention and/or therapeutic intervention are considered. This volume provides an important compilation and analysis of major experimental systems and principles for further preclinical research with translational impact on energy balance and cancer.
Author: Nathan A. Berger
Publisher: Springer
ISBN: 3319167332
Category : Medical
Languages : en
Pages : 302
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Book Description
This volume provides a transdisciplinary and translational review of many of the leading murine models used to study the mechanisms, mediators and biomarkers linking energy balance to cancer. It provides a review of murine models that should be of interest to basic, clinical and applied research investigators as well as nutrition scientists and students that work in cancer prevention, cancer control and treatment. The worldwide obesity pandemic has been extensively studied by epidemiologic and observational studies and even, in some cases, by randomized controlled trials. However, the development and control of obesity, its comorbidities and its impact on cancer usually occurs over such long periods that it is difficult, if not impossible to conduct randomized controlled trials in humans to investigate environmental contributions to obesity, energy balance and their impact on cancer. In contrast, model organisms, especially mice and rats, provide valuable assets for performing these studies under rigorously controlled conditions and in sufficient numbers to provide statistically significant results. In this volume, many of the leading and new murine models used to study the mechanisms and mediators linking cancer with obesity, sleep, exercise, their modification by environment and how they may continue to be used to further elucidate these relations as well as to explore preclinical aspects of prevention and/or therapeutic intervention are considered. This volume provides an important compilation and analysis of major experimental systems and principles for further preclinical research with translational impact on energy balance and cancer.
Author: Jason Asher Goldberg
Publisher:
ISBN:
Category :
Languages : en
Pages : 92
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Book Description
Pancreatic cancer is the fourth leading cause of cancer death in the United States, with a five-year survival rate under 5%. Given the disease's deadliness, increasing our understanding of the molecular nature of the pancreatic cancer is key to developing more effective preventive measures and treatments. Dietary energy restriction (DER) has been shown to have potent anticancer effects in pancreatic cancer, but the mechanism of action has yet to be completely elucidated. Here we investigate the potential of altered microRNA expression as a mechanism by which DER exerts its anticancer effect. Using the Exiqon microRNA Array, we identified several microRNAs of interest for further study. This includes microRNA (mir) 669c, a known regulator of glutathione-S transferases (linked to carcinogen metabolism and oxidative stress) that increases with age. To our knowledge, this is the first exploration of the effects of DER (which is known to suppress oxidative stress and other processes associated with aging and cancer) on microRNA expression. These findings may provide the initial steps towards identifying novel targets for pancreatic cancer prevention or treatment.
Author: Sanford D. Markowitz
Publisher: Springer Science & Business Media
ISBN: 1461423678
Category : Medical
Languages : en
Pages : 192
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Book Description
The gastrointestinal track provides one of the distinct systems where multiple malignancies, including adenocarcinoma of the pancreas, esophagus and colon are each associated with obesity. This unique association is covered in this volume of Energy Balance and Cancer from the epidemiologic, biologic and potential etiologic viewpoint. The focus on possible dietary contribution as well as the role of exercise in prevention and therapy is presented in both animal model and patient based studies. Special focus is provided also on the role of genetic mutations and inflammatory pathways as drivers of these obesity related gastrointestinal malignancies. Overall, this volume on Energy Balance and Gastrointestinal Malignancies should be valuable to Epidemiologists, Gastroenterologists and Oncologists, as well as to students and researchers from multiple disciplines interested in understanding and disrupting the association between obesity and cancer.
Author: William Turbitt
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Book Description
One significant challenge in the field of breast cancer (BC) research is to determine how to reduce and/or eliminate the mortality associated with metastatic BC. Novel therapies, especially non-pharmacological, lifestyle-based interventions that prevent or slow metastatic disease with less severe side effects are greatly needed. Numerous lifestyle factors (including dietary components, body weight, and physical activity patterns) significantly impact BC risk and survival. Emerging population data suggests an inverse relation between physical activity and BC incidence, as well as an important role for exercise in the prevention of cancer recurrence and mortality. The observational nature of these studies limit the ability to determine biological mechanisms and the extent to which exercise, as opposed to changes in body weight, drive beneficial effects. Additionally, very little is known about the mechanisms contributing to the relation between physical activity and survival. Given the importance of metastases in the mortality of women with BC, understanding the role of exercise on metastatic burden may reveal important new targets for secondary and tertiary cancer prevention. The aim of study one was to control for weight and examine the effects of exercise, mild dietary restriction, or the combination of diet and exercise on the inflammation-immune axis and tumor progression in a preclinical metastatic BC model to determine the extent to which exercise or body weight contribute to cancer prevention. Dietary energy restriction-induced weight control (i.e., SED+ER mice) was effective at altering host splenic immunity and the expression of key genes in the tumor microenvironment (TME) related to immunosuppression and metastatic progression; however, this intervention failed to induce changes in primary tumor growth or spontaneous metastases. Moderate exercise in weight stable mice (EX+ER) resulted in a similar reduction in immunosuppressive and metastatic genes in the TME compared with the SED+ER mice; however, in addition, EX+ER mice had the greatest reduction in splenic immunosuppressive cells and plasma insulin-like growth factor-1 (IGF-1). The effects of moderate exercise in weight stable mice culminated in a significant delay in primary tumor growth and spontaneous metastases, suggesting that exercise-induced alterations in metabolic drivers of tumorigenesis, not simply a change in body weight, underlie the protective effects in the dual intervention group. Interestingly the exercise-induced protective effect on the emergence of immunosuppressive factors and reduced tumor burden was lost when mice continued to gain weight over the course of the study, suggesting that weight gain-induced disturbances on hormonal, inflammatory, and/or immunological function can override the exercise-induced benefits. Collectively, study one provided a deeper understanding of the extent to which exercise, and changes in body weight, underlies cancer protection. Few researchers have examined the effect of energy balance interventions on the efficacy of immunotherapeutic strategies. Two subsequent studies were designed to investigate the response to emerging cancer therapeutics in mice randomized to an energy balance paradigm (i.e., sedentary, ad libitum, weight gain [WG] group vs. exercising, mild dietary restriction, weight maintenance [WM] group) to identify potential mechanisms and provide translational support. Study two aimed to determine if there were any additive effects of moderate exercise in weight stable mice and the therapeutic administration of a broad-based, allogeneic, whole tumor cell cancer vaccine (VAX). There was a significant effect of both WM and VAX alone on primary tumor growth; and an additive effect of WM+VAX on primary tumor growth, lung and heart spontaneous metastases, splenocyte count at sacrifice, the number of total splenic myeloid-derived suppressor cells (MDSCs) and granulocytic subset of MDSCs, and plasma levels of IGF-1. Splenic interferon gamma (IFN) secretion in response to re-stimulation with tumor antigens was significantly elevated in response to VAX and WM; however, there was no additive effect of WM+VAX. These results suggested that our whole tumor cell cancer vaccine augmented the weight maintenance (via diet and exercise) effects on primary tumor growth and spontaneous metastasis; and suggested that vaccination may provide an immune stimulus to further promote the protective effects of moderate exercise alone in the metastatic 4T1.2 mammary tumor model.Study three aimed to determine if there were any additive effects of moderate exercise in weight stable mice and the dual therapeutic administration of a whole tumor cell cancer vaccine and programmed cell death protein-1 (PD-1) checkpoint blockade. We observed a cancer prevention effect of PD-1 checkpoint blockade in WG mice on primary tumor growth and spontaneous lung metastasis. However, moderate activity in weight stable mice, independent of PD-1 checkpoint blockade, was effective in reducing primary tumor growth and metastatic burden. The WM+PD-1 group displayed the lowest number of splenic MDSCs and granulocytic MDSCs and maintained its splenic lymphoid populations. Neither the number of tumor-infiltrating immune cells, the effector or activation status of tumor-infiltrating CD4+ helper and CD8+ cytotoxic T cells, nor functional outcomes were significantly different between groups. PD-1 checkpoint blockade in WG mice, moderate exercise in weight stable mice, and PD-1 checkpoint blockade in moderately exercising, weight stable mice showed comparable, albeit subtle differences, in tumor-immune crosstalk gene expression markers that drive the expansion of immunosuppressive cell types and impact metastatic progression. The lack of responsiveness to VAX+PD-1 checkpoint blockade in WM mice suggests that moderate exercise in weight stable mice may be enhancing antitumor immunity and/or reducing protumorigenic factors (i.e., similar mechanisms mediated by VAX+PD-1 checkpoint blockade). Results from the current studies provided insight into the extent to which exercise in weight stable mice underlie cancer protection. Also, results provided insight into potential mechanisms by which exercise can act via the inflammation-immune axis to attenuate the generation of a protumorigenic and immunosuppressive TME. These data demonstrated that preventing weight gain through diet and exercise may be an important recommendation to maintain prolonged antitumor effector responses and improve clinical outcomes. Results from the current studies provided insight into potential mechanisms by which physical activity exerts primary and secondary cancer prevention effects and provides a biological rationale for randomized clinical trials to investigate physical activity strategies to prevent metastatic progression in BC survivors and ultimately improve survival outcomes.
Author: Deborah J. Bowen
Publisher: Springer
ISBN: 3319061038
Category : Medical
Languages : en
Pages : 316
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Book Description
This volume reviews disparities in cancer genetics, etiology, treatment and survivorship that are associated with differences in energy balance and how those differences and disparities may be affected by geography, socioeconomic status, ethnicity, biology, behavior and others. State-of-the-art strategies are outlined to alter these problems at the individual, community and policy levels. The book provides a comprehensive assessment of the multiple contributions of disparities in energy balance and how they affect cancer. this volume should constitute a valuable resource to disparity focused investigators at all levels and serves an important guide to professionals that deal with these issues, especially those who determine and implement policy.
Author: Sanford D. Markowitz
Publisher: Springer
ISBN: 9781461423683
Category : Medical
Languages : en
Pages : 184
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Book Description
The gastrointestinal track provides one of the distinct systems where multiple malignancies, including adenocarcinoma of the pancreas, esophagus and colon are each associated with obesity. This unique association is covered in this volume of Energy Balance and Cancer from the epidemiologic, biologic and potential etiologic viewpoint. The focus on possible dietary contribution as well as the role of exercise in prevention and therapy is presented in both animal model and patient based studies. Special focus is provided also on the role of genetic mutations and inflammatory pathways as drivers of these obesity related gastrointestinal malignancies. Overall, this volume on Energy Balance and Gastrointestinal Malignancies should be valuable to Epidemiologists, Gastroenterologists and Oncologists, as well as to students and researchers from multiple disciplines interested in understanding and disrupting the association between obesity and cancer.
Author: Kara L. Hall
Publisher: Springer Nature
ISBN: 303020992X
Category : Psychology
Languages : en
Pages : 633
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Book Description
Collaborations that integrate diverse perspectives are critical to addressing many of our complex scientific and societal problems. Yet those engaged in cross-disciplinary team science often face institutional barriers and collaborative challenges. Strategies for Team Science Success offers readers a comprehensive set of actionable strategies for reducing barriers and overcoming challenges and includes practical guidance for how to implement effective team science practices. More than 100 experts--including scientists, administrators, and funders from a wide range of disciplines and professions-- explain evidence-based principles, highlight state-of the-art strategies, tools, and resources, and share first-person accounts of how they’ve applied them in their own successful team science initiatives. While many examples draw from cross-disciplinary team science initiatives in the health domain, the handbook is designed to be useful across all areas of science. Strategies for Team Science Success will inspire and enable readers to embrace cross-disciplinary team science, by articulating its value for accelerating scientific progress, and by providing practical strategies for success. Scientists, administrators, funders, and others engaged in team science will also leave equipped to develop new policies and practices needed to keep pace in our rapidly changing scientific landscape. Scholars across the Science of Team Science (SciTS), management, organizational, behavioral and social sciences, public health, philosophy, and information technology, among other areas of scholarship, will find inspiration for new research directions to continue advancing cross-disciplinary team science.
Author: Tricia Wallace Moore
Publisher:
ISBN:
Category :
Languages : en
Pages : 290
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Book Description
Energy balance refers to the relationship between energy intake and energy expenditure. Epidemiological studies have established a clear association between energy balance and cancer, however the underlying mechanisms are unclear. The objective of the current study was to evaluate the impact of caloric consumption on epithelial carcinogenesis and identify potential mechanisms of inhibition or enhancement. Using ICR female mice, we demonstrated that positive energy balance enhanced, while negative energy balance inhibited susceptibility to multistage carcinogenesis in mouse skin. We next evaluated diet-induced changes in the epidermal proliferative response. Calorie restriction (CR) significantly reduced epidermal hyperproliferation, in the presence and absence of tumor promotion, as compared to diet-induced obesity (DIO). Additional studies were conducted to determine the impact of dietary manipulation on TPA-induced growth factor signaling. CR reduced, while DIO increased insulin like growth factor-1 receptor (IGF-1R) and epidermal growth factor receptor (EGFR) activation, which subsequently modulated signaling downstream to Akt and mTOR. These diet-induced changes in growth factor signaling were confirmed under steady-state conditions in multiple epithelial tissues (i.e., skin, liver and dorsolateral prostate) in multiple mouse strains (FVB/N, C57BL/6 and ICR). Further analyses demonstrated that caloric consumption directly correlated with levels of cell cycle progression related proteins and inversely correlated with levels of cell cycle inhibitory proteins. Genetic reduction of circulating IGF-1, liver IGF-1 deficient (LID) mouse model, inhibited two-stage skin carcinogenesis, reduced epidermal hyperproliferation and attenuated IGF-1R and EGFR growth factor signaling during tumor promotion, similar to CR, suggesting a potential for IGF-1R and EGFR crosstalk. Further studies, demonstrated that IGF-1 induced EGFR activation in cultured mouse keratinocytes, possibly due to IGF-1R and EGFR heterodimerization or IGF-1 induced changes in EGFR mRNA expression. In vivo, CR reduced, while DIO increased IGF-1R and EGFR association during tumor promotion. Furthermore, CR attenuated EGFR ligand mRNA expression both in the presence and absence of TPA treatment. Collectively, these findings suggest that dietary energy balance modulates epithelial carcinogenesis, at least in part due to diet-induced changes in levels of circulating IGF-1, which then modulate IGF-1R and EGFR crosstalk and downstream signaling to cell cycle related proteins, subsequently altering epidermal hyperproliferation.
Author: Sanford D. Markowitz
Publisher: Springer Science & Business Media
ISBN: 146142366X
Category : Medical
Languages : en
Pages : 192
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Book Description
The gastrointestinal track provides one of the distinct systems where multiple malignancies, including adenocarcinoma of the pancreas, esophagus and colon are each associated with obesity. This unique association is covered in this volume of Energy Balance and Cancer from the epidemiologic, biologic and potential etiologic viewpoint. The focus on possible dietary contribution as well as the role of exercise in prevention and therapy is presented in both animal model and patient based studies. Special focus is provided also on the role of genetic mutations and inflammatory pathways as drivers of these obesity related gastrointestinal malignancies. Overall, this volume on Energy Balance and Gastrointestinal Malignancies should be valuable to Epidemiologists, Gastroenterologists and Oncologists, as well as to students and researchers from multiple disciplines interested in understanding and disrupting the association between obesity and cancer.
