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Author: Publisher: Academic Press ISBN: 0128225351 Category : Science Languages : en Pages : 258
Book Description
Carcinogen-Driven Mouse Models of Oncogenesis, Volume 163 contains a series of protocols written by world-leading experts in the field. Each manuscript provides a detailed methodological description to drive carcinogen-mediated oncogenesis in mice. Chapters in this new release include Chemical carcinogenesis in mice as a model of human cancer: Pros and cons, MPA/DMBA-driven mammary carcinomas, Dimethylbenz(a)anthracene-Induced Mammary Tumorigenesis in mice, Urethane-induced lung carcinogenesis, Methylcholanthrene-induced fibrosarcomas, BBN-driven bladder carcinomas, Oral squamous cell carcinomas driven by 4NQO, Analyzing skin tumor development in mice by the DMBA/TPA model, and much more. Other sections cover DSS/AOM-driven colorectal carcinomas, Diethylnitrosamine-induced liver tumorigenesis in mice, Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice, Lung carcinomas induced by NNK and LPS, Pristane-induced mammary carcinomas, The 4-NQO mouse model: an update on a well-established in vivo model of oral carcinogenesis, and more. Provides protocols provided by renowned experts in the field Presents detailed descriptions of protocols, hence allowing appropriate reproduction of the models Includes author notes for each protocol, covering useful tips and troubleshooting
Author: Publisher: Academic Press ISBN: 0128225351 Category : Science Languages : en Pages : 258
Book Description
Carcinogen-Driven Mouse Models of Oncogenesis, Volume 163 contains a series of protocols written by world-leading experts in the field. Each manuscript provides a detailed methodological description to drive carcinogen-mediated oncogenesis in mice. Chapters in this new release include Chemical carcinogenesis in mice as a model of human cancer: Pros and cons, MPA/DMBA-driven mammary carcinomas, Dimethylbenz(a)anthracene-Induced Mammary Tumorigenesis in mice, Urethane-induced lung carcinogenesis, Methylcholanthrene-induced fibrosarcomas, BBN-driven bladder carcinomas, Oral squamous cell carcinomas driven by 4NQO, Analyzing skin tumor development in mice by the DMBA/TPA model, and much more. Other sections cover DSS/AOM-driven colorectal carcinomas, Diethylnitrosamine-induced liver tumorigenesis in mice, Two-stage 3-methylcholanthrene and butylated hydroxytoluene-induced lung carcinogenesis in mice, Lung carcinomas induced by NNK and LPS, Pristane-induced mammary carcinomas, The 4-NQO mouse model: an update on a well-established in vivo model of oral carcinogenesis, and more. Provides protocols provided by renowned experts in the field Presents detailed descriptions of protocols, hence allowing appropriate reproduction of the models Includes author notes for each protocol, covering useful tips and troubleshooting
Author: Bradley J. Kubick Publisher: ISBN: Category : Languages : en Pages : 192
Book Description
Cancer develops as the end product of a multistep process in which cells and/or their microenvironments accumulate alterations, either genetic or epigenetic, which enable uncontrolled growth. During the early steps of this process, altered cells constituting the precursors to cancer are subject to the constraints of natural selection. As such, variations within the population of transformed cells which lead to increased relative fitness are reproductively favored by the various selective pressures of the local microenvironment. Anti-tumor immunity is an important arm of this pre-malignant niche. Consequently, for cancer to develop, at least one of the following four possibilities must occur: 1) the transformed cells progress to cancer without ever becoming immunogenic, 2) the transformed cells are immunogenic, but are able to proliferate faster than they are eliminated, 3) the host immune system becomes compromised or tolerized, or 4) from within the transformed population, new clones evolve adaptations that enable evasion of anti-tumor immunity. This final possibility has been termed “cancer immunoediting” and it includes three distinct stages of cancer-immune interaction: elimination, equilibrium, and escape. As a result of this process, every immunogenic cancer that develops in an immunocompetent host is intrinsically immune-evasive as a result of its past triumphs over anti-tumor immunity. Here, I describe a genetically engineered mouse model developed in order to study this process directly, via in vivo confocal microscopy. This model accurately recapitulates the cancer immunoediting process which occurs as a result of common mutations that drive human carcinomas. Using this model, I identified a previously unknown mechanism of early survival in which transformed cells use an immune-privileged niche as a surrogate for immune evasion. This project also provides a means to further characterize the adaptations that mediate the transitions between the stages of immunoediting. Finally, and perhaps most importantly, this model acts as a prototype for discovery of new biomarkers of human immunoediting as well as a screening tool for therapeutic interventions that could form the basis of rational cancer prevention strategies.
Author: Jeffrey E. Green Publisher: Springer Science & Business Media ISBN: 0387698051 Category : Medical Languages : en Pages : 639
Book Description
Genetically-engineered mouse models for cancer research have become invaluable tools for studying cancer biology and evaluating novel therapeutic approaches. This volume focuses on state-of-the-art methods for generating, analyzing and validating such models for studying aspects of human cancer biology. Additionally, these models are emerging as important pre-clinical systems in which to test cancer prevention and therapeutic strategies in order to select compounds for testing in clinical trials.
Author: Daniel Bassi Publisher: Biota Publishing ISBN: 1615045090 Category : Medical Languages : en Pages : 60
Book Description
Many proprotein convertases (PC), especially furin and PACE4, are involved in pathological processes such as viral infection, inflammation, hypercholesterolemia, and cancer, and have been postulated as therapeutic targets for some of these diseases. In this chapter, we review mostly our work using animal models of squamous cancers that have been induced by chemical or UV carcinogenesis protocols to highlight the role of PCs in the development and progression of experimental tumors. After demonstrating in wild type mice the role of PACE4 in tumor progression as well as detecting the expression of PACE4 and furin in human non-melanoma skin cancers, we developed transgenic mice that over-express either PACE4 or furin in squamous epithelia, including the epidermis. This was accomplished by targeting the expression of the corresponding PC by using the promoter of the bovine keratin 5. Both K5-PACE4 and K5-Furin transgenic mice showed increased susceptibility to a two-stage carcinogenesis protocol of chemical carcinogenesis. Similar studies conducted in K5-PACE4 mice also showed an increased sensitivity to ultraviolet B radiation carcinogenesis. In most of these experiments, we were able to demonstrate that compared to the control wild type mice, the over-expression of the transgene in the epidermis increased the number of benign and malignant skin tumors and also had an effect on tumor progression as evidenced by the presence of less differentiated tumors and more frequent local and distant metastases in many of the transgenic lines. Interestingly, double transgenic mice in which PACE4 and furin are targeted to the epidermis did not show any additive effect, pointing to a probable in vivo overlap of functions at least in cutaneous tissues. The tumor-enhancing effects of PACE4 and furin further support their possible role as therapeutic targets. Furthermore, a proof of principle for PC inhibition as a therapeutic tool has been substantiated by an in vivo experiment in which the PC-inhibitor, decanoyl-RVKRchloromethylketone, was topically administrated to the skin of wild type and transgenic mice treated with chemical carcinogenesis protocols, resulting in a significant decrease of tumor development and progression.
Author: Elizabeth K. Weisburger Publisher: Springer Science & Business Media ISBN: 9400925263 Category : Medical Languages : en Pages : 210
Book Description
but also the possibility of intervention in specific stages. In Human behavior, including stress and other factors, plays an important role in neoplasia, although too little is known addition, variables which affect cancer development as well on the reasons for such development. Carcinogens, which as some endogenous factors can be better delineated help initiate the neoplastic process, may be either synthetic through such investigations. The topics of this volume encompass premalignant non or naturally-occurring. Cancer causation may be ascribed to invasive lesions, species-specific aspects of carcinogenicity, certain chemicals, physical agents, radioactive materials, viruses, parasites, the genetic make-up of the organism, and radiation, viruses, a quantum theory of carinogenesis, onco bacteria. Humans, eumetazoan animals and vascular plants genes, and selected environmental carcinogens. are susceptible to the first six groups of cancer causes, whe reas the last group, bacteria, seems to affect only vascular plants. Neoplastic development may begin with impairment ofJmdy defenses by a toxic material (carcinogen) which acts as an initiator, followed by promotion and progression to an overt neoplastic state. Investigation of these processes Series Editor Volume Editor allows not only a better insight into the mechanism of action Hans E. Kaiser Elizabeth K. Weisburger vii ACKNOWLEDGEMENT Inspiration and encouragement for this wide ranging project on cancer distribution and dissemination from a comparative biological and clinical point of view, was given by my late friend E. H. Krokowski.
Author: Rajesh Uthamanthil Publisher: Academic Press ISBN: 0128040610 Category : Medical Languages : en Pages : 486
Book Description
Patient Derived Tumor Xenograft Models: Promise, Potential and Practice offers guidance on how to conduct PDX modeling and trials, including how to know when these models are appropriate for use, and how the data should be interpreted through the selection of immunodeficient strains. In addition, proper methodologies suitable for growing different type of tumors, acquisition of pathology, genomic and other data about the tumor, potential pitfalls, and confounding background pathologies that occur in these models are also included, as is a discussion of the facilities and infrastructure required to operate a PDX laboratory. Offers guidance on data interpretation and regulatory aspects Provides useful techniques and strategies for working with PDX models Includes practical tools and potential pitfalls for best practices Compiles all knowledge of PDX models research in one resource Presents the results of first ever global survey on standards of PDX development and usage in academia and industry
Author: Keiko Hiyama Publisher: Springer Science & Business Media ISBN: 1603278796 Category : Medical Languages : en Pages : 375
Book Description
Telomerase, an enzyme that maintains telomeres and endows eukaryotic cells with immortality, was first discovered in tetrahymena in 1985. In 1990s, it was proven that this enzyme also plays a key role in the infinite proliferation of human cancer cells. Now telomere and telomerase are widely accepted as important factors involved in cancer biology, and as promising diagnostic tools and therapeutic targets. Recently, role of telomerase in “cancer stem cells” has become another attractive story. Until now, there are several good books on telomere and telomerase focusing on biology in ciliates, yeasts, and mouse or basic sciences in human, providing basic scientists or students with updated knowledge.
Author: Publisher: ISBN: Category : Government publications Languages : en Pages : 728
Book Description
This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.
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Author: Bradley J. Kubick
Author: Jeffrey E. Green
Author: Daniel Bassi
Author: Alecsandru Ioan Baba
Author: Elizabeth K. Weisburger
Author: Rajesh Uthamanthil
Author: Keiko Hiyama
Author: 
Author: Helen Rosenbaum