Inflammation And Cancer

This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.

This second edition volume expands on the previous edition with an update on the broad spectrum of research models, techniques, and protocols used in laboratories by basic and clinical researchers. The chapters in this book are divided into two parts. Part One discusses the latest findings on the development and characterization of representative research models for chronic immune-based diseases and inflammation-associated cancers. Part Two covers biochemical, molecular, and cellular biological techniques that are commonly used to dissect the molecular mechanisms and cellular processes that drive the pathogenesis of certain disease states. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Cutting-edge and comprehensive, Inflammation and Cancer: Methods and Protocols, Second Edition is a valuable resource for those with a diverse range of laboratory-based experience, ranging from novice undergraduate students to established basic or clinical researchers who wish to diversify their existing portfolio of practical knowledge in the field.

This revised second edition is improved linguistically with multiple increases of the number of figures and the inclusion of several novel chapters such as actin filaments during matrix invasion, microtubuli during migration and matrix invasion, nuclear deformability during migration and matrix invasion, and the active role of the tumor stroma in regulating cell invasion.

This book offers a summary and discussion of the advances of inflammation and infection in various cancers. The authors cover the classically known virus infections in cancer, novel roles of other pathogens (e.g. bacteria and fungi), as well as biomarkers for diagnosis and therapy. Further, the chapters highlight the progress of immune therapy, stem cells and the role of the microbiome in the pathophysiology of cancers. Readers will gain insights into complex microbial communities, that inhabit most external human surfaces and play a key role in health and disease. Perturbations of host-microbe interactions often lead to altered host responses that can promote cancer development. Thus, this book highlights emerging roles of the microbiome in pathogenesis of cancers and outcome of therapy. The focus is on mechanistic concepts that underlie the complex relationships between host and microbes. Approaches that can inhibit infection, suppress chronic inflammation and reverse the dysbiosis are discussed, as a means for restoring the balance between host and microbes. This comprehensive work will be beneficial to researchers and students interested in infectious diseases, microbiome, and cancer as well as clinicians and general physiologists.

In recent years there have been various discoveries connecting inflammation and lung cancer and clearly there is growing interest in this area of cancer research. The link between unresolved inflammation and cancer has been well established with estimates that 15% of cancer deaths are inflammation‐related. Evidence for this link includes the following: a) some inflammatory diseases are associated with increased risk of cancer development; b) inflammatory mediators are present surrounding and within most tumors; c) overexpression of inflammatory cytokines increases cancer development and progression in murine studies; d) inhibition of inflammatory mediators decreases cancer development and progression; and e) the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) has been found to decrease cancer incidence and delay progression. The volume will present aspects of the inflammatory tumor microenvironment (TME), its many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of micro‐RNAs (miRNAs) and an increase in a stem cell phenotype. The book will also cover the mechanisms of inflammatory mediators. Chronic overexpression of inflammatory mediators in the TME, as seen in smokers and patients with non‐small cell lung cancer (NSCLC), can also lead to increased tumor initiation, progression, invasion and metastasis. The volume will provide a comprehensive perspective of the latest findings and summaries of progress made regarding inflammation and its connection to lung cancer.

Inflammation and Oral Cancer: From Bench to Bedside discusses all aspects surrounding the relationship between inflammation and oral cancer, from basic science to the translational research that helps in the optimization of clinical management strategies. The book discusses topics such as chronic inflammation and cancer in oral cavity, the role of HPV in oral inflammation and cancer, rodent models of oral cancer, and epigenetics in oral inflammation and cancer. This is a valuable resource for cancer researchers, oncologists and members of biomedical field who are interested in learning more about the diverse aspects of inflammation and oral cancer. Inflammation in oral mucosa can remodel the topography of the overlying epithelium. If such inflammation is chronic, it can have fundamental clinical consequences, the principal of which can be premalignant lesions throughout the alimentary tract. Furthermore, mucosal inflammation, even if subtle, is the single most common pathway for oral cancer - therefore it is very important to understand these interactions in detail. Presents animal models of oral cancers for use in research Discusses epigenetics in oral cancers, along with risk factors such as tabaco and alcohol Encompasses detailed information on human papilloma virus (HPV) and its risk in oral inflammation and cancer

A link between inflammation and cancer has been established many years ago, yet it is only recently that the potential significance of this connection has become apparent. Although several examples of chronic inflammatory conditions, often induced by persistent irritation and/or infection, developing into cancer have been known for some time, there has been a notable resistance to contemplate the possibility that this association may apply in a causative way to other cancers. Examples for such progression from chronic inflammation to cancer are colon carcinoma developing with increased frequency in patients with ulcerative colitis, and the increased incidence of bladder cancer in patients suffering from chronic Schistosoma infection. Inflammation and cancer have been recognized to be linked in another context for many years, i.e., with regards to pathologies resembling chronic lacerations or 'wounds that do not heal.' More recently, the immunology of wound healing has given us clues as to the mechanistic link between inflammation and cancer, in as much as wounds and chronic inflammation turn off local cell-mediated immune responses and switch on growth factor release as well the growth of new blood vessels - angiogenesis. Both of these are features of most types of tumours, which suggest that tumours may require an immunologically shielded milieu and a growth factor-rich environment.

An overview of the current systems biology-based knowledge and the experimental approaches for deciphering the biological basis of cancer.