How are cancer and inflammation interrelated mechanistically and clinically? Though extensive literature exists on the topic "Cancer and Inflammation", there are relatively few texts that have truly integrated the two in spite of the many common mechanisms shared by their processes. Certainly, areas such as cytokines, growth factors, proliferation, signal transduction and angiogenesis, for example, are found in both. Yet, the dynamics of how these common mechanisms are maybe interrelated in the pathologies of the two is not widely covered. Such coverage, as presented in this volume, may help further understanding and bring new approaches to therapeutics. The first section of the book discusses inflammatory mechanisms, studied in cellular and animal studies. The second part concentrates on clinical studies with antiinflammatory drugs in cancer treatment. The volume is written for biomedical researchers in the health care industry and in academia who are working in these areas.

A new perspective on the link between inflammation and cancer Inflammation is the human body’s normal biological response to threats in the modern world, as well as a defense against the harmful influence of pathogens, the environment, and poor nutrition. But what happens when the inflammatory response is triggered repeatedly and sustained for long periods of time? Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects discusses the mechanisms by which chronic inflammation can lead to cancer, the various causative agents, and possible prevention methods. A compilation of the latest information coming out of the various fields of cancer research, this book provides a detailed look at inflammation-related carcinogenesis from the perspective of researchers at the forefront of the field. It takes an interdisciplinary approach to the topic, and provides comprehensive information about the major factors at work in inflammation, cancer, and the intersection of the two conditions. Topics include: A general overview of inflammation-related cancer The biochemistry of inflammation and its effects on DNA Molecular biology and the role of microRNA in carcinogenesis Specific causative agents including oncogenic viruses, asbestos, and nanomaterial Anti-inflammatories, nutraceuticals, and other preventative measures A deeper understanding of the mechanisms behind inflammation-related carcinogenesis can lead to better patient outcomes by improving diagnostics and prevention, as well as altering the approach to treatment. Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects provides the knowledge base researchers need to push the field forward.

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.

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.

Chronic inflammation predisposes to some forms of cancer and the host response to malignant disease shows several parallels with inflammation and wound healing. The cells involved in inflammation are detected in a range of common cancers, together with the inflammatory cytokines and members of the chemokine ligand/receptor systems. Neutralization or deletion of the gene for some inflammatory cytokines confers resistance to tumour induction and experimental metastasis. Over-expression of such cytokines in tumour cells may enhance malignant potential. Certain chemokines are likely to subvert antitumour immunity by favouring development of ineffective Type 2 responses. Tumour cells may even utilize chemokine receptors in homing to lymph nodes and other organs. Thus, the cells, cytokines and chemokines found in tumours are more likely to contribute to tumour growth, progression and immunosuppression than they are to mount an effective host antitumour response. This book draws together contributions from an international group of scientists and clinicians from diverse disciplines, ranging from epidemiology to immunology, cell biology, molecular oncology, molecular medicine and pharmacology to debate these and related issues. Topics covered include the epidemiological links between cancer and inflammation, the parallels between inflammation and cancer, the role of inflammation in cancer, inflammatory genes as risk factors for cancer initiation and progression, inflammation and cancer angiogenesis, and preventative and therapeutic strategies. Related Novartis Foundation symposia: 252 Generation and effector functions of regulatory lymphocytes Chair: Jean-François Bach Immunoinformatics: bioinformatic strategies for better understanding of immune function Chair: Hans-Georg Rammensee

A link between inflammation and cancer was initially made by Rudolf Virchow back in the 19th century. Nowadays many cancers are considered dependent on inflammatory responses to microbial and damaged-self stimuli and both arms of immunity, innate and adaptive, are playing a role in promoting cancer. Moreover, besides environmental factors, opportunistic pathogens contribute to inflammation and cancer. Nevertheless, microbial influence on chronic disease is sometimes difficult to discern, especially in the context of polymicrobial communities, such as those found in the digestive tract. In this light, model organisms provide important insights into immune and growth signals that promote cancer, and suggest therapies that will selectively target potentially harmful microbes or modulate host responses. A number of review and opinion articles in this series address novel aspects and paradigms of the interactions between the microbiota and the host in relation to inflammation and 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

Immunology is the branch of biomedical sciences to study of the immune system physiology both in healthy and diseased states. Some aspects of autoimmunity draws our attention to the fact that it is not always associated with pathology. For instance, autoimmune reactions are highly useful in clearing off the excess, unwanted or aged tissues from the body. Also, generation of autoimmunity occurs after the exposure to the non-self antigen that is structurally similar to the self, aided by the stimulatory molecules like the cytokines. Thus, a narrow margin differentiates immunity from auto-immunity as already discussed. Hence, finding answers for how the physiologic immunity turns to pathologic autoimmunity always remains a question of intense interest. However, this margin could be cut down only if the physiology of the immune system is better understood. The individual chapters included in this book will cover all the possible aspects of immunology and pathologies associated with it. The authors have taken strenuous effort in elaborating the concepts that are lucid and will be of reader's interest.

This volume represents a collection of contributions from the 6th International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Related Diseases held in Boston from September 12-15, 1999. The mission of this meeting was to bring together senior and junior investigators to both announce and examine their recent advancements in cutting-edge research on the roles and actions of lipid mediators and their impact in human physiology and disease pathogenesis. The meeting focused on new concepts in these areas of interest to both clinicians and researchers. The program included several outstanding plenary lectures and presentations by leading experts in the fields of cancer and inflammation. In addition, the Boston meeting presented three Young Investigator awards, one in each of the major focus areas. The meeting was exciting and proved to be very memorable. The program was developed with an emphasis on recent advances in molecular and of lipid mediators relevant in cellular mechanisims involved in the formation and actions inflammation and cancer. Plenary lectures were presented by Prof. Bengt Sammuelsson (Karolinska Institute, Stockholm; 1982 Nobel Laureate in Physiology or Medicine) and Prof. E. 1. Corey (Harvard University; 1990 Nobel Laureate in Chemistry). Both of these plenary lectures were held on Day 1, which set an exciting tone for this meeting. Immediately following these plenary lectures, three simultaneous breakout sessions were held, one of inflammation, a second on cancer and synthesis of novel inhibitors, and a third on enzymes-lipoxygenases/cyclooxygenases and inhibitors.

Over one hundred contributions detail advances in the molecular and cellular biology of eicosanoid production, as well as their role in signal transduction. One of the most exciting developments explored within this collection of articles is the expression of the novel isoform of cyclooxygenase (cox-2), which may play a large role in the development of anti-inflammatory drugs.