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.
A comprehensive resource on the recent developments of stem cell use in wound healing With contributions from experts in the field, Wound Healing offers a thorough review of the most recent findings on the use of stem cells to heal wounds. This important resource covers both the basic and translational aspects of the field. The contributors reveal the great progress that has been made in recent years and explore a wide range of topics from an overview of the stem cell process in wound repair to inflammation and cancer. They offer a better understanding of the identities of skin stem cells as well as the signals that govern their behavior that contributes to the development of improved therapies for scarring and poorly healing wounds. Comprehensive in scope, this authoritative resource covers a wealth of topics such as: an overview of stem cell regeneration and repair, wound healing and cutaneous wound healing, the role of bone marrow derived stems cells, inflammation in wound repair, role and function of inflammation in wound repair, and much more. This vital resource: Provides a comprehensive overview of stem cell use in wound healing, including both the basic and translational aspects of the field Covers recent developments and emerging subtopics within the field Offers an invaluable resource to clinical and basic researchers who are interested in wound healing, stem cells, and regenerative medicine Contains contributions from leading experts in the field of wound healing and care Wound Healing offers clinical researchers and academics a much-needed resource written by noted experts in the field that explores the role of stem cells in the repair and restoration of healing wounds.
This book was prepared as extension of author’s accidental discoveries on experimental models of acute and chronic ocular inflammatory diseases that were established at the University of Pennsylvania in 1980’s. Analyses of original data suggest a series of first evidence for direct link between inflammation and developmental phases of immune dysfunction in multistep tumorigenesis and angiogenesis. The only evidence presented on initial events for interactions and synergies between activated host and recruiting cells toward tumorigenesis. Effective immunity was defined as balance between two highly regulated and biologically opposing arms, Yin and Yang of acute inflammation, an amazingly precise signal communications between immune and non-immune systems requiring differential bioenergetics. Unresolved inflammation is a common denominator mapping aging process and induction of ‘mild’, ‘moderate’ or ‘severe’ immune disorders including cancers. Our knowledge of the fascinating biology of immunity in health or chronic diseases is fragmentary, chaotic and confusing, particularly for cancer science. Lack of progress in curing majority of chronic diseases or cancer is primarily due to the fact that scientists work on isolated molecules/cells or topics that are funded and promoted by decision makers in medical/cancer establishment. Despite existence of over 25 million articles on cancer-related topics, cancer biology and cure remain mysteries to be solved. After a century of cancer research, the failure rates of therapies for solid tumors are 90% (+/-5). Current reductionist views on cancer science are irresponsible, shut-gun approaches and create chaos. Outcomes are loss of millions of precious lives and economic drain to society. Very little is known about initial events that disturb effective immunity whose function is to monitor and arrest growth of cancerous cells or defend against other external or internal hazardous agents that threaten body’s survival. The author demonstrates the serious need for systematic understanding of how immune disruptors and aging process would alter effective immunity. Outcomes of proposed orderly studies are expected to provide logical foundations for cost-effective strategies to promote immunity toward a healthier society. The policy makers and medical/cancer establishment are urged to return to the common sense that our Forefathers used to serve the public.
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.
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
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.
Increasing scientific evidence suggests that the majority of diseases including cancer are driven by oxidative stress and inflammation, attributed to environmental factors. These factors either drive genetic mutations or epigenetically modify expression of key regulatory genes. These changes can occur as early as gestational fetal development, and
