In this state-of-the-art exploration of a hugely dynamic and fast-evolving field of research, leading researchers share their collective wisdom on the role that stem cells could play in the context of physiological stress and lung injury. The text focuses on reviewing the most relevant-and recent-ideas on using local, endogenous, and exogenous progenitor/stem cells in preventing and treating injury to the lung. The lungs are one of the most complex organs in the human body, with a mature adult lung boasting at least 40 morphologically differentiated cell lineages. Our entire blood supply passes through the lung's alveolar units during oxygenation. This interaction with the outside world, along with the intricacies of its structure, makes the lung a highly susceptible organ that is vulnerable to numerous types of injury and infection. This means that the mechanisms of lung repair are in themselves correspondingly complex. Because of their multipotentiality, as well as the fact of the lung's relatively rapid cell turnover, stem cells are thought to be an important alternative cell-base therapy in lung injury. Despite the controversial nature of stem cell research, there has been growing interest in both local and endogenous stem cells in the lung. This highly topical book with chapters on everything from using mesenchymal stem cells in lung repair to the effect of physical activity on the mobilization of stem and progenitor cells, represents an exciting body of work by outstanding investigators and will be required reading for those with an interest in the subject.

Progress in the treatment of cancer over the past two decades has been rapid with many new and novel therapeutic modalities arriving at an unprecedented pace. Overall cancer mortality rates have actually begun to fall in parallel with progress in the diagnosis and treatment of malignant disease. Despite our advances in the understanding of the biology and molecular genetics of cancer, as well as the availability of an increasing array of effective therapies, cancer treatment today and for the foreseeable future will include the traditional modalities of surgery, radiation therapy and chemotherapy. Myelosuppressive agents with their potential hematopoietic toxicities remain the mainstay of systemic treatment for both metastatic and early stage cancer. The complications of cancer chemotherapy have serious impact on a patient's well being and overall quality of life. Fortunately, advances in cancer treatment have been accompanied by equally impressive progress in the availability of a wide array of supportive care modalities which have greatly enhanced the ability of oncologists to minimize the impact of cancer and its treatment on patient quality of life as well improve delivery of potentially curative cancer treatment. Despite the increasing complexity of modern cancer treatment, it is the obligation of the oncologist as well as the entire cancer care team to be certain that cancer patients receive the optimal supportive care available for their disease and its treatment. Among the most serious and potentially life threatening toxicities of cancer treatment are the hematologic toxicities accompanying myelosuppression including anemia and associated asthenia and fatigue, neutropenia and fever associated with infection in the immunocompromised patient and thrombocytopenia and accompanying risk of bleeding. Special supportive care needs arise in the very elderly care patient that may tax the ability of even the most skilled clinician. Despite the considerable progress that has been made with more effective and safer treatment strategies, myelosuppressive chemotherapy will remain the mainstay of systemic treatment for cancer for the foreseeable future. While considerable progress has occurred, better methods and broader application of supportive care measures are needed to reduce the symptomatic effects of cancer and the associated toxicities associated with cancer treatment. No area of cancer supportive care better illustrates the progress that has resulted from advances in our understanding of cellular and molecular biology, genetic engineering and the development of more effective yet often more toxic cancer treatments than that of the hematopoietic growth factors. This volume will review and integrate the major advances in our understanding of the underlying molecular biology and pharmacology of these agents along with the results of well designed and executed randomized controlled trials of the erythroid stimulating agents, the myeloid growth factors and the new thrombopoietic agents each addressing a major threat associated with bone marrow suppression accompanying cancer treatment. The current clinical utilization of these agents is based on numerous randomized controlled trials and meta-analyses along with evidence-based clinical practice guidelines developed by professional societies guiding their appropriate and cost-effective use in clinical care.

At the time of the first edition of Principles of Cancer Biotherapy in 1987, this book represented the first comprehensive textbook on biological therapy. In 1991, when the second edition was published, there was still some doubt on the part of many oncologists and cancer researchers as to the therapeutic value of these new approaches. By 2003 and the fourth edition, it was generally agreed that biopharmaceuticals were producing major opportunities for new cancer therapies. Cancer biotherapy has now truly matured into the fourth modality of cancer treatment. This fifth revised edition describes the tremendous progress that has been made in recent years using biologicals in cancer treatment.

This book summarizes an evolving science and a rapidly changing medical practice in biotherapy. In this new millennium, it is now possible to envision a much more diversified system of cancer research and treatment that will afford greater opportunities for a patient s personalized cancer treatment. This was first envisioned in the 1987 initial edition of this textbook and is now a new and popular approach to cancer treatment. Some forms of cancer biotherapy use the strategy of tumor stabilization and control through continued biological therapy, akin to the use of insulin in the treatment of diabetes.

This textbook illustrates new methods of thinking and new strategies for control of cancer. It is always difficult to move from past dogma to future opportunity, but this fifth edition of Principles of Cancer Biotherapy illustrates why it is so important to the patients for researchers and clinicians to explore and quickly apply these new opportunities in cancer biotherapy."

The book will explain previously unconnected clinical data such as why mammography works better for women age 50-59 than it does for women age 40-49, why adjuvant chemotherapy works best for premenopausal patients with positive lymph nodes, and it may also explain the racial disparity in outcome. In particular, it points to the perioperative period when systemic inflammation persists for a week or so. This can lead to a variety of mechanisms whereby single cancer cells (perhaps from the marrow) begin division and angiogenesis of dormant avascular micrometastases occurs leading to early relapses. With chapters presented from distinguished scientists and physicians in a variety of specialties that relate to and border the effects we present, this volume can be used as a reference for practicing physicians and as a jumping-off point for researchers to explore new therapeutic opportunities.

This volume, which includes contributions from leading scientists and clinicians in the field, provides definitive, state-of-the-art information on STAT inhibitors in a biological and clinical context. It gives an overview of the biology of the STAT family of transcription factors and their role in cancer etiology. Additionally, it describes the raft of therapeutic approaches being used to inhibit STATs in the context of various cancers, covering the full spectrum of therapeutic approaches to inhibiting STATs, and presenting emerging data from clinical trials.

A comprehensive review of the recent developments in DNA repair that have potential for translational and clinical applications. The authors explain in detail the various mechanisms by which cancer cells can circumvent anticancer therapy and limits its usefulness in patients. They also review the clinical impact of such novel inhibitors of DNA repair mechanisms as methylguanine-DNA-methyltransferase. Also examined are inhibitors of other DNA repair enzymes such as PARP and DNA-PK, now under development and close to clinical trials. The book captures-for both cancer researchers and practicing oncologists dealing with hallmark "relapse" or "drug resistance" phenomena on a daily basis-the many exciting new uses of DNA repair inhibitors, either alone or in combination with anticancer therapies.

The increase in new medical technology and experimental treatments has made the study of medical ethics essential for practitioners on all levels. This book brings together experts in the fields of pediatric hemotology/oncology, ethics, and law to examine legal and ethical issues surrounding the treatment of children with cancer or blood disease. The contributors present thoughtful discussions of ethical considerations of such practices as bone marrow transplantation, caring for hemophiliacs, preventing sickle cell disease, informing patients of treatment side effects, the statistical design of clinical trials, and the activities of the Institutional Review Board.

This book concisely reviews our current understanding of hypoxia, molecular targeting, DNA repair, cancer stem cells, and tumor pathophysiology, while also discussing novel strategies for putting these findings into practice in daily clinical routine. Radiotherapy is an important part of modern multimodal cancer treatment, and the past several years have witnessed not only substantial improvements in radiation techniques and the use of new beam qualities, but also major strides in our understanding of molecular tumor biology and tumor radiation response. Against this backdrop, the book highlights recent efforts to identify reasonable and clinically applicable biomarkers using broad-spectrum tissue microarrays and high-throughput systems biology approaches like genomics and epigenomics. In particular, it describes in detail how such molecular information is now being exploited for diagnostic imaging and imaging throughout treatment using the example of positron emission tomography. By discussing all these issues in the context of modern radiation oncology, the book provides a broad, up-to-date overview of the molecular aspects of radiation oncology that will hopefully foster its further optimization.

A comprehensive collection of classic and innovative methodologies used in many laboratories for the investigation of multiple myeloma. These readily reproducible techniques range from the standard Plasma Cell Labeling Index methodology to a final chapter on making sense of microarrays, and include the full spectrum of cytogenetic and molecular diagnostic methods. The protocols follow the successful Methods in Molecular Medicine (TM) series format, each offering step-by-step laboratory instructions, an introduction outlining the principle behind the technique, lists of the necessary equipment and reagents, and tips on troubleshooting and avoiding known pitfalls. These proven techniques are ideal for studying the pathogenesis of multiple myeloma and identifying new therapeutic targets.

As cells mature they naturally stop dividing and enter a period called senescence. But cellular senescence can also be induced prematurely by certain oncogenes involved in cancer development. Cellular senescence, a growth-arrest program that limits the lifespan of mammalian cells and prevents unlimited cell proliferation, is attracting considerable interest because of its links to tumor suppression.

This volume will explore the latest findings in research into the genetics of breast and reproductive cancers, covering the epidemiological aspects of these cancers, their etiology, the effect of environment on genes and cancer etiology, and how research in this area can lead to development of preventative measures and treatments.

Experts from around the world review the current field of the immunobiology of heat shock proteins, and provide a comprehensive account of how these molecules are spearheading efforts in the understanding of various pathways of the immune system. This one-stop resource contains numerous images to both help illustrate the research on heat shock proteins, and better clarify the field for the non-expert. Heat shock proteins (HSPs) were discovered in 1962 and were quickly recognized for their role in protecting cells from stress. Twenty years later, the immunogenicity of a select few HSPs was described, and for the past 30 years, these findings have been applied to numerous branches of immunology, including tumor immunology and immunosurveillance, immunotherapy, etiology of autoimmunity, immunotherapy of infectious diseases, and expression of innate receptors. While HSPs can be used to manipulate immune responses by exogenous administration, they appear to be involved in initiation of de novo immune responses to cancer and likely in the maintenance of immune homeostasis.

This volume explores the epigenetic alterations and their association with various human cancers. Considering one of human cancer as an example, individual chapters are focused on defining the role of epigenetic regulators and underlying mechanisms in cancer growth and progression. Epigenetic alteration including DNA methylation, histone modification, nucleosome positioning and non-coding RNAs expression are involved in a complex network of regulating expression of oncogenes and tumor suppressor genes and constitute an important event of the multistep process of carcinogenesis. Recent advances in the understanding of the epigenetic regulation and detailed information of these epigenetic changes in various cancers provide new avenues of advancements in diagnostics, prognostics, and therapies of this highly fatal disease.

Neurofibromatosis type 1 (NF1), caused by mutational inactivation of the "NF1" tumour suppressor gene, is one of the most common dominantly inherited human disorders, affecting 1 in 3000 individuals worldwide. This book presents in concise fashion, but as comprehensively as possible, our current state of knowledge on the molecular genetics, molecular biology and cellular biology of this tumour predisposition syndrome.

Written by internationally recognized experts in the field, the 44 chapters that constitute this edited volume provide the reader with a broad overview of the clinical features of the disease, the structure and expression of the "NF1" gene, its germ line and somatic mutational spectra and genotype-phenotype relationships, the structure and function of its protein product (neurofibromin), NF1 modifying loci, the molecular pathology of NF1-associated tumours, animal models of the disease, psycho-social aspects and future prospects for therapeutic treatment.

A collection of both well-established and cutting-edge methods for investigating breast cancer biology not only in the laboratory, but also in clinical settings. These readily reproducible techniques solve a variety of problems, ranging from how to collect, store, and prepare human breast tumor samples for analysis, to analyzing cells in vivo and in vitro. Additional chapters address the technology of handling biopsies, new methods for analyzing genes and gene expression, markers of clinical outcome and progress, analysis of tumor-derived proteins and antigens, validating targets, and investigating the biology of newly discovered genes.

This book contextualizes translational research and provides an up to date progress report on therapies that are currently being targeted in lung cancer. It is now well established that there is tremendous heterogeneity among cancer cells both at the inter- and intra-tumoral level. Further, a growing body of work highlights the importance of targeted therapies and personalized medicine in treating cancer patients. In contrast to conventional therapies that are typically administered to the average patient regardless of the patient's genotype, targeted therapies are tailored to patients with specific traits. Nonetheless, such genetic changes can be disease-specific and/or target specific; thus, the book addresses these issues manifested in the somatically acquired genetic changes of the targeted gene. Each chapter is written by a leading medical oncologist who specializes in thoracic oncology and is devoted to a particular target in a specific indication. Contributors provide an in-depth review of the literature covering the mechanisms underlying signaling, potential cross talk between the target and downstream signaling, and potential emergence of drug resistance.

This book discusses the emergence of a new class of genes with a specific anticancer activity. These genes, recently defined as "Anticancer Genes", are reviewed in individual chapters on their mode of action, the specific cell death signals they induce, and the status of attempts to translate them into clinical application. Anticancer Genes provides an overview of this nascent field, its genesis, current state, and prospect. It discusses how Anticancer Genes might lead to the identification of a repertoire of signaling pathways directed against cellular alterations that are specific for tumor cells. With contributions from experts worldwide, Anticancer Genes is an essential guide to this dynamic topic for researchers and students in cancer research, molecular medicine, pharmacology and toxicology and genetics as well as clinicians and clinical researchers interested in the therapeutic potential of this exciting new field.

This teaching monograph on systems approaches to cancer research and clinical applications provides a unique synthesis, by world-class scientists and doctors, of laboratory, computational, and clinical methods, thereby establishing the foundations for major advances not possible with current methods. Specifically, the book: 1) Sets the stage by describing the basis of systems biology and bioinformatics approaches, and the clinical background of cancer in a systems context; 2) Summarizes the laboratory, clinical, data systems analysis and bioinformatics tools, along with infrastructure and resources required; 3) Demonstrates the application of these tools to cancer research; 4) Extends these tools and methods to clinical diagnosis, drug development and treatment applications; and 5) Finishes by exploring longer term perspectives and providing conclusions. This book reviews the state-of-the-art, and goes beyond into new applications. It is written and highly referenced as a textbook and practical guide aimed at students, academics, doctors, clinicians, industrialists and managers in cancer research and therapeutic applications. Ideally, it will set the stage for integration of available knowledge to optimize communication between basic and clinical researchers involved in the ultimate fight against cancer, whatever the field of specific interest, whatever the area of activity within translational research.

We present an in-depth description of resistance to targeted therapies in breast cancer. Targeted therapies discussed here include those used to treat ER+ or Her2+ breast cancers (i.e., Tamoxifen or trastuzumab) or those targeting signaling pathways aberrantly activated in triple negative breast cancer (i.e., EGFR and Wnt signaling). We have also provided an overview of standard of care as an introduction into the importance of targeted therapy. It is our hope that this volume gives an insight into the landscape of breast cancer treatment, the challenges of targeted therapy, and a glimpse into the future of breast cancer therapy.

Mast cells are versatile, tissue-homing secretory cells, which were first described by Paul Ehrlich in 1878. Mast cells have long been implicated in the pathogenesis of allergic reactions and certain protective responses to parasites. Their functional role, however, has been discovered to be increasingly complex and multifarious. Mast cells have been implicated in various cell-mediated immune reactions, being found in tissues from multiple disease sites, and as a component of the host reaction to bacteria, parasite, and even virus infections. They have also been shown to participate to angiogenic and tissue repair processes after injury. The importance of a possible functional link between chronic inflammation and cancer has long been recognized. As most tumours contain inflammatory cell infiltrates, which often include plentiful mast cells, the question as to the possible contribution of mast cells to tumour development has progressively been emerged. In this book, the general biology of these cells, their development, anatomical distribution and phenotype as well as their secretory products will first be discussed. The biology of tumour cells, their structural and molecular characteristics, the specificity of the tumour microenvironment and the development of a vascular network in the tumour context will be analyzed. The involvement of mast cells in tumour biology and tumour fate will then be considered, with particular emphasis on the capacity of these cells to stimulate tumour growth by promoting angiogenesis and lymphangiogenesis. The last chapter suggest that mast cells may serve as a novel therapeutic target for cancer treatment.

This handbook provides a useful guide for the day-to-day management of people with breast cancer. It covers the journey from diagnosis to post-treatment comprehensive care. It explains when and why different treatment modalities are used, what the complications of both the disease and treatments are and how to manage them. Although this book has been written for students and health personnel working in a general hospital, it will be useful for those in specialist breast units as well. Dr Jenny Edge is a surgeon and head of Breast and Endocrine Surgery at the University of Stellenbosch. Dr Ines Buccimazza is head of the Breast Unit, member of the Multidisciplinary Breast Team and a senior specialist in the Department of Surgery at the Nelson R. Mandela School of Medicine at the University of KwaZulu-Natal in Durban.

Receptor Tyrosine Kinase: Structure, Functions and Role in Human Disease, for the first time, systematically covers the shared structural and functional features of the RTK family. Receptor Tyrosine Kinases (RTKs) play critical roles in embryogenesis, normal physiology and several diseases. And over the last decade they have become the Number 1 targets of cancer drugs. To be able to conduct fundamental research or to attempt to develop pharmacological agents able to enhance or intercept them, it is essential first to understand the evolutionary origin of the 58 RTKs and their roles in invertebrates and in humans, as well as downstream signaling pathways. The assembly of chapters is written by experts and underscores commonalities between and among the RTKs. It is an ideal companion volume to The Receptor Tyrosine Kinase: Families and Subfamilies, which proceeds, family by family through all of the specific subfamilies of RTKs, along with their unique landmarks.