The discovery of microRNAs and its role as gene expression regulators in human carcinogenesis represents one of the most important scientific achievements of the last decade. More recently, other non-coding RNAs have been discovered and its implications in cancer are emerging as well, suggesting a broader than anticipated involvement of the non-coding genome in cancer. Moreover, completely new and unexpected functions for microRNAs are being revealed, leading to the identification of new anticancer molecular targets. This book represents a comprehensive guide on non-coding RNAs and cancer, spanning from its role as cancer biomarkers, to providing the most useful bioinformatic tools, to presenting some of the most relevant discoveries, which indicates how these fascinating molecules act as fine orchestrators of cancer biology.

This book reviews recent breakthroughs in anti-cancer drug discovery. Building on the previous volume in the series, it outlines some of the most significant developments that have occurred in the field in the subsequent period that have led to new drug approvals or promising clinical candidates. The volume is divided into chapters that each relate to a specific protein or protein class. Each chapter provides an overview of the underlying biology and then emphasises the medicinal chemistry strategies and tactics that led to the most significant drugs and drug candidates. A summary of clinical data and the future outlook for the field is also provided. Each chapter is authored by experts in the topic and who have themselves made significant contributions to their respective fields.

This volume constitutes, in part, the proceedings of the Hong Kong Conference on "Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury" held in Hong Kong in October 1995. It contains papers by the symposium speakers, as well as poster contributions from researchers in this field. Since the discovery of "PROSTAGLANDIN-LIKE' substances 60 years ago. much has been learned. EICOSANOID is the new term that is used to include prostaglandins. thromboxanes, leukotrienes, lipoxins, isoprostanes, depoxilins, hydroxy acids, epoxy and hydroperoxy fatty acids. The conference focussed on recent development in underatanding the role of EICOSANOIDS in inflammation, cancer, and radiation damage. At the confer- ence, we also highlighted advances in newly developing areas such as "NO," "A POP- TOSIS and "ANANDAMIDE." The discovery of the structures of genes that encode several key enzymes and receptors of the Eicosanoid cascade, has allowed us to include reports in the "Alteration of the Gene Expression" section that reflects the most recent de- velopments in regulation for PGH-synthase and lipoxygenases. The editors are convinced that this volume will be an up-to-date and useful reference for investigators in both basic and clinical research.

This volume, with contributions from the most recognized experts in preventive strategies in breast cancer, presents the accepted as well as the novel ideas that have been introduced for the prevention of breast cancer. There is no single preventive agent that can stop the incidence of breast cancer-the malignant disease most frequently diagnosed in women of all races and nationalities. Furthermore, its incidence around the globe is increasing in industrialized countries. The worldwide incidence of breast cancer has increased 30-40% since the 1970s, reaching an excess of 1,390,000 new cases and a mortality of more than 460,000 cases in 2015. Therefore, what is needed is the development of rational strategies for the prevention of this fatal disease.

This volume reviews the current state of research on immune checkpoints and offers novel concepts. It discusses the two most important immune checkpoints: T lymphocyte-associated antigen-4 (CTLA-4) and programmed cell death-1 (PD-1). It shows that antagonistic antibodies against these two molecules are highly effective in the treatment of various cancers and that PD-1 and CTLA-4 have been linked to the suppression of T-cell receptor signaling and co-stimulatory molecules. Further, the volume examines other agents, a number of cells, receptors and signaling molecules, that are also involved in the regulation of T-cell activation and extends the concept of immune checkpoints to "molecules and cells that negatively regulate T-cell activation". Playing essential roles in immune homeostasis, they could offer new targets for cancer immunotherapy, and for the therapy of autoimmune diseases. Written by internationally respected scientists, this book will appeal to basic scientists, clinicians, drug development researchers, and advanced students alike.

Leland H. Hartwell Director, Fred Hutchinson Cancer Research Center, Nobel Laureate for Medicine, 2001 Yeast has proved to be the most useful single-celled organism for studying the fundamental aspects of cell biology. Resources are now available for yeast that greatly simplify and empower new investigations, like the presence of strains with each gene deleted, each protein tagged and databases on protein-protein interactions, gene regulation, and subcellular protein location. A powerful combination of genetics, cell biology, and biochemistry employed by thousands of yeast researchers has unraveled the complexities of numerous cellular processes from mitosis to secretion and even uncovered new insights into prion diseases and the role of prions in normal biology. These insights have proven, time and again, to foretell the roles of proteins and pathways in human cells. The collection of articles in this volume explores the use of yeast in pathway analysis and drug discovery. Yeast has, of course, supplied mankind's most ubiquitous drug for thousands of years. In one aspect, the role of yeast in drug discovery is much like the role of yeast in other areas of biology. Yeast offers the power of genetics and a repetoire of resources available in no other organism. Using yeast in the study of drug targets and metabolism can help to make a science of what has been largely an empirical activity. A science of drug discovery would permit rigorous answers to important questions.

This book covers all aspects of thyroid cancer. Heavily illustrated and including pathology, thyroid and whole-body scans, ultrasounds and other nuclear medicine and radiological studies, the book addresses important issues that physicians should cover when dealing with their patients.

The text is designed for physicians, endocrinologists, nuclear medicine physicians, general and head and neck surgeons, oncologists and radiation oncologists, and primary care doctors. Other groups are residents, medical students, and nurse practitioners researching a patient-related problem.

This book provides a comprehensive coverage and a succinct overview of the current status of supportive cancer care with Chinese medicine written by leading experts in the field. The chapters coherently present an overview on the major treatment approaches of Chinese medicine and progresses made with different important aspects on supportive cancer care with acupuncture, herbal therapy and qigong. Moreover, there are reviews on the evidences and efficacies of Chinese medicine for controlling radiation-induced injuries, chemotherapy-related side effects, as well as pain control with Chinese medicine. In order to provide information from basic science at the bench to the patient's bedside, modern researches and clinical trials would be overviewed so as to give an up-to-date and realistic evaluation of a therapy's utility for cancer patients. It is also worth noting that toxicology, safety and herb-drug interactions are the main concerns of using Chinese medicine combined with western medicine. A chapter will expound on these issues and there will also be chapters discussing integrative Chinese and Western medicine, as well as cancer prevention with Chinese medicine. This book presents state-of-the-art knowledge on supportive cancer care with Chinese medicine, which will appeal to anyone involved in cancer care. This is a precious book for all types of readers, including but not limited to oncologists, cancer researchers, pharmacologists, pharmaceutical specialists, traditional Chinese medicine practitioners, Chinese medicine educators, medicine postgraduates and undergraduates, cancer caregivers, cancer survivors, and family members of cancer patients who want to expand their knowledge in supportive cancer care.

Despite recent progress in many areas of treatment and control, cancer remains a frightening threat to everyone. While scientists have known for decades that the majority of human cancers are caused by environmental agents such as radiation and the chemicals in cigarette smoke, not everyone who smokes gets lung cancer. Furthermore, many people who assiduously avoid all possible risk from smoking, diet, and pollution still succumb to some form of cancer later in life. Does this mean that there is an element of blind chance in the underlying mechanisms of human carcinogenesis? To what extent do genetic influences play a role in determining the cancer risk of individuals? A number of `cancer families', in which several closely related individuals have suffered from various specific forms of cancer, have been studied by genetic epidemiologists. However, for the majority of cancer cases, little or no discernible genetic influence or family history is found. Recent research has discovered that for many of these `sporadic' (non-familial) cancer cases, defects or aberrations in certain metabolic genes not previously associated with genetic cancer risk may contribute to either causing the disease or at least increasing the chances of developing cancer. It is therefore possible that much of what has previously passed for `bad luck' may turn out to be a new type of `bad genes'. Genetic Susceptibility to Cancer explains that this new idea of `bad genes' may contain an unexpected positive side. The carcinogenic effects of these metabolic genes, unlike those of the oncogenes and tumor suppressor genes that are responsible for the inherited cancer syndromes, can potentially be overcome or nullified. Genetic Susceptibility to Cancer will provide a valuable reference for health professionals, researchers, clinicians and biomedical scientists who are interested in the current thinking in this critically important area of cancer management.

For the past decade or so, research regarding women's health has become a major source of concern among health professionals. Due to the vast amounts of research, it has been difficult to amass a comprehensive source describing the challenges of physicians in this area of medical treatment and care. The Handbook of Research on Oncological and Endoscopical Dilemmas in Modern Gynecological Clinical Practice is a pivotal reference source that provides vital research on the application of clinical practices in regards to the health of women and prevention of severe, life-threatening diseases. While highlighting topics such as mental health, women's health, and preventative care, this publication provides an insight into critical dilemmas and issues in modern gynecologic oncology and endoscopy as well as the methods of daily clinical practice. This book is ideally designed for obstetricians, gynecologists, specialized physicians, medical professionals, academicians, researchers, and medical students.

Revealing essential roles of the tumor microenvironment in cancer progression, this book provides a comprehensive overview of the latest research in the field. A variety of topics are covered, including metabolism in the tumor microenvironment, stellate cells and endothelial progenitors in the tumor microenvironment, as well as the effects of HIV, viral hepatitis, and inflammation in the tumor microenvironment, and more. Taken alongside its companion volumes, Tumor Microenvironment: State of the Science updates us on what we know about various aspects of the tumor microenvironment, as well as future directions. This book is essential reading for advanced cell biology and cancer biology students as well as researchers seeking an update on research in the tumor microenvironment.

Cancer is a complex disease. Only 5-10% of human cancers are hereditary in nature. Many of us think of environmental agents when we think of carcinogens. The environment includes all that surrounds us, and environmental influences include not only chemical, physical and biological toxicants, but also diet and lifestyle. In this broadest sense, the environment contributes substantially in the development of human cancer. This book will describe how environment contributes to malignant transformation leading to profound changes in the genetic and signaling networks that control the functioning of the cell. It will critically discuss the understanding of the effects of environment on the development, progression and metastasis of cancer with current knowledge of the signaling networks that support functioning of transformed human cells. Genes and environmental factors that influence the origins of cancer are not necessarily the same as those that contribute to its progression and metastasis. Susceptibility gene variants for each specific cancer are being identified with emerging evidence of gene environment interaction. Gene-environment interactions will be discussed through each specific cancer-based approach to address the question of how genetic variations can influence susceptibility to the individual type of cancer. It will also highlight and summarize epigenetic changes that increase the risk for susceptibility to a particular type of cancer, particularly in the presence of specific environmental factors. Thus, this book will contain chapters from the world s experts focused on the current evidences that support the role of environment in the cancer etiology and in the growth of malignant lesions, and discuss who may be susceptible to environmental influences."

1 Characteristics of Multidrug Resistance in Human Tumor Cells.- 2 Development of Multidrug Resistance in Rodent Cell Lines.- 3 Cloning and Characterization of Mouse mdr Genes.- 4 Isolation and Characterization of the Human MDR (P-Glycoprotein) Genes.- 5 Amplification of Several Different Genes in Multidrug-Resistant Chinese Hamster Cell Lines.- 6 Molecular and Cytogenetic Analysis of Multidrug Resistance-Associated Gene Amplification in Chinese Hamster, Mouse Sarcoma, and Human Neuroblastoma Cells.- 7 Karyotype and Amplicon Evolution during Stepwise Development of Multidrug Resistance in Djungarian Hamster Cell Lines.- 8 Chromosome Localization of P-Glycoprotein Genes in Drug-Sensitive and -Resistant Human Cells.- 9 Structure and Evolution of P-Glycoproteins.- 10 Drug Accumulation and Binding in P-Glycoprotein-Associated Multidrug Resistance.- 11 Binding of Drugs and ATP by P-Glycoprotein and Transport of Drugs by Vesicles from Human Multidrug-Resistant Cells.- 12 Protein Changes in Multidrug-Resistant Cells.- 13 Membrane Lipids of Multidrug-Resistant Cells: Chemical Composition and Physical State.- 14 Expression of the MDR1 Gene in Normal Human Tissues.- 15 Expression of the Multidrug Resistant Gene in Human Cancer.- 16 Immunohistochemical Analysis of P-Glycoprotein Expression in Normal and Tumor Tissues in Humans.- 17 Quantitative Estimation of MDR1 mRNA Levels by Polymerase Chain Reaction.- 18 Collateral Sensitivity of Multidrug-Resistant Cells.- 19 Reversal of Multidrug Resistance by Calcium Channel Blockers and Other Agents.- 20 Growth Inhibition of Multidrug-Resistant Cells by Monoclonal Antibodies against P-Glycoprotein.- 21 P-Glycoprotein-Mediated Drug Resistance: Puzzles and Perspectives.

In the past, many tumor marker laboratory tests have not been sensitive enough for the very early detection of cancer. However, many of them have nonetheless proved useful in monitoring therapy, following the course of the tumor, and predicting prog- nosis. Today, cancer may be viewed as a genetic disease with various specific chromo- somal and nucleotide aberrations, such as mutations, deletions, gene amplification, gene rearrangements, and translocations occurring during the transformation of a nor- mal cell into a malignant cell. The considerable advances in technology during the past several years have greatly enhanced our ability to detect human cancers in the very early stages of tumor forma- tion. These technologies include: (1) nucleotide molecular assays (genomics); (2) proteomics (multiplex protein measurements); (3) DNA microarrays; and (4) bio- informatics. Many of these technologies are already helping in the integration and use of multiple biomarkers for tumors. Although the individual biomarkers may reveal only limited information, the use of multiple biomarkers can help markedly elevate the diagnostic capabilities for early detection of tumors.

This volume presents the most current reviews on how cancer stem cells (CSCs) hypothesis dictates that the continued proliferation of a tumor is dependent on a sub-population of self-renewing and asymmetrically dividing neoplastic stem cells that supply a largely differentiated tumor. This volume provides a comprehensive overview of the characteristics of CSCs, their role in central nervous system (CNS) tumors, and the recent CSC-specific treatment modalities being used. The emerging focus on CSCs in brain tumors represents a paradigm shift in our understanding of the pathogenesis of these neoplasms. Importantly, the realization that a distinct sub-population of cells contributes disproportionately to the growth and sustenance of central nervous system tumors has important implications for the treatment of such tumors. To treat CNS tumors, there is now a growing need to treat CSCs to achieve adequate tumor control.

This book focuses on issues in clinical practice and research that are of general interest. The articles primarily focus on understanding the pathogenic mechanisms of diseases, their prevention, and therapy. The topics addressed include cardiovascular regulation with regard to blood pressure and heart rate variability, and to coupling blood pressure changes with subarachnoid fluid oscillations. In addition, the book discusses recent advances in the diagnostics of and targeted molecular therapy for renal and pancreatic malignancies, growth disorders, vitamin D and calcium homeostasis in children in the context of neonatal urolithiasis, and neurosurgical interventions in multifarious age-related diseases of the vertebrae. Neuropsychological aspects of patients' quality of life and of shaping medical staff's attitude toward patients are also addressed. The respective articles are intended to build a bridge between basic and clinical research. Further, the book enhances the current body of knowledge on diagnostics and patient treatment and offers valuable new perspectives on practical clinical issues. As such, it offers a unique resource for clinicians, family physicians, medical scholars, and professionals engaged in patient management.

This book focuses on how obesity and sedentary lifestyles adversely affect cancer risk and survival for individuals as well as mechanisms that may underlie those associations. However, evidence is accumulating rapidly on the cost of obesity and sedentary lifestyles to society. For example, obesity is estimated to lead to costs of $147 billion in the US.6 While research on individual level interventions for weight loss and increasing physical activity have identified efficacious approaches, these changes in behavior are not maintained by many in the current environments in the US and worldwide that promote weight gain and inactivity. Research on environmental and policy approaches for addressing these problems at the societal level is needed7, 8 and is a major component of the President's Report on Childhood Obesity released in April 2010. The epidemic of overweight and obesity and the increasing sedentary lifestyles will impact the magnitude and quality of the cancer problem globally. Increasing the knowledge of scientists, clinicians, and policy experts will aid in defining new prevention and treatment methods, to reduce the impact of energy balance on cancer, with the goal to eventually reduce the burden of cancer. Hopefully, this knowledge can be translated into incentives for the general public, persons at high risk, and cancer patients and survivors to increase physical activity, reduce excess weight, and maintain energy balance lifelong.

This volume is based on the Workshop on Systems Biology of Tumor Dormancy meeting, held July 25th to July 28th, 2011. The first annual CCSB workshop brought together biologists, clinicians, mathematicians, and computer scientists to discuss various aspects of tumor dormancy and develop novel mathematical/computational models with the keynote speakers. Specific topics included the angiogenic switch, immune system interactions, cancer stem cells and signaling.

The annual research conference for 1996 of the American Institute for Cancer Re search was again held at the Loews L'Enfant Plaza Hotel in Washington, DC, August 29 and 30. The topic for this, the seventh in the series, was "Dietary Fat and Cancer: Genetic and Molecular Mechanisms. " Two separate presentations were given as the conference overview. "Fat and Cancer: The Epidemiologic Evidence in Perspective" noted that die tary fat can be saturated, largely from animal or dairy sources, or mono- or polyunsatu rated, mostly from plant sources. Unlike animal fats, fish contain relatively high levels of protective omega-3 fatty acids. Although the hypothesis that dietary fat is associated with cancer is plausible, the mechanisms involved are reasonable, and many animal studies support the hypothesis, there are many obstacles in any direct extrapolation to humans, in cluding imprecise measures of dietary fat intake, variability in individual diets, and spe cies variations. Despite these limitations, there is a weak positive correlation between colon cancer and dietary fat intake, but with substantial differences for various ethnic groups. In the case of breast cancer, there is substantial variation among countries and eth nic groups, but the overall evidence indicated an association with fat in the diet. Epidemiologic studies of dietary fat and prostate cancer are more consistent and most show a positive relationship. However, it was not clear which types of dietary fat were im plicated in the effect."

1 Biochemical, Immunological, and Molecular Markers of Hemopoietic Precursor Cells.- 1. Introduction.- 2. Biochemical Markers.- 2.1. Terminal Deoxynucleotide Transferase.- 2.2. Enzymes in Nucleotide Metabolism.- 3. Immunological Markers.- 4. Molecular Markers.- 5. Analysis of Human Hemopoietic Ontogenesis by Immunological and Molecular Markers.- 6. New Opportunities for Immunological and Molecular Markers: Minimal Residual Disease Detection and Therapeutical Approaches.- 7. References.- 2 Cell Surface Markers in Leukemia and Lymphoma.- 1. Introduction.- 2. B Cells.- 2.1. Normal B-Cell Ontogeny.- 2.2. B-Cell Leukemias and Lymphomas.- 3. T Cells.- 3.1. Normal T-Cell Ontogeny.- 3.2. T-Cell Leukemias and Lymphomas.- 4. Myeloid Cells.- 4.1. Normal Myeloid Ontogeny.- 4.2. Myeloid Leukemias.- 5. Summary.- 6. References.- 3 Cytoskeletal Organization of Normal and Leukemic Lymphocytes and Lymphoblasts.- 1. Introduction.- 2. Microfilaments in Normal and Leukemic Lymphocytes and Lymphoblasts.- 2.1. Actin and Actin-Associated Proteins in Nonmuscle Cells.- 2.2. Actin Isoforms.- 2.3. Organization of Actin in Normal Lymphocytes.- 2.4. Interactions between Actin and Surface Antigens in Lymphocytes.- 2.5. Actin in Leukemic Lymphocytes and Lymphoblasts.- 3. Intermediate-Size Filaments in Normal and Leukemic Lymphocytes and Lymphoblasts.- 3.1. The Intermediate Filament System.- 3.2. Distribution of Vimentin in Lymphocytes in Normal Conditions.- 3.3. Vimentin in Neoplastic Lymphocytes and Lymphoblasts.- 3.4. Expression of Cytokeratin in Lymphoid Tissues.- 4. Microtubules in Lymphoid Cells.- 5. Organization of Spectrin in Lymphocytes.- 6. Conclusions.- 7. References.- 4 Signaling Events in T-Lymphocyte-Dependent B-Lymphocyte Activation.- 1. Introduction.- 2. B-Cell Antigen Receptor-Mediated Signaling.- 3. Molecular Bases of T-Cell-Mediated B-Cell Signaling.- 4. Biological Evidence for Ia-Mediated Signal Transduction.- 5. Biochemical Evidence for Ia-Mediated Signal Transduction.- 6. Conclusions.- 7. References.- 5 IgE Receptors on Lymphocytes and IgE-Binding Factors.- 1. Introduction.- 2. Historical Overview.- 3. Fc?RII on Lymphocytes.- 3.1. Fc?RII-Bearing Cells.- 3.2. Function of Fc?RII.- 3.3. Molecular Properties of Fc?RII.- 3.4. Regulation of Fc?RII Expression on Lymphocytes.- 4. IgE-Binding Factors.- 4.1. Rat.- 4.2. Murine.- 4.3. Human.- 5. Glycosylation-Regulating Factors: GEF and GIF.- 5.1. Rat.- 5.2. Murine.- 6. Interleukin 4 and Gamma Interferon.- 7. CD23 Antigen.- 8. Conclusion.- 9. References.- 6 Lymphocyte-Mediated Cytolysis: Role of Granule Mediators.- 1. Role of Granules and Perform in Lymphocyte-Mediated Killing.- 1.1. The Granule Exocytosis or Secretion Model for Cell Killing.- 1.2. Cytoplasmic Granules and Perform as Mediators of Cytotoxicity.- 1.3. A Family of Serine Esterases Localized in Lymphocyte Granules.- 1.4. Proteoglycans.- 1.5. Leukalexins and Cytokines Related to Tumor Necrosis Factor and Lymphotoxin.- 2. Other Candidate Mechanisms of Lymphocyte-Mediated Killing.- 3. Resistance of Lymphocytes to Self-Mediated Killing.- 4. Conclusion.- 5. References.- 7 CR1-Cytoskeleton Interactions in Neutrophils.- 1. Introduction.- 2. Detergent Extraction of Cells.- 3. Receptor-Cytoskeleton Interactions.- 4. The C3b Receptor (CR1).- 5. References.- 8 The Flow of Granular Organelles in Leukocyte Differentiation.- 1. Introduction.- 2. Biogenesis of Membrane-Bound Organelles.- 2.1. Introduction.- 2.2. Endoplasmic Reticulum.- 2.3. Golgi Complex.- 2.4. Lysosomes.- 2.5. Communication between Compartments: Endosomes.- 2.6. Secretory Granules.- 3. Leukocyte Granules are Major Determinants of Function.- 3.1. Neutrophils.- 3.2. Platelets.- 3.3. Cytotoxic Lymphocytes.- 4. Granules Interact with the Plasma Membrane.- 4.1. Neutrophils.- 4.2. Platelets.- 5. Pathology of Myeloid Granules and Plasma Membranes.- 5.1. Nonneoplastic.- 5.2. Leukemic.- 6. Conclusion.- 7. References.- 9 The Elusive Oxidase: The Respiratory Burst Oxidase of Human Phagocytes...

Research over the past decades has firmly established the genetic basis of cancer. In particular, studies on animal tumour viruses and chromosome rearrangements in human tumours have concurred to identify so-called 'proto-oncogenes' and 'tumour suppressor genes', whose deregulation promotes carcinogenesis. These important findings not only explain the occurrence of certain hereditary tumours, but they also set the stage for the development of anti-cancer drugs that specifically target activated oncogenes. However, in spite of tremendous progress towards the elucidation of key signalling pathways involved in carcinogenesis, most cancers continue to elude currently available therapies. This stands as a reminder that "cancer" is an extraordinarily complex disease: although some cancers of the haematopoietic system show only a limited number of characteristic chromosomal aberrations, most solid tumours display a myriad of genetic changes and considerable genetic heterogeneity. This is thought to reflect a trait commonly referred to as 'genome instability', so that no two cancers are ever likely to display the exact same genetic alterations. Numerical and structural chromosome aberrations were recognised as a hallmark of human tumours for more than a century. Yet, the causes and consequences of these aberrations still remain to be fully understood. In particular, the question of how genome instability impacts on the development of human cancers continues to evoke intense debate.

In Hormone Therapy in Breast and Prostate Cancer, many of today's leading researchers and clinicians describe the principles underlying targeted hormonal treatments, assess the actions of new and established agents, and illustrate the new applications of hormonal chemoprevention for breast cancer. Topics range from preclinical and clinical antiestrogens to the inhibition of estrogen synthesis and the effects of androgen withdrawal. A wide variety of proven and new agents are discussed-antiestrogens, including aromatase inhibitors (anastrozole, letrozole, and others), SERMs (tamoxifen, raloxifene, and others), and such antiandrogenic strategies as goserelin and bicalutamide.