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.

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

This volume will be the first to provide a comprehensive description of tumor dormancy. It will define the clinical and biological aspects of this phenomenon, as well as the cellular and molecular mechanisms associated with tumor dormancy. Chapters will be authored by world-renewed experts who are conducting cutting-edge research in the field. A unique feature will be a conclusive paragraph detailing future development and foreseeable clinical applications at the end of each chapter. The volume will serve as a fundamental instrument for every researcher and clinician interested in the field of tumor dormancy as well as a means of disseminating stimulating concepts and prompting the development of innovative technological solutions.

Understanding Cancer from a Systems Biology Point of View: From Observation to Theory and Back starts with a basic question, why do we sometimes observe accelerated metastatic growth after resection of primary tumors? Next, it helps readers understand the systemic nature of cancer and how it affects treatment approaches and decisions. The book puts together aspects of cancer that many readers have most likely never combined, using unfamiliar, novel methods. It is a valuable resource for cancer researchers, cancer biologists, mathematicians and members of the biomedical field who are interested in applying systems biology methodologies for understanding and treating cancer. Explains the systemic nature of cancer and how it affects decisions on treatment Brings a variety of methods together, showing, in detail, the logical approach to finding answers to complex questions Discusses the theoretical underpinnings of cancer as a systemic disease, providing the reader with valuable information on applicable cases

The book shows how mathematical and computational models can be used to study cancer biology. It introduces the concept of mathematical modeling and then applies it to a variety of topics in cancer biology. These include aspects of cancer initiation and progression, such as the somatic evolution of cells, genetic instability, and angiogenesis. The book also discusses the use of mathematical models for the analysis of therapeutic approaches such as chemotherapy, immunotherapy, and the use of oncolytic viruses.

In this second volume in the series exploring Tumor Dormancy, Quiescence, and Cellular Senescence, discussion is focused on the role of tumor dormancy in diseases such as breast cancer, melanoma, prostate cancer, liver cancer and lung cancer. M. A. Hayat, the series editor, writes in the preface that little is known of factors regulating the transition of residual cancer into a dormant state or the subsequent reinitiation of growth. A majority of us, he says, have in situ tumors that may remain dormant or may progress into a lethal form of cancer; the former are prevented from recruiting their own blood supply. Section I covers Molecular Mechanisms, with chapters on the role of NAE inhibitor MLN4924; oncogene-induced senescence; the role played by mitogen-activated protein kinase in the induction of cellular senescence; mechanisms of premature cell senescence and other topics. Section II examines Tumor and Cancer, discussing defects in chromatin structure and diseases; the role of fibrosis in tumor progression and the dormant to proliferative switch; the function of ING proteins in cancer and senescence and more. The final section is devoted to Stem Cells and Cancer Stem Cells, featuring chapters showing that senescent-derived pluripotent stem cells are able to redifferentiate into fully rejuvenated cells; that the transcription factor Gata2 regulates quiescence in haematopoietic stem and progenitor cells; and discussing dormancy and recurrence of cancer stem cells in bone. The contributors point out that the quiescent state regulates hematopoietic stem cells and muscle stem cells, and detail the role of kinase in the mediation of reversible quiescent state in a subset of ovarian, pancreatic, and colon cancers. Molecular mechanisms underlying stress-induced cellular senescence and accumulation of reactive oxygen species and induction of premature senescence are also presented. Discussion includes the important role of microRNAs in oxidative stress-induced apoptosis and senescence and the effect of microRNA as a modulator of cell proliferation in lung cancer. The book includes an explanation of the suppression of cellular senescence in glioblastoma brain tumor. Taking a broad and varied perspective, this volume was written by 70 contributors representing 11 countries.

This important book provides up-to-date information on a series of topical issues relating to the approach to minimal residual disease in breast cancer patients. It first explains how the study of minimal residual disease and circulating and disseminated tumor cells (CTCs/DTCs) can assist in the understanding of breast cancer metastasis. A series of chapters then discuss the various technologies available for the detection and characterization of CTCs and DTCs, pinpointing their merits and limitations. Detailed consideration is given to the relevance of CTCs and DTCs, and their detection, to clinical research and practice. The role of other blood-based biomarkers is also addressed, and the closing chapters debate the challenges facing drug and biomarker co-development and the use of CTCs for companion diagnostic development. This book will be of interest and assistance to all who are engaged in the modern management of breast cancer.

With a particular emphasis on tumor dormancy in breast, lung, prostate, and liver cancers, as well as in melanoma, this first volume of a new Springer series focuses on the interrelationship between biological processes of aging and tumors—both dormant and quiescent. With detail supplied by numerous international researchers at the forefront of cancer research, the book examines a host of differing aspects of the topic. Featured contributions analyze the role of the quiescent state in regulating hematopoietic and muscle stem cells. They also explore the mediation, by the kinase, in the reversible quiescent state of a subset of ovarian, pancreatic, and colon cancers. The book includes key research on the molecular mechanisms underlying stress-induced cellular senescence, in addition to those governing the accumulation of reactive oxygen species, and the induction of premature senescence. It also provides information on suppressing cellular senescence in the most common, and most aggressive malignant primary brain tumor in humans, glioblastoma multiforme. With comprehensive and cutting-edge information on therapeutic interventions and on the correct diagnosis of relevant neoplasms, and with numerous color illustrations, this is the most up-to-date assessment of current medical knowledge in this crucial area of medical research.

The unprecedented amount of data produced with high-throughput experimentation forces biologists to employ mathematical representation and computation to glean meaningful information in systems-level biology. Applying this approach to the underlying molecular mechanisms of tumorgenesis, cancer research is enjoying a series of new discoveries and biological insights. Unique in its dualistic approach, this book introduces the concepts and theories of systems biology and their applications in cancer research. It presents basic cancer biology and cutting-edge topics of cancer research for computational biologists alongside systems biology analysis tools for experimental biologists.