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 third volume in the series Tumor Dormancy, Quiescence, and Senescence discusses the role of tumor dormancy and senescence in a number of diseases, including breast cancer, ovarian cancer and leukemia. The contents are organized under five subheadings: General Applications, Role in Breast Cancer, Role in Ovarian Cancer, Role in Leukemia and Role in Cardiovascular Disease. The first section includes basic information on the definition of dormancy, how cells become senescent and what they do, along with an appraisal of the current state of research on dormancy. Section Two explores dormancy in breast cancer, including the progression of hormone-dependent mammary tumors after dormancy. Section Three details the resistance of Type II ovarian tumors, in which the resistant tumor cell population persists after chemotherapy in a state of dormancy, with recurrent tumors arising upon transformation of such dormant cells back to malignant growth. This section explains how lineage, histological subtypes and grade influence the differential response of ovarian cancer resistance to platinum drugs. The fourth section explores leukemia, discussing regulation of the promyelocytic leukemia protein and its role in premature senescence. The final section explores the role of senescence and autophagy in age-related cardiovascular diseases and the observation that autophagy seems to retard cardiac senescence. Like the two preceding volumes in the series, Volume 3 stands out for its comprehensive approach, its roster of some 26 expert contributors representing seven different countries and its up-to-date review of leading-edge technology and methods.

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.

Chromatin Readers in Health and Disease, Volume 35, a new release in the Translational Epigenetics series, gathers and makes actionable our current understanding of how chromatin readers regulate access to genetic information, and how their aberrant regulation can contribute to human pathologies. Chromatin readers discussed include 14-3-3 Dinshaw, ADD, Ankyrin, BAH, BET, BIR, BRCT, bromodomains and Kac readers, chromodomains and chromobarrel readers, citrullination readers, macrodomains and poly-ADP-ribose readers, MBT, PHD and double PHD, PWWP, SUMO (H4K12) readers, Tudor and TTD, UDR and ubiquitin, WD40, YEATS (crotonyl reader), MBD, SRA, and Methyl-RNA readers.In the book, more than a dozen leaders in the field examine a range of protein readers, their relationship to human disease, and the early therapeutics that act as chromatin signaling factors to treat cancers and Huntington's disease, among other disorders. - Enables researchers and clinicians to understand chromatin signaling mechanisms that regulate gene expression through chromatin readers - Highlights the role of chromatin readers in a variety of human pathologies, as well as early therapeutics that act on chromatin signaling - Includes chapter contributions from international leaders in the field

Phospholipases in Physiology and Pathology presents a comprehensive overview on the physiology and pathology of phospholipases. This seven-volume set considers the biochemical and molecular mechanisms of normal and abnormal cell function upon dysregulation of phospholipases in different diseases. Volumes cover signal transduction mechanisms, implications in cancer, infectious diseases, neural diseases, cardiovascular diseases and other diseases, implications in inflammation, apoptosis, gene expression and non-coding RNAs, the role of natural and synthetic compounds, and stem cell therapies, nanotechnology-based therapies, and more. Together, these volumes give researchers critical insight on the mechanistic and therapeutic aspects of phospholipases. - Discusses the biochemical and molecular mechanisms of normal and abnormal cell function in different disease processes - Covers a wide range of basic and translational research appropriate for scientists engaged in studying the regulation of phospholipases from interdisciplinary perspectives - Features state-of-the-art chapter contributions from international leaders in the field

This detailed volume explores methods and protocols that aim to increase our understanding of how cells enter a quiescent state during homeostasis and how cells exit quiescence and re-enter differentiating cell divisions to restore damaged tissues, essential for developing new approaches in regenerative medicine in the future. The chapters in this book were designed to address cellular quiescence in prokaryote and eukaryote organisms, detection of quiescence (Hoechst/pyronin Y, FUCCI, CFSE, BrdU, H2B-GFP, CyTOF), quiescence in stem cells (skin, intestinal, neuronal, hematopoietic), genomic regulation (gene expression, transcription factors, lncRNA, RNA methylation), as well as analysis of the heterogeneity of quiescence by computer modeling. Written for the highly successful Methods in Molecular Biology series, 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. Authoritative and practical, Cellular Quiescence: Methods and Protocols offers a broad view of basic and cutting-edge technology to inspire research in this emerging field of cell biology.

Advances in Cancer Research, Volume 150, the latest release in this ongoing series, covers the relationship(s) between autophagy and senescence, how they are defined, and the influence of these cellular responses on tumor dormancy and disease recurrence. Specific sections in this new release include Autophagy and senescence, converging roles in pathophysiology, Cellular senescence and tumor promotion: role of the unfolded protein response, autophagy and senescence in cancer stem cells, Targeting the stress support network regulated by autophagy and senescence for cancer treatment, Autophagy and PTEN in DNA damage-induced senescence, mTOR as a senescence manipulation target: A forked road, and more. - Addresses the relationship between autophagy and senescence in cancer therapy - Covers autophagy and senescence in tumor dormancy - Explores autophagy and senescence in disease recurrence

Foreword from the Editor: With the second installment in the Quarterly Highlights series, Frontiers in Oncology has once again had a strong quarter, and continues to publish important research, with submissions from across the globe - and readership from across the globe. In this quarter, we saw a number of different impact metrics become updated using recent data. The 2019 impact metrics reflect our competitive and respectable status in the field and amongst competitors. We find it very encouraging to see that our impact has remained high, and thank the entirety of the Editorial Board and Office for their contributions and hard work in doing so. Once again with a record-breaking number of papers to choose from, this Special Edition takes an interdisciplinary approach to highlight important recent findings across the different areas of cancer research. We have opted for a selection of papers that we feel best demonstrates the interdisciplinary and international nature of the journal. We are pleased to announce that we have begun our work on launching a new section in the journal. The new section, which will be our 19th, will focus on dermatological malignancies and cancers of the skin. Given the importance and relevance of skin cancers in today’s climate, we are very excited to be moving forward with this. The journal has been active and present at a number of conferences including the 1st International Lung Cancer Summit, the 15th International Conference on Malignant Lymphoma, and ESMO’s World Congress on Gastrointestinal Cancers. The Editorial Office will also be present at the ESMO 2019 Congress in Barcelona next month (Booth P425) and look forward to meeting our readers and Editors there. Giuseppe Giaccone

It is now established that dysregulated cell stress response pathways play a critical role in tumorigenesis, and a refined mechanistic understanding of this phenomenon at the molecular level promises to open new avenues for targeted therapeutic strategies that may benefit cancer patients in the near future. Coauthored by recognized leaders in cancer research from five continents, this novel book provides a comprehensive perspective on cell stress response pathways and therapeutic opportunities. Focusing on the role of genotoxic, proteotoxic, oxidative, metabolic, and inflammatory stress in tumorigenesis, the book is essential reading for students, basic researchers, and biomedical health care professionals interested in cancer and therapeutic development.

The collection of chapters in this proceeding volume reflects the latest research presented at the Aegean meeting on Tumor Microenvironment and Cellular Stress held in Crete in Fall of 2012. The book provides critical insight to how the tumor microenvironment affects tumor metabolism, cell stemness, cell viability, genomic instability and more. Additional topics include identifying common pathways that are potential candidates for therapeutic intervention, which will stimulate collaboration between groups that are more focused on elucidation of biochemical aspects of stress biology and groups that study the pathophysiological aspects of stress pathways or engaged in drug discovery.