Apoptosis Senescence And Cancer
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| Author | : David A. Gewirtz |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 596 |
| Release | : 2007-10-23 |
| Genre | : Medical |
| ISBN | : 1597452211 |
This book provides insight into established practices and research into apoptosis and senescence. The volume thoroughly examines novel and emerging techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics that still hold mysteries for researchers. In total, this volume provides basic scientists and clinicians with a deeper and more complete understanding of the cellular responses of malignancies which may determine the effectiveness of treatment, both in the initial stages of the disease as well as in disease recurrence.
| Author | : Seamus J. Martin |
| Publisher | : S. Karger AG (Switzerland) |
| Total Pages | : 0 |
| Release | : 1997 |
| Genre | : Apoptosis |
| ISBN | : 9783805565790 |
The past five years have witnessed an explosion of research efforts in the study of how cells die. This book provides an up-to-date overview of our current knowledge of apoptosis and how discoveries in this area impact on our understanding of cancer. By synthesizing many of the recent developments in this area and placing them in perspective, it fulfills an important need. All the contributions are written by experts in their respective fields. The first two chapters give a basic introduction to the cell death machinery and its role in tumor development and progression; subsequent chapters cover current aspects of apoptosis research, including the involvement of cell cycle-related proteins (e.g. cyclin-dependent kinases) in apoptosis, the role of Bcl-2, Bcr-Abl, Rb, p53 and myc in the regulation of cell death, and apoptosis in the context of specific neoplasms such as cancer of the prostate, kidney, leukemia and neuroblastoma. It is also discussed how insights into the regulation of apoptosis may be exploited for designing new drugs aimed at eliminating malignant cells. Compiling the most recent research results on the relationship between apoptosis and cancer in one handy volume, this book will provide a valuable reference for scientists working in cancer research as well as newcomers to the field.
| Author | : M.A. Hayat |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 336 |
| Release | : 2013-11-29 |
| Genre | : Science |
| ISBN | : 9400777264 |
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.
| Author | : |
| Publisher | : Academic Press |
| Total Pages | : 384 |
| Release | : 2021-04-13 |
| Genre | : Medical |
| ISBN | : 0128241594 |
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
| Author | : Kenneth Charles Calman |
| Publisher | : |
| Total Pages | : 180 |
| Release | : 1980 |
| Genre | : Medical |
| ISBN | : |
| Author | : Peter D. Adams |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 274 |
| Release | : 2010-01-23 |
| Genre | : Medical |
| ISBN | : 1441910751 |
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.
| Author | : M.A. Hayat |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 332 |
| Release | : 2013-03-14 |
| Genre | : Medical |
| ISBN | : 9400759584 |
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.
| Author | : Daniel Muñoz-Espin |
| Publisher | : Springer Nature |
| Total Pages | : 226 |
| Release | : 2020-04-27 |
| Genre | : Science |
| ISBN | : 3030449033 |
This book offers comprehensive information on the new and rapidly evolving science of identifying and targeting senescent cells, and on the exciting prospect of new diagnostic and therapeutic opportunities for stopping, and even reversing, the progression of disease and the deterioration of the human body due to ageing. According to recent United Nations data, by 2050 one in six people worldwide will be older than age 65, with peaks rising to one in four people in Europe and North America. Remarkably, the number of persons aged 80 years or older is expected to triple, from 143 million in 2019 to 426 million in 2050. First documented in the 1960s, the concept of cellular senescence as an underlying cause of ageing has been established in the course of the last decade. Using genetically engineered mouse models, researchers have demonstrated that the selective elimination of senescent cells can block and even reverse a number of age-related dysfunctions and pathologies, promoting both better health and longer life in the elderly. These include cardiovascular diseases; neurological disorders; type 1 and type 2 diabetes; inflammatory diseases; fibrosis; geriatric syndromes; chronic diseases resulting in organ dysfunction; the integrity of the musculoskeletal system; and cancer. Some senolytic agents have already progressed into trials. These include UBX0101 for the treatment of osteoarthritis (now in phase II), a cocktail of dasatinib and quercetin for the management of idiopathic pulmonary fibrosis and chronic kidney disease, and ABT-263 in combination with senescence-inducing chemotherapies for the treatment of advanced solid tumours. In addition, the book discusses pathways to early phase clinical trials and translational approaches in medicine and ageing, highlighting new opportunities as well as current limitations, challenges and alternatives. Given its scope, it will benefit a broad audience of advanced educators, researchers, graduate students and practitioners.
| Author | : Razmik Mirzayans |
| Publisher | : Nova Science Publishers |
| Total Pages | : 0 |
| Release | : 2009 |
| Genre | : Cancer |
| ISBN | : 9781606926765 |
Normal human cells have a limited life span when grown in culture. Aging cells enter a state of permanent growth arrest called replicative senescence, which is regulated by multiple signal transduction pathways involving p53 and other cancer-associated proteins. Senescent cells exhibit flattened and enlarged morphology, retain cell membrane integrity, remain metabolically active, but cease to divide when explanted in culture. Exposure of young (early passage) human cells to genotoxic agents such as ionising radiation and cancer therapeutic drugs can also trigger a state of permanent growth arrest. One mechanism of stress-induced growth arrest is similar to replicative senescence and is commonly termed accelerated or premature senescence. Whereas some normal human cell types (e.g., skin fibroblasts) lose their clonogenic potential in response to genotoxic stress primarily through the process of premature senescence, it has been generally assumed that cancer-derived cells die through necrosis or programmed cell death (apoptosis) but do not exhibit premature senescence following exposure to genotoxic agents. Recently, however, it has become evident that exposure of human solid tumour-derived cells to genotoxic agents can trigger not only premature senescence, but also growth arrest by an ill-defined process leading to the development of multinucleated/polyploid cells. Here the author provides evidence reinforcing the notion that ionising radiation-triggered premature senescence in cancer cells is generally dependent on the wild-type p53 function, and that the development of giant cells is a response of p53-deficient cells, presumably reflecting their failure to engage the premature senescence program.
| Author | : Hong-Gang Wang |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 267 |
| Release | : 2013-03-30 |
| Genre | : Medical |
| ISBN | : 1461465613 |
With the explosion of information on autophagy in cancer, this is an opportune time to speed the efforts to translate our current knowledge about autophagy regulation into better understanding of its role in cancer. This book will cover the latest advances in this area from the basics, such as the molecular machinery for autophagy induction and regulation, up to the current areas of interest such as modulation of autophagy and drug discovery for cancer prevention and treatment. The text will include an explanation on how autophagy can function in both oncogenesis and tumor suppression and a description of its function in tumor development and tumor suppression through its roles in cell survival, cell death, cell growth as well as its influences on inflammation, immunity, DNA damage, oxidative stress, tumor microenvironment, etc. The remaining chapters will cover topics on autophagy and cancer therapy. These pages will serve as a description on how the pro-survival function of autophagy may help cancer cells resist chemotherapy and radiation treatment as well as how the pro-death functions of autophagy may enhance cell death in response to cancer therapy, and how to target autophagy for cancer prevention and therapy − what to target and how to target it.
