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Author: Peter D. Adams
Publisher: Springer Science & Business Media
ISBN: 1441910751
Category : Medical
Languages : en
Pages : 274
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Book Description
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: Peter D. Adams
Publisher: Springer Science & Business Media
ISBN: 1441910751
Category : Medical
Languages : en
Pages : 274
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Book Description
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: Martine Extermann
Publisher: Springer
ISBN: 9783319574141
Category : Medical
Languages : en
Pages : 1150
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Book Description
This book is intended as a comprehensive resource for clinicians and researchers seeking in-depth information on geriatric oncology. The coverage encompasses epidemiology, the biology and (patho)physiology of aging and cancer, geriatric assessment and management, hematologic malignancies, solid tumors, issues in patient care, and research methods. Since cancer is a disease of aging and people are living longer, most cancer patients are now aged 70 and older. Yet the more we age, the more diverse we become in terms of our health, biologic fitness, and cancer behavior. Typically, however, general oncology clinical trials address only a selected healthier and younger population of patients. Geriatric oncology is the area of oncology that addresses these issues but while a wealth of knowledge has been accumulated, information is often difficult to retrieve or insufficiently detailed. The SpringerReference program, in which this book is published, offers an ideal format for overcoming these limitations since it combines thorough coverage with access to living editions constantly updated chapter by chapter via a dynamic peer-review process, ensuring that information remains current and pertinent.
Author: M.A. Hayat
Publisher: Springer Science & Business Media
ISBN: 9400777264
Category : Science
Languages : en
Pages : 336
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Book Description
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: Manuel Serrano
Publisher: Academic Press
ISBN: 0128225157
Category : Science
Languages : en
Pages : 474
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Book Description
Winner of the 2023 PROSE award in Biomedicine and Neuroscience! Research in the field of senescence has boomed recently due to the gradual realization that senescent cells are associated with a significant number of diseases. The genetic or pharmacological elimination of senescent cells can cause widespread benefits and improves outcomes for most of those diseases. Cellular Senescence in Diseases presents an updated review of the role of cellular senescence in multiple pathologies. Focus is given to those diseases where the implication of senescence has been more extensively documented, such as (cancer, lung and liver diseases, diabetes, Neurodegenerative diseases and others). The Editors recruited a group of worldwide experts in each individual pathology to review the role of cellular senescence in each one of them, aiming at identifying potential therapeutic pathways. The first two chapters provide an overview of the cellular senescence principles. Next, the chapters are divided into specific diseases. Cancer, including premalignant lesions (OIS), Advanced disease (TIS), and Metastasis are covered. The following condition covered is Lund diseases, including IPF, COPD, and Pulmonary Hypertension. Next Liver Diseases are covered, including Fibrosis and Cirrhosis, and Fatty liver disease. Next there is coverage for Kidney implications, including fibrosis and transplantation. Vascular diseases are covered next including infarction and hear fibrosis, and atherosclerosis. Both diabetes types 1 and 2 are covered next. Following chapters cover Obesity, Sarcopenia, and Bone and Cartilage disorders, respectively. Neurodegenerative diseases are covered next, focusing on Alzheimer and Parkinson. The next chapter discusses accumulation of senescent cell in tissues during aging. The two final chapters cover current developments and conclusions. Cellular Senescence in Diseases is designed for researchers and clinicians with a focus on the cellular mechanisms of diseases. All chapters cover current experimental therapeutic approaches to eliminate or cancel the pathological effects of senescent cells. Pharmaceutical scientists may also benefit from the contents of the book in the exploration of novel therapeutic opportunities. 2023 PROSE Awards - Winner: Category: Biomedicine and Neuroscience: Association of American Publishers Provides a thorough introduction to Cellular Senescence Covers all major pathologies for which cellular senescence has shown evidence of involvement Focuses on possible therapeutic pathways Edited and authored by worldwide experts
Author: M.A. Hayat
Publisher: Springer Science & Business Media
ISBN: 9400759584
Category : Medical
Languages : en
Pages : 332
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Book Description
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:
Publisher: Academic Press
ISBN: 0128241594
Category : Medical
Languages : en
Pages : 384
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Book Description
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: Wang Zhiwei
Publisher: BoD – Books on Demand
ISBN: 9535109979
Category : Medical
Languages : en
Pages : 162
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Book Description
Senescence is a biological process that causes a progressive deterioration of structure and function of all organs chronologically. Recent studies have revealed the detailed molecular mechanisms of senescence using cell culture system and experimental organisms. It is thought that senescence is a potential cause for the development of various age-related disorders such as cancer, cardiovascular and neurodegenerative disorders. This book discusses in detail senescence and its related diseases by distinguished researchers and practicing clinicians. The cumulative knowledge from the studies could lead to developing new approaches for anti-senescence interventions.
Author: M.A. Hayat
Publisher: Springer
ISBN: 9401793255
Category : Science
Languages : en
Pages : 160
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Book Description
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.
Author: L. Robert
Publisher: Karger Medical and Scientific Publishers
ISBN: 3318026530
Category : Medical
Languages : en
Pages : 226
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Book Description
Aging inspired a large number of theories trying to rationalize the aging process common to all living beings. In this publication the most important environmental and intrinsic mechanisms involved in the aging process and in its pathological consequences are reviewed. Furthermore theoretical and experimental evidence of the most important theoretical elements based on Darwinian evolution, cellular aging, role of cell membranes, free radicals and oxidative processes, receptor-mediated reactions, the extracellular matrix and immune functions as well as the most important environmental and intrinsic mechanisms involved in the aging process and in its pathological consequences are discussed. These presentations of theories and related experimental facts give a global overview of up to date concepts of the biology of the aging process and are of essential reading not only for specialists in this field but also for practitioners of scientific, medical, social and experimental sciences.
Author: Razmik Mirzayans
Publisher: Nova Science Publishers
ISBN: 9781606926765
Category : Cancer
Languages : en
Pages : 0
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Book Description
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.
