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Provides insight into established practices and research into apoptosis and senescence by examining techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics which still hold mysteries for researchers. This book concludes with established cancer therapies.
Book Synopsis Apoptosis, Senescence and Cancer by : David A. Gewirtz
Download or read book Apoptosis, Senescence and Cancer written by David A. Gewirtz and published by Springer Science & Business Media. This book was released on 2007-12-17 with total page 596 pages. Available in PDF, EPUB and Kindle. Book excerpt: Provides insight into established practices and research into apoptosis and senescence by examining techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics which still hold mysteries for researchers. This book concludes with established cancer therapies.
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.
Book Synopsis Tumor Dormancy, Quiescence, and Senescence, Volume 2 by : M.A. Hayat
Download or read book Tumor Dormancy, Quiescence, and Senescence, Volume 2 written by M.A. Hayat and published by Springer Science & Business Media. This book was released on 2013-11-29 with total page 336 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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 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.
Book Synopsis Geriatric Oncology by : Martine Extermann
Download or read book Geriatric Oncology written by Martine Extermann and published by Springer. This book was released on 2020-01-30 with total page 1150 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
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
Book Synopsis Autophagy and Senescence in Cancer Therapy by :
Download or read book Autophagy and Senescence in Cancer Therapy written by and published by Academic Press. This book was released on 2021-04-13 with total page 384 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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
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.
Book Synopsis Apoptosis and Cancer by : Seamus J. Martin
Download or read book Apoptosis and Cancer written by Seamus J. Martin and published by S. Karger AG (Switzerland). This book was released on 1997 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
In the second half of the twentieth century, life expectancy was prolonged, and the number of elderly people increased. The effect of population aging increases in the frequency of neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, epilepsy, and stroke. Also, a higher incidence of infections, autoimmune diseases, and malignant cancers is observed in elderly people. The aging process is difficult to define. Are physiological changes in elderly people controlled by specific genes? Is aging process a pathophysiology affecting different organs with different severity? Finding answers to these questions may help prevent age-related diseases and improve the quality of life of old people. This book was made as a compendium on contemporary challenges in senescence.
Book Synopsis Senescence by : Jolanta Dorszewska
Download or read book Senescence written by Jolanta Dorszewska and published by BoD – Books on Demand. This book was released on 2017-08-30 with total page 167 pages. Available in PDF, EPUB and Kindle. Book excerpt: In the second half of the twentieth century, life expectancy was prolonged, and the number of elderly people increased. The effect of population aging increases in the frequency of neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, epilepsy, and stroke. Also, a higher incidence of infections, autoimmune diseases, and malignant cancers is observed in elderly people. The aging process is difficult to define. Are physiological changes in elderly people controlled by specific genes? Is aging process a pathophysiology affecting different organs with different severity? Finding answers to these questions may help prevent age-related diseases and improve the quality of life of old people. This book was made as a compendium on contemporary challenges in senescence.
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.
Book Synopsis Cellular Senescence by : Razmik Mirzayans
Download or read book Cellular Senescence written by Razmik Mirzayans and published by Nova Science Publishers. This book was released on 2009 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
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.
Book Synopsis Cellular Senescence and Tumor Suppression by : Peter D. Adams
Download or read book Cellular Senescence and Tumor Suppression written by Peter D. Adams and published by Springer Science & Business Media. This book was released on 2010-01-23 with total page 274 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
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.
Book Synopsis Tumor Dormancy, Quiescence, and Senescence, Volume 1 by : M.A. Hayat
Download or read book Tumor Dormancy, Quiescence, and Senescence, Volume 1 written by M.A. Hayat and published by Springer Science & Business Media. This book was released on 2013-03-14 with total page 332 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.
Addressing a major field of interest for oncologists, cell biologists, and other biomedical researchers, Beyond Apoptosis provides an overview of how different biological mechanisms of cell death, senescence and mitotic catastrophe stop the growth of tumor cells treated with anticancer agents. Written by internationally renowned contributors, this text includes: morphological illustrations, as well as a DVD containing documents and video clips from various time-lapse microscopic studies of cell death and mitotic catastrophe the role and limitations of apoptosis as a determinant of the toxicity of anticancer agents alternative mechanisms of the antiproliferative actions of anticancer drugs and radiation, such as non-apoptotic cell death, cell senescence, and mitotic catastrophe non-apoptotic forms of cell death, such as necrosis, paraptosis, autophagic cell death, and others morphological and kinetic differences of the various forms of cell death
Book Synopsis Beyond Apoptosis by : Igor B Roninson
Download or read book Beyond Apoptosis written by Igor B Roninson and published by CRC Press. This book was released on 2019-08-30 with total page 376 pages. Available in PDF, EPUB and Kindle. Book excerpt: Addressing a major field of interest for oncologists, cell biologists, and other biomedical researchers, Beyond Apoptosis provides an overview of how different biological mechanisms of cell death, senescence and mitotic catastrophe stop the growth of tumor cells treated with anticancer agents. Written by internationally renowned contributors, this text includes: morphological illustrations, as well as a DVD containing documents and video clips from various time-lapse microscopic studies of cell death and mitotic catastrophe the role and limitations of apoptosis as a determinant of the toxicity of anticancer agents alternative mechanisms of the antiproliferative actions of anticancer drugs and radiation, such as non-apoptotic cell death, cell senescence, and mitotic catastrophe non-apoptotic forms of cell death, such as necrosis, paraptosis, autophagic cell death, and others morphological and kinetic differences of the various forms of cell death
