Mechanisms Leading to Escape from Oncogene-induced Senescence PDF Download
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Author: Priyanka L. Patel
Publisher:
ISBN:
Category :
Languages : en
Pages : 284
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Author: Priyanka L. Patel
Publisher:
ISBN:
Category :
Languages : en
Pages : 284
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Author: Alketa Stefa
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ISBN:
Category :
Languages : en
Pages : 0
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Author: Samantha Garnett
Publisher:
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Category :
Languages : en
Pages :
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"Cancer is caused by the accumulation of genetic mutations that promote the abnormal growth of cells. Oncogene Induced Senescence (OIS), a tumour suppressive mechanism, provides a robust barrier to proliferation promoted by commonly mutated oncogenes, such as Raf or Ras, and the bypass of this barrier is a critical event on the path to malignancy. The mechanisms involved in OIS bypass are not yet fully understood. Many questions remain such as whether the timing of genetic mutations is relevant, whether additional mutations can permit escape from OIS, what cellular processes are required to establish OIS, and how senescent tumour cells can contribute to the tissue microenvironment.Using a Flp-activated Braf allele paired with a Cre-conditionally null p53 allele, p53 was ablated at six independent timepoints following the initiation of BrafV600E lung adenomas in the mouse lung, allowing for temporal dissection of tumour progression and OIS. Using this dual-recombinase system, it was determined that p53 loss after OIS is established is not sufficient to permit malignant adenocarcinoma (LUAD) development. BrafV600E adenomas are stably restrained from malignancy by OIS by approximately 24 weeks after BrafV600E expression, and several senescence and SASP markers can be detected in those adenomas. Interestingly, the length of time until OIS establishment could be modulated by the initiating viral titres of adenoviral-Flp. Lower initiating adenoviral titre produced lower tumour density in the lung that was correlated with smaller, more proliferative tumours. Lower-density tumour environments also permitted bypass of OIS and LUAD development at 24-32 weeks, suggesting that higher proliferation is due to delay in OIS. Finally, a search for new modulators of OIS was conducted. Using an shRNA-based lentiviral genetic screen, IAPP or amylin, a small metabolic regulator, was shown to be required for BRAF induced senescence. Both loss of IAPP, and its receptor RAMP3, permitted bypass of oncogene induced senescence. IAPP is a glycolysis inhibitor and this thesis links IAPP-regulated metabolic programming to OIS and the functions of the chromatin remodellers known as Jumonji Histone Demethylases. Together this work contributes new insight into the mechanisms underlying OIS and how these might be bypassed in the case of cancer development"--
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: Cristina Bernadó Morales
Publisher:
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Category :
Languages : en
Pages : 0
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Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 46
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Author: David P. Bazett-Jones
Publisher: Springer
ISBN: 3319388827
Category : Science
Languages : en
Pages : 501
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Book Description
This book gives an in-depth overview on nuclear structure and function. It clearly shows that the epigenome and the three-dimensional organization of the nucleus are not independent properties. The intimate relationship between the location and the epigenetic modifications of gene loci is highlighted. Finally, it shows that the complex three-dimensional organization of the nucleus is not just of academic interest: The structure, composition and function of virtually all of the sub-nuclear compartments identified so far can be implicated to a list of human genetic diseases. Hence, a detailed elucidation of how these domains are assembled and function will provide new opportunities for therapeutic intervention in clinical practice.
Author: Michael Piepkorn
Publisher: Springer Science & Business Media
ISBN: 0387216197
Category : Medical
Languages : en
Pages : 432
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Book Description
Highly acclaimed and considered the leading reference in the field, Pathology of Melanocytic Nevi and Malignant Melanoma has now been fully revised and updated to accomodate rapid advances in the field of melanoma pathology. Drs. Michael Piepkorn and Klaus Busam have now joined Dr. Barnhill, world-renowned expert in dermatology and pathology, to expand the text with new sections on the genetics and cytogenetics of melanoma, sentinal lymph node biopsy, the new AJCC TNM staging system for melanoma, the mechanisms of melanoma metastasis. The successful focus and format of the first edition have been preserved. Each lesion and diagnosis is clearly illustrated, now with more than 340 new, digitally enhanced full-color photomicrographs and over 125 tables. A corresponding precis, or concise description of the clinical features, histopathology, differential diagnosis, and outstanding characteristics of each lesion provides readers with a quick yet comprehensive overview of each topic covered. With the inclusion of recent advances in cancer research and new techniques, the second edition of Pathology of Melanocytic Nevi and Malignant Melanoma is the essential reference for every practicing dermatopathologist, pathologist, dermatologist, and cancer research scientist today.
Author: Lorenzo Galluzzi
Publisher: Humana Press
ISBN: 9781627032384
Category : Science
Languages : en
Pages : 0
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Book Description
Cell senescence is the process whereby cells permanently lose the possibility to proliferate without undergoing cell death, and occurs in a plethora of distinct model organisms. In Cell Senescence: Methods and Protocols, expert researchers in the field detail the methods that are now commonly used to study cell senescence, in model organisms encompassing bacteria, fungi, worms, flies, zebrafish, and mammalian cells. These techniques cover the study of all the morphological, biochemical and functional manifestations of senescence at the cellular level and include protocols for population analyses and high-throughput approaches in suitable model organisms. Written in the highly successful Methods in Molecular BiologyTM series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls.
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.
