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Author: Chris Maxwell
Publisher: Springer
ISBN: 3319121367
Category : Medical
Languages : en
Pages : 252
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Book Description
Metastasis is the primary cause of mortality associated with cancer, and tumor genomic heterogeneity is a likely source for the cells that support cancer progression, resistance to therapy, and disease relapse. This book connects cancer metastasis with genomic instability in a comprehensive manner. Section 1 outlines the fundamental mechanisms responsible for these cellular and tissue phenotypes. Section 2 discusses in silico, in vitro, and in vivo models used for the experimental study of these processes. Section 3 reviews emerging themes (ex., microenvironment, mechanotransduction, and immunomodulation), and Section 4 highlights new therapeutic approaches to overcome the unique challenges presented by the heterogeneous and metastatic tumor. This book is intended for undergraduates and postgraduates with an interest in the areas of medicine, oncology, and cancer biology as well as for the content expert searching for thorough reviews of current knowledge in these areas.
Author: Chris Maxwell
Publisher: Springer
ISBN: 3319121367
Category : Medical
Languages : en
Pages : 252
Get Book Here
Book Description
Metastasis is the primary cause of mortality associated with cancer, and tumor genomic heterogeneity is a likely source for the cells that support cancer progression, resistance to therapy, and disease relapse. This book connects cancer metastasis with genomic instability in a comprehensive manner. Section 1 outlines the fundamental mechanisms responsible for these cellular and tissue phenotypes. Section 2 discusses in silico, in vitro, and in vivo models used for the experimental study of these processes. Section 3 reviews emerging themes (ex., microenvironment, mechanotransduction, and immunomodulation), and Section 4 highlights new therapeutic approaches to overcome the unique challenges presented by the heterogeneous and metastatic tumor. This book is intended for undergraduates and postgraduates with an interest in the areas of medicine, oncology, and cancer biology as well as for the content expert searching for thorough reviews of current knowledge in these areas.
Author: Nosheen Masood
Publisher: Springer Nature
ISBN: 9811510679
Category : Medical
Languages : en
Pages : 499
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Book Description
This book concisely describes the role of omics in precision medicine for cancer therapies. It outlines our current understanding of cancer genomics, shares insights into the process of oncogenesis, and discusses emerging technologies and clinical applications of cancer genomics in prognosis and precision-medicine treatment strategies. It then elaborates on recent advances concerning transcriptomics and translational genomics in cancer diagnosis, clinical applications, and personalized medicine in oncology. Importantly, it also explains the importance of high-performance analytics, predictive modeling, and system biology in cancer research. Lastly, the book discusses current and potential future applications of pharmacogenomics in clinical cancer therapy and cancer drug development.
Author: Erich A. Nigg
Publisher: Springer Science & Business Media
ISBN: 1402037643
Category : Medical
Languages : en
Pages : 509
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Book Description
Research over the past decades has firmly established the genetic basis of cancer. In particular, studies on animal tumour viruses and chromosome rearrangements in human tumours have concurred to identify so-called ‘proto-oncogenes’ and ‘tumour suppressor genes’, whose deregulation promotes carcinogenesis. These important findings not only explain the occurrence of certain hereditary tumours, but they also set the stage for the development of anti-cancer drugs that specifically target activated oncogenes. However, in spite of tremendous progress towards the elucidation of key signalling pathways involved in carcinogenesis, most cancers continue to elude currently available therapies. This stands as a reminder that “cancer” is an extraordinarily complex disease: although some cancers of the haematopoietic system show only a limited number of characteristic chromosomal aberrations, most solid tumours display a myriad of genetic changes and considerable genetic heterogeneity. This is thought to reflect a trait commonly referred to as ‘genome instability’, so that no two cancers are ever likely to display the exact same genetic alterations. Numerical and structural chromosome aberrations were recognised as a hallmark of human tumours for more than a century. Yet, the causes and consequences of these aberrations still remain to be fully understood. In particular, the question of how genome instability impacts on the development of human cancers continues to evoke intense debate.
Author: Eleanor J. Gloscow
Publisher: Nova Publishers
ISBN: 9781600213205
Category : Medical
Languages : en
Pages : 312
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Book Description
Many cancer biologists now believe that genomic instability not only initiates carcinogenesis, but also allows the tumour cell to become metastatic and evade drug toxicity. The loss of stability of the genome is becoming accepted as one of the most important aspects of carcinogenesis. One of the hallmarks of the cancer cell is the inherent instability of its genome. This book presents important research in this exciting field.
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 76
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Book Description
Author: Enrico Mihich
Publisher: Springer Science & Business Media
ISBN: 1461553652
Category : Medical
Languages : en
Pages : 410
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Book Description
Proceedings of the Eighth Annual Pezcoller Symposium held in Trento, Italy, June 17-19, 1996
Author: Gajanan V. Sherbet
Publisher: Elsevier
ISBN: 0080521908
Category : Science
Languages : en
Pages : 261
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Book Description
Genetic recombination is a process of combining genes that leads to the generation of cell variants that possess different characteristics. This process is important to the evolution of a species and to embryonic growth and differentiation. However, this process can also lead to the development of abnormal, cancerous cells. This book reviews the role of genetic recombination in the generation of various cancers and how genetic alterations have been or could be employed to elicit clinically useful information. * Provides detailed discussion of the genetic mechanisms that result in the generation of normal and abnormal cells* Examines the role of genetic recombination in cancer including cancer invasion and metastasis* Information is presented in a manner that is useful and accessible to everyone from graduate students to established cancer researchers
Author:
Publisher: Academic Press
ISBN: 0323855628
Category : Science
Languages : en
Pages : 286
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Book Description
Chromatin and DNA Repair in Cancer, Volume 364 in the International Review of Cell and Molecular Biology series reviews and details current advances in cell and molecular biology. Chapters in this new release cover Genomic Instability and metabolism in cancer, Histones variants and Histones modifications in cancer and Aging, DNA Double-stranded breaks Repair in Cancer, Reactive oxygen species and DNA damage response in cancer, Transcription-Associated DNA Breaks and Cancer: A Matter of DNA Topology, Mechanisms of Base Excision Repair: Its Significance to Human Health, and more. The IRCMB series has a worldwide readership, maintaining a high standard by publishing invited articles on important and timely topics that are authored by prominent cell and molecular biologists. The articles published in IRCMB have a high impact and an average cited half-life of 9 years. This great resource ranks high amongst scientific journals dealing with cell biology. Publishes only invited review articles on selected topics Authored by established and active cell and molecular biologists, drawn from international sources Offers a wide range of perspectives on specific subjects
Author: Michael B. Kastan
Publisher: Springer Science & Business Media
ISBN: 3642605052
Category : Medical
Languages : en
Pages : 189
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Book Description
M. B. KASTAN Cancer is a disease resulting from alterations of cellular genes which cause phe notypic changes in somatic cells. Usually, when we think about genetic diseases, we think about inheriting one or two abnormal genes from our parents and these gene abnormalities confer the disease phenotype. In contrast, in the majority of cancers, no such inherited gene abnormalities can be identified (which does not mean that they do not exist) and there is no obvious family history suggesting an inherited disease. The vast majority of genes which are altered in the cancer cells are not transmitted through the germ line, but rather become abnormal in somatic cells sometime during the lifetime of the individual. Thus, the critical question which arises is "how do these genetic changes occur in somatic cells?". Epidemiologic data suggest that exposure to environmental carcinogens con tributes to the genesis of at least 80% of all human cancers (DOLL and PETO 1981). Thus, it is natural to suspect that the genetic changes in somatic cells which con tribute to the transformed phenotype arise from DNA damage caused by such exposures. Therefore, understanding how cells respond to DNA-damaging agents is likely to be an important component of our understanding of the genesis of human tumors.
Author: Pragya Shah
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
Cancer metastasis is the process by which cells from the primary tumor invade into the surrounding extracellular matrix and neighboring tissue and spread to distant organs in the body through the blood or lymphatic system. This process is responsible for majority of cancer related deaths. During metastasis, cancer cells encounter very tiny interstitial spaces, smaller than the size of the cell's nucleus. Migration through such confined spaces, puts considerable pressure on the nucleus, which is the largest and stiffest organelle in the cell. The nucleus experiences severe deformations and in some cases, nuclear envelope rupture as well as DNA damage during this migration. Here, we investigated the cause of DNA damage and the impact of DNA damage repair kinases during confined migration. We also examined the role of nuclear envelope protein lamin A/C in promoting confined cancer cell migration in breast cancers. Using cell-lines, live-cell imaging and microfluidic devices that mimic the interstitial spaces found in vivo, we show that DNA damage is caused by two distinct but overlapping events - nuclear deformation and nuclear envelope rupture. The main cause of DNA damage, varies for each cell line. Moreover, nuclear deformation during confined migration or due to nuclear compression leads to increased replication stress, possibly due to replication fork stalling. Our findings suggest that nuclear deformation during confined migration, causes DNA damage by increasing replication stress. We also evaluated the role of DNA damage repair kinase ATM in promoting confined migration. Using chemical inhibitors, stable and conditional depletion of ATM, we show that ATM regulates levels of nuclear lamin A protein. Furthermore, lack of ATM makes nuclei more deformable and increases migration speed through confined spaces, similar to those encountered during metastasis. Additionally, we examined the role of A-type lamins in modulating nuclear deformability and promoting breast cancer progression. Our results indicate that more aggressive breast cancers have low lamin A/C expression which correlates to increased nuclear deformability in those cells. Moreover, increasing lamin A levels reduces nuclear deformability and impedes migration through confined spaces in aggressive breast cancer cells. Lamin A levels also modulate cell shape and proliferation rates and are associated with poor disease-free survival in breast cancer patients. Thus we have identified a new role for ATM in modulating nuclear mechanics by regulating lamin levels and established A-type lamins as a potential clinical marker to predict breast cancer patient outcomes. This thesis, thus, provides mechanistic insights into the cause of DNA damage as well as the role of nuclear envelope proteins (like lamins) and DNA damage repair proteins (like ATM) during confined migration.
