Characterizing The Mechanism Of Continued Primer Synthesis At Stalled Replication Forks And Its Contribution To Checkpoint Activation

This book is a printed edition of the Special Issue "DNA Replication Controls" that was published in Genes

Genome Duplication provides a comprehensive and readable overview of the underlying principles that govern genome duplication in all forms of life, from the simplest cell to the most complex multicellular organism. Using examples from the three domains of life - bacteria, archaea, and eukarya - Genome Duplication shows how all living organisms store their genome as DNA and how they all use the same evolutionary-conserved mechanism to duplicate it: semi-conservative DNA replication by the replication fork. The text shows how the replication fork determines where organisms begin genome duplication, how they produce a complete copy of their genome each time a cell divides, and how they link genome duplication to cell division. Genome Duplication explains how mistakes in genome duplication are associated with genetic disorders and cancer, and how understanding genome duplication, its regulation, and how the mechanisms differ between different forms of life, is critical to the understanding and treatment of human disease.

Since the establishment of the DNA structure researchers have been highly interested in the molecular basis of the inheritance of genes and of genetic disorders. Scientific investigations of the last two decades have shown that, in addition to oncogenic viruses and signalling pathways alterations, genomic instability is important in the development of cancer. This view is supported by the findings that aneuploidy, which results from chromosome instability, is one of the hallmarks of cancer cells. Chromosomal instability also underpins our fundamental principles of understanding tumourigenesis: It thought that cancer arises from the sequential acquisition of genetic alterations in specific genes. In this hypothesis, these rare genetic events represent rate-limiting ‘bottlenecks’ in the clonal evolution of a cancer, and pre-cancerous cells can evolve into neoplastic cells through the acquisition of somatic mutations. This book is written by international leading scientists in the field of genome stability. Chapters are devoted to genome stability and anti-cancer drug targets, histone modifications, chromatin factors, DNA repair, apoptosis and many other key areas of research. The chapters give insights into the newest development of the genome stability and human diseases and bring the current understanding of the mechanisms leading to chromosome instability and their potential for clinical impact to the reader.

Now completely up-to-date with the latest research advances, the Seventh Edition retains the distinctive character of earlier editions. Twenty-two concise chapters, co-authored by six highly distinguished biologists, provide current, authoritative coverage of an exciting, fast-changing discipline.

This book is a state-of-the-art summary of the latest achievements in cell cycle control research with an outlook on the effect of these findings on cancer research. The chapters are written by internationally leading experts in the field. They provide an updated view on how the cell cycle is regulated in vivo, and about the involvement of cell cycle regulators in cancer.

In this book leading researchers in the field discuss the state-of-the-art of many aspects of SAPK signaling in various systems from yeast to mammals. These include various chapters on regulatory mechanisms as well as the contribution of the SAPK signaling pathways to processes such as gene expression, metabolism, cell cycle regulation, immune responses and tumorigenesis. Written by international experts, the book will appeal to cell biologists and biochemists.