Cancer is a multifaceted and genomically complex disease and data obtained through high throughput technologies has provided near complete resolution of the landscape of how genomic, genetic and epigenetic mutations in cancerous cells effectively influence homeostasis of signaling networks within these cells, between cancerous cells, tumor microenvironment and at the organ level. Increasingly sophisticated information has helped us in developing a better understanding of the underlying mechanisms of cancer, and it is now known that intra-tumor genetic heterogeneity, cellular plasticity, dysregulation of spatio-temporally controlled signaling cascades, and loss of apoptosis are contributory in cancer development, progression and the development of resistance against different therapeutics. It is becoming progressively more understandable that earlier detection of pre-existing or emerging resistance against different therapeutics may prove to be helpful in personalizing the use of targeted cancer therapy. Despite the fact that there is a continuously increasing list of books, being guest edited by researchers, books on the subject are often composed of invited reviews without proper sequence and continuity and designed for a particular readership. This book progressively shifts and guides the readers from basic underlying mechanisms to translational approaches to treat cancer.

Diabetes mellitus is a very common disease which affects approximately 150,000,000 worldwide. With its prevalence rising rapidly, diabetes continues to mystify and fascinate both practitioners and investigators by its elusive causes and multitude of This textbook is written for endocrinologists, specialists in other disciplines who treat diabetic patients, primary care physicians, housestaff and medical students. It covers, in a concise and clear manner, all aspects of the disease, from its pathogenesis on the molecular and cellular levels to its most modern therapy.

This volume contains cutting-edge techniques to study the function of enhancers and promoters in depth. Chapters are divided into six sections and describe enhancer-promoter transcripts, nucleosome occupancy, DNA accessibility, chromatin interactions, protein-DNA interactions, functional analyses, and DNA methylation assays. Written in the Methods in Molecular Biology series format, chapters include comprehensive introductions, lists of the necessary materials and reagents, step-by-step laboratory protocols, and useful suggestions for troubleshooting. Authoritative and cutting-edge, Enhancers and Promoters: Methods and Protocols is a useful guide for future experiments.

This book systematically reviews the most important findings on cancer immune checkpoints, sharing essential insights into this rapidly evolving yet largely unexplored research topic. The past decade has seen major advances in cancer immune checkpoint therapy, which has demonstrated impressive clinical benefits. The family of checkpoints for mediating cancer immune evasion now includes CTLA-4, PD-1/PD-L1, CD27/CD70, FGL-1/LAG-3, Siglec-15, VISTA (PD-1L)/VSIG3, CD47/SIRPA, APOE/LILRB4, TIGIT, and many others. Despite these strides, most patients do not show lasting remission, and some cancers have been completely resistant to the therapy. The potentially lethal adverse effects of checkpoint blockade represent another major challenge, the mechanisms of which remain poorly understood. Compared to the cancer signaling pathways, such as p53 and Ras, mechanistic studies on immune checkpoint pathways are still in their infancy. To improve the responses to checkpoint blockade therapy and limit the adverse effects, it is essential to understand the molecular regulation of checkpoint molecules in both malignant and healthy cells/tissues. This book begins with an introduction to immune checkpoint therapy and its challenges, and subsequently describes the regulation of checkpoints at different levels. In closing, it discusses recent therapeutic developments based on mechanistic findings, and outlines goals for future translational studies. The book offers a valuable resource for researchers in the cancer immunotherapy field, helping to form a roadmap for checkpoint regulation and develop safer and more effective immunotherapies.

Medicinal Chemistry of Anticancer Drugs, Second Edition, provides an updated treatment from the point of view of medicinal chemistry and drug design, focusing on the mechanism of action of antitumor drugs from the molecular level, and on the relationship between chemical structure and chemical and biochemical reactivity of antitumor agents. Antitumor chemotherapy is a very active field of research, and a huge amount of information on the topic is generated every year. Cytotoxic chemotherapy is gradually being supplemented by a new generation of drugs that recognize specific targets on the surface or inside cancer cells, and resistance to antitumor drugs continues to be investigated. While these therapies are in their infancy, they hold promise of more effective therapies with fewer side effects. Although many books are available that deal with clinical aspects of cancer chemotherapy, this book provides a sorely needed update from the point of view of medicinal chemistry and drug design. - Presents information in a clear and concise way using a large number of figures - Historical background provides insights on how the process of drug discovery in the anticancer field has evolved - Extensive references to primary literature

Scientists often look askance at their colleagues whose research appears too strongly focused on a single gene or gene product. We are supposed to be interested in the “big picture” and excessive zeal in pursuit of a single pixel might seem to border on an obsession that is likely to yield only details. However as this volume of Current Topics in Microbiology and Immunology demonstrates, this is certainly not the case for myc. Intense study of this en- matic proto-oncogene over the last twenty years has only broadened our view of its functions and led to insights into mechanisms relating to transcriptional regulation as well as to cell growth, proliferation, differentiation, apoptosis and organismal development. The myc gene originally came to light as a retroviral oncogene (v-myc) associated with a wide range of acute neoplasms. It was later shown to be a virally transduced cellular gene (c-myc) which is a member of family of on- genes (c-myc,N-myc,L-myc). These family members are themselves subject to a bewildering assortment of genetic rearrangements associated with many different types of tumors derived from many different types of cells. These rearrangements (including chromosomal translocation, viral integration, and gene ampli?cation) act to uncouple expression of the myc family genes from their normal physiological regulators. The chapter by LIU and LEVENS - scribes the key pathways leading to regulation of myc expression, showing that such regulation occurs at several different levels and through multiple mechanisms.