This book addresses possible analogies between cancer and developmental biology. An international group of experts provides a multidisciplinary approach, allowing biological or clinical scientists involved with cancer research to integrate specific information from diverse areas. Five concepts of cancer are presented, and developmental biology is reviewed at five levels. These are integrated in discussions of failure in organisation as a basis of cancer and its control. The book will be a valuable reference for both newcomers as well as experienced biological and clinical scientists. Features
Demonstrating how the malfunction of normal molecular pathways and components can lead to cancer, this text explores how our understanding of these defective mechanisms can be harnessed to develop new targeted therapeutic agents.
A concise overview of the fundamental concepts of cancer biology, ideal for those with little or no background in the field. From cancer epidemiology and the underlying mechanisms, through to tumour detection and treatment, the comprehensive picture revealed will enable students to move into the cancer field with confidence.
This textbook takes you on a journey to the basic concepts of cancer biology. It combines developmental, evolutionary and cell biology perspectives, to then wrap-up with an integrated clinical approach. The book starts with an introductory chapter, looking at cancer in a nut shell. The subsequent chapters are detailed and the idea of cancer as a mass of somatic cells undergoing a micro-evolutionary Darwinian process is explored. Further, the main Hanahan and Weinberg “Hallmarks of Cancer” are revisited. In most chapters, the fundamental experiments that led to key concepts, connecting basic biology and biomedicine are highlighted. In the book’s closing section all of these concepts are integrated in clinical studies, where molecular diagnosis as well as the various classical and modern therapeutic strategies are addressed. The book is written in an easy-to-read language, like a one-on-one conversation between the writer and the reader, without compromising the scientific accuracy. Therefore, this book is suited not only for advanced undergraduates and master students but also for patients or curious lay people looking for a further understanding of this shattering disease
Tumor progression is driven by mutations that confer growth advantages to different subpopulations of cancer cells. As a tumor grows, these subpopulations expand, accumulate new mutations, and are subjected to selective pressures from the environment, including anticancer interventions. This process, termed clonal evolution, can lead to the emergence of therapy-resistant tumors and poses a major challenge for cancer eradication efforts. Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine examines cancer progression as an evolutionary process and explores how this way of looking at cancer may lead to more effective strategies for managing and treating it. The contributors review efforts to characterize the subclonal architecture and dynamics of tumors, understand the roles of chromosomal instability, driver mutations, and mutation order, and determine how cancer cells respond to selective pressures imposed by anticancer agents, immune cells, and other components of the tumor microenvironment. They compare cancer evolution to organismal evolution and describe how ecological theories and mathematical models are being used to understand the complex dynamics between a tumor and its microenvironment during cancer progression. The authors also discuss improved methods to monitor tumor evolution (e.g., liquid biopsies) and the development of more effective strategies for managing and treating cancers (e.g., immunotherapies). This volume will therefore serve as a vital reference for all cancer biologists as well as anyone seeking to improve clinical outcomes for patients with cancer.
Decades of research on the tumor suppressor p53 have revealed that it plays a significant role as a "guardian of the genome," protecting cells against genotoxic stress. In recent years, p53 research has begun to move into the clinic in attempts to understand how p53 is frequently inactivated in-and sometimes even promotes-human cancer. Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine covers the rapid progress that has recently been made in basic and clinical research on p53. The contributors review new observations about its basic biology, providing updates on the functions of its isoforms and domains, the myriad stresses and signals that trigger its activation or repression, and its downstream effects on genome stability and the cell cycle that enforce tumor suppression in different cell and tissue types. They also discuss how p53 dysfunction contributes to cancer, exploring the various inherited and somatic mutations in the human TP53 gene, the impact of mutant p53 proteins on tumorigenesis, and the prognostic value and clinical outcomes of these mutations. Drugs that are being developed to respond to tumors harboring aberrant p53 are also described. This book is therefore essential reading for all cancer biologists, cell and molecular biologists, and pharmacologists concerned with the treatment of this disease.
Incorporating the most important advances in the fast-growing field of cancer biology, the text maintains all of its hallmark features. It is admired by students, instructors, researchers, and clinicians around the world for its clear writing, extensive full-color art program, and numerous pedagogical features.
This volume provides the reader with an overview of the diverse functions of the RUNX family of genes. As highlighted in the introduction and several of the 29 chapters, humans and other mammals have three RUNX genes that are known to play specific roles in blood, bone and neuronal development. However, their evolutionary history has recently been traced back to unicellular organisms and their involvement in many well-known signaling pathways (Wnt, TGFb, Notch, Hippo) is indicative of a more general function in cell biology. Their documented roles in cell fate decisions include control of proliferation, differentiation, survival, senescence and autophagy. The pleiotropic effects of RUNX in development are mirrored in cancer, where RUNX genes can function as oncogenes that collaborate strongly with Myc family oncogenes or as tumour suppressor genes. In the latter role, they display hallmarks of both ‘gatekeepers’ that modulate p53 responses and ‘caretakers’ that protect the genome from DNA damage. Several chapters focus on the importance of these genes in leukemia research, where RUNX1 and CBFB are frequently affected by chromosomal translocations that generate fusion oncoproteins, while recent studies suggest wider roles for RUNX modulation in solid cancers. Moreover, RUNX genes are intimately involved in the development and regulation of the immune system, while emerging evidence suggests a role in innate immunity to infectious agents, including HIV. At the biochemical level, the RUNX family can serve as activators or repressors of transcription and as stable mediators of epigenetic memory through mitosis. Not surprisingly, RUNX activity is controlled at multiple levels, this includes miRNAs and a plethora of post-translational modifications. Several chapters highlight the interplay between the three mammalian RUNX genes, where cross-talk and partial functional redundancies are evident. Finally, structural analysis of the RUNX/CBFB interaction has led to the development of small molecule inhibitors that provide exciting new tools to decipher the roles of RUNX in development and as targets for therapy. This volume provides a compendium and reference source that will be of broad interest to cancer researchers, developmental biologists and immunologists.
