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This volume covers classic and modern cell and molecular biology of prostate cancer, as well as novel biomarkers, inflammation, centrosome pathologies, microRNAs, cancer initiation novel biomarkers, inflammation, centrosome pathologies, microRNAs, cancer initiation and genetics, epigenetics, mitochondrial dysfunctions and apoptosis, cancer stem cells, angiogenesis and progression to metastasis, and treatment strategies including clinical trials related to prostate cancer. Cell & Molecular Biology of Prostate Cancer is one of two companion books comprehensively addressing the biology and clinical aspects of prostate cancer. Prostate Cancer: Molecular & Diagnostic Imaging and Treatment Stategies, the companion volume, discusses both classic and the most recent imaging approaches including analysis of needle biopsies, applications of nanoparticle probes and peptide-based radiopharmaceuticals for detection, early diagnosis and treatment of prostate cancer. Taken together, these volumes form one comprehensive and invaluable contribution to the literature.
The purpose of this book is to provide a contemporary overview of the causes and consequences of prostate cancer from a cellular and genetic perspective. Written by experts in the fields of epidemiology, toxicology, cell biology, genetics, genomics, cell-cell interactions, cell signaling, hormone signaling, and transcriptional regulation, the text covers aspects of prostate cancer from disease initiation to metastasis. Chapters explore in depth the cells of origin for prostate cancer, its genomic subtypes, neural transcription factors in disease progression, epigenetic regulation of chromatin, and many other topics. This book distinguishes itself from other texts on prostate cancer by its focus on cellular and genetic mechanisms, as opposed to clinical diagnosis and management. As a result, this book will be of broad interest to basic and translational scientists with familiarity of these topics, as well as to trainees at earlier stages of their research careers.
These proceedings of the 5th Prouts Neck Meeting on Prostate Cancer, held in October, 1989, highlight the many advances in the understanding of prostatic growth and function at the cellular and molecular levels which have been registered since the first Prouts Neck Meeting in 1985, a meeting which also focused on the then current concepts and basic approaches to understanding prostate cancer. Inter vening Prouts Neck Meetings in 1986, 1987 and 1988 were devoted to treatment, image cytometry and clinical markers. As before, the Prouts Neck tradition of bringing together an international, multidiscipli nary group of experts for 3 days to exchange ideas and new data, in the relaxed atmosphere of an old iun on the scenic Maine coast, proved to be an ideal combination for a highly successful conference. Accordingly, the Organ System Program of the National Cancer Institute plans to use the Prouts Neck model for future conferences on other solid tumors (bladder in 1990 and kidney in 1991) and will return to the prostate in 1992. A new dimension was added to the current program through the inclusion of a poster session to recognize the research of pre-and postdoctoral investigators. The posters were judged by Drs. Collette Freeman, Frank French, Shutsung Liao, Robert Matusik and Henry Sun. The three winners, in alphabeti cal order, were John Fabian, Robert Getzenberg and Ming Fong-Lin.
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.
A fundamental and groundbreaking reassessment of how we view and manage cancer When we think of the forces driving cancer, we don’t necessarily think of evolution. But evolution and cancer are closely linked because the historical processes that created life also created cancer. The Cheating Cell delves into this extraordinary relationship, and shows that by understanding cancer’s evolutionary origins, researchers can come up with more effective, revolutionary treatments. Athena Aktipis goes back billions of years to explore when unicellular forms became multicellular organisms. Within these bodies of cooperating cells, cheating ones arose, overusing resources and replicating out of control, giving rise to cancer. Aktipis illustrates how evolution has paved the way for cancer’s ubiquity, and why it will exist as long as multicellular life does. Even so, she argues, this doesn’t mean we should give up on treating cancer—in fact, evolutionary approaches offer new and promising options for the disease’s prevention and treatments that aim at long-term management rather than simple eradication. Looking across species—from sponges and cacti to dogs and elephants—we are discovering new mechanisms of tumor suppression and the many ways that multicellular life-forms have evolved to keep cancer under control. By accepting that cancer is a part of our biological past, present, and future—and that we cannot win a war against evolution—treatments can become smarter, more strategic, and more humane. Unifying the latest research from biology, ecology, medicine, and social science, The Cheating Cell challenges us to rethink cancer’s fundamental nature and our relationship to it.
Prostate cancer is the commonest male cancer with over 5 million survivors in US alone. Worldwide, the problem is staggering and has attracted significant attention by media, scientists and cancer experts. Significant research, discoveries, innovations and advances in treatment of this cancer have produced voluminous literature which is difficult to synthesize and assimilate by the medical community. Prostate Cancer: A Comprehensive Perspective is a comprehensive and definitive source which neatly resolves this problem. It covers relevant literature by leading experts in basic science, molecular biology, epidemiology, cancer prevention, cellular imaging, staging, treatment, targeted therapeutics and innovative technologies. Prostate Cancer: A Comprehensive Perspective, is a valuable and timely resource for urologists and oncologists.
Candidate gene based studies have identified a handful of aberrant CpG DNA methylation events in prostate cancer (Brooks et al. 1998; Yegnasubramanian et al. 2004). However, large scale DNA methylation profiles have not been examined for normal prostates or prostate tumors. Additionally, the mechanisms behind these DNA methylation alterations are unknown. In this thesis, I describe the results of my efforts to better understand these previously unexplored areas of biology. For the study presented in this thesis, I quantitatively profiled 95 primary prostate tumors and 86 healthy prostate tissue samples for their DNA methylation levels at 26,333 CpGs representing 14,104 gene promoters by using the Illumina HumanMethylation27 platform. When the profiles of the prostate tissue samples were compared, I observed a substantial number of tumor-specific DNA methylation alterations. A 2-class Significance Analysis of this dataset revealed 5,912 CpG sites with increased DNA methylation and 2,151 CpG sites with decreased DNA methylation in tumors (FDR
This book covers all the practical issues related to the interpretation of prostatic biopsies in day-to-day practice, including: biopsy sampling and processing; the diagnosis of limited cancer; differentiation of prostate cancers from benign lesions and recognition of histologic variants; the recognition and clinical significance of “atypical” diagnoses and HGPIN; the identification of recently described entities; the contemporary approach to Gleason grading; the utility of immunohistochemical markers and emerging molecular markers; and the reporting of prostate biopsies. Algorithms, flow charts, and tables are used throughout to simulate the thought and decision-making process upon encountering common clinical scenarios during sign-out of prostate biopsy. The book is richly illustrated with carefully selected, high-quality color images and will appeal especially to practicing surgical pathologists as well as pathology residents and fellows in training.