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This textbook presents concise chapters written by internationally respected experts on various important aspects of cancer-associated metabolism, offering a comprehensive overview of the central features of this exciting research field. The discovery that tumor cells display characteristic alterations of metabolic pathways has significantly changed our understanding of cancer: while the first description of tumor-specific changes in cellular energetics was published more than 90 years ago, the causal significance of this observation for the pathogenesis of cancer was only discovered in the post-genome era. The first 10 years of the twenty-first century were characterized by rapid advances in our grasp of the functional role of cancer-specific metabolism as well as the underlying molecular pathways. Various unanticipated interrelations between metabolic alterations and cancer-driving pathways were identified and currently await translation into diagnostic and therapeutic applications. Yet the speed, quantity, and complexity of these new discoveries make it difficult for researchers to keep up to date with the latest developments, an issue this book helps to remedy.
In 1920s, Otto Warburg described the phenomenon of ‘aerobic glycolysis’, the ability of tumour cells to convert glucose to lactate in the presence of normal oxygen conditions. Warburg’s hypothesis of an altered metabolism in cancer cells found no immediate acceptance, though it was latter confirmed for most human tumours. With the advent of molecular biology the focus in tumour research has shifted towards the search for oncogenes. However, the interest in cancer molecular profiling eventually led to a renaissance of the Warburg effect trying to combine genetic alterations with effects on metabolism with the help of modern analytic technologies to rapidly analyze broad varieties of metabolites in various tissues and bodyfluids (metabonomics).
The four sections of this book cover cell and molecular biology of tumor metabolism, metabolites, tumor microenvironment, diagnostics and epigenetics. Written by international experts, it provides a thorough insight into and understanding of tumor cell metabolism and its role in tumor biology. The book is intended for scientists in cancer cell and molecular biology, scientists in drug and diagnostic development, as well as for clinicians and oncologists.
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 an...
- Provides a forum for discussion of new discoveries, approaches, and ideas in molecular biology - Includes contributions from leaders in their fields - Abundantly referenced
New genomic information has revealed the crucial role that protein-protein interactions (PPIs) play in regulating numerous cellular functions. Aberrant forms of these interactions are common in numerous diseases and thus PPIs have emerged as a vast class of critical drug targets. Despite the importance of PPIs in biology, it has been extremely challenging to convert targets into therapeutics and targeting PPIs had long been considered a very difficult task. However, over the past decade the field has advanced with increasing growth in the number of successful PPI regulators. Protein-Protein Interaction Regulators surveys the latest advances in the structural understanding of PPIs as well as recent developments in modulator discovery.
The papers in this book were presented at the 14th Mechanisms in B-cell Neoplasia meeting that was held in Bethesda, Maryland October 21-23, 1996. In 1995 the organizers decided that the format of the meeting would be changed and that specific topics relevant to B-cell neoplasia would be discussed. This year's topic is on the c-myc oncogene in B-cell neoplasia which has been discussed in virtually every previous meeting. Some of the presentations announced for the first time dramatic advances in our understanding of c-myc and because this subject has become highly complex it was thought that devoting the whole meeting to this theme would be appropriate. The book, therefore, repre sents a rev...
Nearly a century of scientific research has revealed that mitochondrial dysfunction is one of the most common and consistent phenotypes of cancer cells. A number of notable differences in the mitochondria of normal and cancer cells have been described. These include differences in mitochondrial metabolic activity, molecular composition of mitochondria and mtDNA sequence, as well as in alteration of nuclear genes encoding mitochondrial proteins. This book, Mitochondria and Cancer, edited by Keshav K. Singh and Leslie C. Costello, presents thorough analyses of mitochondrial dysfunction as one of the hallmarks of cancer, discusses the clinical implications of mitochondrial defects in cancer, and as unique cellular targets for novel and selective anti-cancer therapy.
The fifth Annual Pezcoller Symposium entitled, Apoptosis, was held in Trento, Italy, June 9-1I, 1993 and was focused on the specific phenomena leading to Programmed Cell Death (PCD) or Apoptosis, and the mechanisms involved. With presentations at the cutting edge of progress and stimulating discussions, this Symposium addressed the genetics and molecular mechanisms determining PCD and the role of this suicidal process in cancer and the immune system. The functions of pS3, c myc and bel 2 in affecting apoptosis in different cell types and the role of ions and intracellular pH changes and that of intranuelear endonueleases are given particular emphasis as are the effects of anticancer agents, ...
Oncogenes and tumor suppressor genes had been traditionally studied in the context of cell proliferation, differentiation, senescence, and survival, four relatively cell-autonomous processes. Consequently, in the late ’80s-early ’90s, neoplastic growth was described largely as an imbalance between net cell accumulation and loss, brought about through mutations in cancer genes. In the last ten years, a more holistic understanding of cancer has slowly emerged, stressing the importance of interactions between neoplastic and various stromal components: extracellular matrix, basement membranes, fibroblasts, endothelial cells of blood and lymphatic vessels, tumor-infiltrating lymphocytes, etc. The commonly held view is that changes in tumor microenvironment are “soft-wired”, i.e., epigenetic in nature and often reversible. Yet, there exists a large body of evidence suggesting that well-known mutations in cancer genes profoundly affect tumor milieu. In fact, these non-cell-autonomous changes might be one of the primary reasons such mutations are preserved in late-stage tumors.