This book, part contributed volume, part proceedings, discusses state-of-the-art advances on human cell transformation in cell models for the study of cancer and aging. Several of the chapters are from the Human Cell Transformation: Advances in Cell Models for the Study of Cancer and Aging conference that was held in June 2018 at McGill University. The authors represent international expertise on a wide variety of topics ranging from different types of cancer (prostate, bone, breast, etc.) to tumor microenvironment, tumor progression, homogeneity, and possible therapies and treatments.

Forty years ago, three medical researchers--Oswald Avery, Colin MacLeod, and Maclyn McCarty--made the discovery that DNA is the genetic material. With this finding was born the modern era of molecular biology and genetics.

Telomerase, an enzyme that maintains telomeres and endows eukaryotic cells with immortality, was first discovered in tetrahymena in 1985. In 1990s, it was proven that this enzyme also plays a key role in the infinite proliferation of human cancer cells. Now telomere and telomerase are widely accepted as important factors involved in cancer biology, and as promising diagnostic tools and therapeutic targets. Recently, role of telomerase in “cancer stem cells” has become another attractive story. Until now, there are several good books on telomere and telomerase focusing on biology in ciliates, yeasts, and mouse or basic sciences in human, providing basic scientists or students with updated knowledge.

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

It has been recognized for almost 200 years that certain families seem to inherit cancer. It is only in the past decade, however, that molecular genetics and epidemiology have combined to define the role of inheritance in cancer more clearly, and to identify some of the genes involved. The causative genes can be tracked through cancer-prone families via genetic linkage and positional cloning. Several of the genes discovered have subsequently been proved to play critical roles in normal growth and development. There are also implications for the families themselves in terms of genetic testing with its attendant dilemmas, if it is not clear that useful action will result. The chapters in The Genetics of Cancer illustrate what has already been achieved and take a critical look at the future directions of this research and its potential clinical applications.

Cancer research has reached a major turning point. The quality and quantity of information gathered about this disease in the past twenty years has revolutionized our understanding of its origins and behavior. No one is better qualified to comment on these dramatic leaps forward than molecular biologist Robert A. Weinberg, director of one of the leading cancer research centers in the world. In One Renegade Cell , Weinberg presents an accessible and state-of-the-art account of how the disease begins and how, one day, it will be cured. Weinberg tells how the roots of cancer were uncovered in 1909 and when the first cancer-causing virus was discovered. He then moves forward to the discovery of the role of chemical carcinogens and radiation in triggering cancer, and relates the remarkable story of the discoveries of oncogenes and tumor suppressor genes, the master controllers of normal and malignant cell proliferation. This book, which presumes little prior knowledge of biology, describes the revolution in biomedical research that has finally uncovered the forces driving malignant growth. Drawing on insights that simply were not available until recently, the discoveries presented in One Renegade Cell have already begun to profoundly alter the way that we diagnose and treat human cancers.

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.