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The genomic era has allowed enormous strides in our understanding of the molecular changes that underlie malignant transformation. Mutations have been discovered that are critical drivers of large cross-sections of human cancers. These discoveries have allowed us to find drugs that target these drivers and make important strides in treatment. Genomics and high-throughput technologies have illuminated the complexity of cancer and the facility with which cancers adapt during their natural history. The field is evolving rapidly with new discoveries and new drugs reported monthly. This book is a timely foundation for understanding in context the origins of molecular oncology and its future directions. The content reviews available technologies for the analysis of cancer tissues and genes; summaries of key oncogenic pathways from a molecular perspective; the technologies, pathways and targeted therapies of a wide range of human malignancies; and new pharmacologic therapies that have a common mechanistic target.
This book was conceived more than five years before its publication date. It was intended to provide a resource that summarized technology, biochemistry, molecular pathophysiology, and targeted therapeutics. As contributors were being recruited and chapters written the field that was being described changed at an accelerating pace. It is a tribute to scientific progress that volumes like this are out-of-date as they are published, but books like this are not meant to contain the most current laboratory discovery or report the most recent FDA approval.
While this book was being written there have been major advances in molecular oncology. The Cancer Genome Atlas (cancergenome.nih.gov) has demonstrated the broad spectrum of mutations in an expanding list of cancers. DNA sequence analysis alone has demonstrated that as cancers grow, metastasize, and develop treatment resistance, individual tumor sites within a single patient evolve differently and demonstrate increasingly complex spectra of driver and passenger mutations. These findings alone strongly support the Darwinian view of tumor progression. The complexities of cellular dysregulation in cancer may arise from DNA sequence changes, but extend to other levels of gene regulation. During the writing of this book the role of micro-RNAs (miRNAs) in cancer was elucidated. Aberrations in epigenetics such as DNA methylation and histone acetylation were demonstrated. Cancer drug development has also proceeded at increasing rates. In the period 2008–2012 there were 51 approvals of new drugs for cancer treatment by the US Food and Drug Administration. Many of these approvals resulted from impressive data in Phase II trials that clearly demonstrated efficacy where no agents have worked before.