Molekularbiologie Menschlicher Krebserkrankungen

Over the last three decades, knowledge on the molecular biology of human cancers has vastly expanded. A host of genes and proteins involved in cancer development and progression have been defined and many mechanisms at the molecular, cellular and even tissue level have been, at least partly, elucidated. Insights have also been gained into the molecular mechanisms underlying carcinogenesis by chemical, physical, and biological agents and into inherited susceptibility to cancer.

Accordingly, Part I of the book presents many of the molecules and mechanisms generally important in human cancers. Following an overview on the cancer problem, individual chapters deal with cancer genetics and epigenetics, DNA damage and repair, oncogenes, tumor suppressors, regulatory pathways in cancer, apoptosis, cellular senescence, tumor invasion, and metastasis.

A consensus is emerging that while these common mechanisms and molecules are all relevant to human cancers, in each cancer type (or even subtype) a selection of them are extremely important. For selected cancers, the route from genetic and epigenetic changes to their biological and clinical behavior can already be traced. Part II of the book presents a broad, but exemplary selection of cancers that serve as paradigms to illustrate this point.

In fact, cancer research has now reached a critical stage, in which the accumulated knowledge on molecular mechanisms is gradually translated into improved prevention, diagnosis, and treatment. The state, pitfalls, and potential of these efforts are summarized in Part III.

More than ever, cancer research is now an interdisciplinary effort which requires a basic knowledge of commonly used terms, facts, issues, and concepts. The aim of this book is to provide advanced students and practitioners of different disciplines with this basis, bridging the gap between standard textbooks of molecular biology, pathology, and oncology on the one hand and the specialized cancer literature on the other.