DNA Repair and Cancer: From Bench to Clinic PDF

Foreword

Cancer is the major cause of pre-mature death and the search for treatments started long before the birth of modern science. Most treatments were ineffective and only a handful of ideas stood the test of time, such as treating cancer with Röntgen beams, chemical weapons (mustard gas), or with nucleoside analogues. Only with modern science did we understand that most if not all of these effective treatments work by introducing DNA damage.

Today, we know not only that DNA damage is an effective way of eradicating cancer cells; cancer is also caused by DNA lesions that are turned into genetic mutations that transform the normal cell into cancer. Central to understanding cancer development and treatment is the understanding of how DNA lesions are dealt with in the cell. Loss of effective DNA repair results in more genetic mutations and cancer, but may also render these cells more sensitive to DNA damaging anti-cancer agents. Information on DNA repair capacity of both normal and cancer cells can also be used to identify a therapeutic window for selective targeting.

One of the main reasons patients die from cancer is the development of resistance to DNA damaging drugs. Such resistance may arise by increasing the DNA repair capacities or altering the DNA damage response. Hence, inhibition of DNA repair may be an effective way to prevent emerging drug resistance.

There are of course many other ways DNA repair can be exploited for cancer treatment. We know that cancer cells have inherently higher levels of DNA damage, in some cases as a result of loss of one DNA repair pathway. In such circumstances, another DNA repair pathway(s) may become critical for repair and survival of the cancer cell, and could be targeted for treatments. Normal cells may be spared as their DNA repair pathways are intact and since they have an overall lower level of DNA damage.

Here, the world's opinion leaders in translational DNA repair have examined the current status on how DNA repair impacts current anti-cancer treatments and outline the opportunities to improve cancer therapy with novel inhibitors of DNA repair. This book will prove to be an invaluable resource to graduate students, as well as the perfect guidebook for basic science researchers and clinical investigators, who are interested in understanding the mechanisms of DNA repair and the emerging strategies to eradicate tumour cells through DNA repair manipulation. I want to leave you with a quote from Dr Bruce Alberts, Editor-in-Chief of Science:

"If I were the czar of cancer research, I would give a higher priority to recruiting more of our best young scientists to decipher the detailed mechanisms of both apoptosis and DNA repair, and I would give them the resources to do so"