Molecular Genetics of Cancer

2004-2005

From left: Jerry Adams (joint Division Head), Suzanne Cory (joint Division Head), Ora Bernard, Philippe Bouillet, David Huang, Ruth Kluck, Geoff Lindeman, Andreas Strasser, David Vaux, Anne Verhagen & Jane Visvader.

• Research Focus
• Overview
• Email the Molecular Genetics of Cancer Division

Research Focus

• Differentiation and proliferation
• Control of cell death (apoptosis)
• Malignancy and therapy

Overview

Our Division is exploring how cancers arise, with the eventual aim of creating better approaches to their diagnosis and treatment. A tumour represents the unrestrained growth of a single colony of cells, due to several alterations in the DNA of those cells. Hence we are attempting to understand how our tissues normally maintain the appropriate numbers of cells by clarifying how cells develop from ancestral (stem) cells and how their proliferation and death is controlled.

For some years scientists around the world have attempted to identify the stem cell that creates the breast. That rare cell has been keenly sought not only because it can clarify how this complex tissue develops but also because some types of breast cancer may originate directly from the stem cell. Our breast cancer laboratory has now purified these remarkable cells and shown that indeed a single one can generate the entire breast.

Understanding the programmed death of cells, termed apoptosis, is important for cancer research both because impaired apoptosis often leads to cancer and because it renders the tumour cells less sensitive to chemotherapy drugs. The decision of a cell to undergo apoptosis (‘to be or not to be’) is decided largely by a battle between three factions of the Bcl2 family of intracellular proteins, two of which promote cell death while the other favours cell life. Our apoptosis groups have now established that one key killer protein is held firmly by two specific pro-life relatives, until members of the other pro-death group overwhelm the guardians and free the killer. Because these proteins all interact through a short protein segment called BH3, we and others are now attempting to develop drugs that mimic BH3 to kill tumour cells more efficiently.