Control of the cell cycle and apoptosis

Abstract

Our understanding of the molecular mechanisms controlling cell proliferation underwent a revolution over the past decade with the discovery and description of the cell cycle clock apparatus. This molecular machinery, operating in the cell nucleus, functions as the master controller governing the decision of the cell to proliferate, to enter into reversible quiescence, or to enter into a postmitotic differentiation state. Before this machinery was uncovered, many believed that oncogene proteins and the products of tumour suppressor genes would provide us with a reasonably complete explanation of proliferation control. Now we know that these proteins, aberrant versions of which are often found in cancer cells, are nothing more than peripheral players that function by funneling their signals to the central decision-making machinery—the cell cycle clock—the ultimate governor of the cell’s fate. Dr Ante Lundberg is a post-doctoral fellow at the Whitehead Institute for Biomedical Research, and a Research Fellow at Harvard Medical School. He received his B.Sc. degree in Biology from Massachusetts Institute of Technology, and his MD degree from Stanford Medical School. He completed his training in Internal Medicine at the Brigham and Women's Hospital, and in Adult Oncology at Dana-Farber Cancer Institute, both in Boston, Massachusetts, U.S.A. The goal of his research is to understand how the cell cycle clock machinery regulates the growth of normal cells, and how alterations within this machinery contribute to the unrestrained growth of cancer. Dr Robert A. Weinberg is a founding member of the Whitehead Institute for Biomedical Research and the Daniel K. Ludwig Professor for Cancer Research at the Massachusetts Institute of Technology. He has been an American Cancer Society Research Professor at Whitehead and MIT since 1985. Dr Weinberg and his colleagues discovered the first human cancer-causing gene, the ras oncogene, and the first known tumour suppressor gene, Rb, the retinoblastoma gene. The principal goal of his research programme is to determine how oncogenes, their normal counterparts (proto-oncogenes), and tumour suppressor genes fit together in the complex circuitry that controls cell growth. He is particularly interested in applying this knowledge to improve the diagnosis and treatment of breast cancer. He is an elected member of the US National Academy of Sciences and Fellow of the American Academy of Arts and Sciences.