KEY POINTS

1. Cancer arises from genetic dysfunction in the regulation of the cell cycle, cell life span, and cell suicide.

Control of the Cell Cycle (Proliferation)

1. Cell division is the result of a clocklike cell cycle.

2. Cyclin-dependent kinases are the "engines" driving the cell cycle.

3. The CDK "engines" are controlled by both throttle (oncogene) and brake (tumor suppressor) controls.

Growth Factor Pathway: Principal Stimulator of Cell Proliferation

1. The cell cycle is stimulated by growth factors that bind to and activate receptor tyrosine kinases.

2. The ras oncogene contributes to many cancers and serves as a model for understanding "small G proteins."

3. The MAP kinase pathway leads to the expression of cyclins and other stimulators of the cell cycle.

4. The MAP kinase pathway also mediates the stimulation of the cell cycle by cell adhesion.

Tumor Suppressors: Inhibitors of Cell Cycle

1. Checkpoints in the cell cycle are manned by tumor suppressors.

2. The retinoblastoma and p53 proteins are the main "gatekeepers" for the cell cycle.

Mechanisms Regulating Cell Suicide and Cell Life Span

1. Apoptosis is the process of cell suicide.

2. Resistance to apoptosis via the intrinsic pathway is a hallmark of cancer.

3. Cellular life span is determined by DNA sequences at the ends of chromosomes.

Tumor Origin and the Spread of Cancer

1. Cancer cells may be related to stem cells.

2. Death by cancer is usually the result of its spread, not the original tumor.

3. Growth of solid tumors depends on development of new blood vessels.

Prospective CancerTherapy

1. Cancer therapy has a hopeful but challenging future.