MODIFIED from a slide show by Kim Foglia

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Presentation transcript:

MODIFIED from a slide show by Kim Foglia

INTERPHASE = G 1, S, G 2 G 1 - Gap 1 Grow by producing proteins & organelles G 2 - Gap 2 Grow Produce molecules & organelles needed for cell division S- Synthesis DNA replication Some can return to cycle with signal (Ex; Liver cells respond to injury) Some never divide again (Ex: Mature nerve, muscle cells) MITOSIS G 0 - Cell leaves cycle and stops dividing Most body cells in this phase

Cyclin-dependent kinases (Cdk’s) are present all the time but inactive unless combined with cyclins Presence of MPF triggers passage past G 1 & G 2 checkpoints KINASES- Enzymes that work by adding a phosphate group to other molecules

Cyclin levels change throughout cell cycle Fluctuating levels of different Cyclin-Cdk complexes seem to control all stages of cell cycle

CANCER CELLS Don’t respond to control signals Lose density-dependent inhibition Lose anchorage dependence Telomerase enzymes maintain/replace telomeres Transformation- process that changes a normal cell into a cancer cell

Telomeres protect DNA from being degraded Telomeres become shorter with each replication; shorter in older cells Telomerase enzyme lengthens telomeres Cancer cells have increased telomerase activity Jack Szostak Carol Greider Elizabeth Blackburn Nobel Prize Physiology/Medicine Discovery of Telomeres

Most cells divide times in culture; then stop, age, die Cancer cells are “immortal” -HeLa cells from a tumor removed from a woman (Henrietta Lacks) in 1951 are still reproducing in culture