1. CANCER MODULE Units 1.3, 2.2, 2.3, 2.4, 2.5

2. REGULATION OF THE CELL CYCLE Drivers Checkpoints Divide!!Don’t divide!!

3. Cell Cycle Checkpoints Is environment ok? Is my DNA intact? G 1 Checkpoint/ Restriction Point G 2 Checkpoint Is my DNA correctly replicated? Are chromosomes ready for separation? Mitosis Checkpoint

4. Cyclin/Driver Function G 1 Driver Cyclin D S Driver 1 Cyclin E S Driver 2 Cyclin A G 2 /M Driver Cyclin B

5. Cell Signaling PDGF Receptor PDGF Transcription Factor TP G1 driver gene Outside Cytoplasm Nucleus Rb

6. Cancer cells behave like stem cells … Specialization is normally a one way trip! More specialized Divides less Less Specialized Divides more Cancer cellsNormal cells Cancer cells lose their specialized functions …  Genetic Changes - Mutated genes are expressed when they shouldn’t be.  Epigenetic Changes – Genes expressed at the wrong time.

7. Cancer and Genetic/Epigenetic Mutations

8. Oncogenes Examples HER-2/neu (erbB-2): a growth factor receptor.HER-2/neu (erbB-2) ras: a signal transduction moleculeras myc: a transcription factormyc src: a protein tyrosine kinase.src hTERT: an enzyme that functions in DNA replication.hTERT Bcl-2: a membrane associated protein that functions to prevent apoptosis.Bcl-2

9. Tumor Suppressor Genes Examples  INK proteins  p53  Rb  BRCA1  BRCA2  APC

10. p53 External signals: Lack of Oxygen Stress Tissue Damage Internal signals: DNA damage Cell Cycle Arrest p53

11. Apoptosis Apoptosis proteins open pore in mitochondria ‘Die’ signals from p53 Mitochondria release ‘death’ proteins Apoptosis! Once pore is open, it cannot be closed! Mitochondria

12. Apoptosis, cont The cell blebs Nucleus condenses Nucleus fragments The blebs float away & are phagocytosed blebs nucleus blebs nucleus