Chapter 8 (Part 1): Mitosis Cell Cycle Regulation & Cancer (Part 1) Pgs Objective: I can describe and explain how cancer involves a disruption in the regulation of the cell cycle and mitosis. But first, how is cell cycle regulated normally ?

Regulation of the Cell Cycle Checkpoints exist in different phases  If cell passes, then allowed to proceed to next phase  Checkpoints NOT at end of phase

Cell Cycle Control System G 1 checkpoint – near end of G 1  Checks if cell grew enough? DNA damaged?  If bad, will put into G 0 (rest period) OR will activate apoptosis (cell suicide) G 2 checkpoint – near end of G 2  Checks if DNA replicated OK, enough organelles? M checkpoint – at metaphase of mitosis  Checks if chromosomes lined up correctly, so that each cell gets all the DNA they need (homologous pairs, singled, etc.) Regulation enzymes: Cdk & cyclins (and others) Enzymes encoded for by genes

G1 Checkpoint (Example)

G1 Checkpoint (Detailed Example) Regulated by Cdk & cyclins, etc., but also controlled by a very special protein called  p53 (made by gene p53) Specifically checks if DNA damaged  If damaged, p53 signals other enzymes to repair it during G 0  If too badly damaged, p53 starts apoptosis

Cancer A growth disorder of cells: when cell regulation (checkpoints) not functioning, so cells divide uncontrollably  Creates a mass of cells called tumor Benign tumors are contained (won’t spread)  can still grow large

Cancer (cont’d) Malignant tumors will spread – cancer cells will break off tumor and travel through blood stream to start tumor elsewhere  Process of spreading cells = metastasis

Why is cancer bad? Tumor growth can put physical pressure on other important organs, etc. Cancer cells still need oxygen, glucose, blood, etc. to live  Will send out signals to make blood vessels feed “useless” cancer cells (VEGF)  Good cells die  You die

Causes of Cancer Chemicals (tobacco), radiation (UV rays) Damage/change DNA: mutation If specific damaged gene controls cell cycle (protein at checkpoint), may result in cancer  Proto-oncogenes: stimulate cell division If mutated to work too much, turn into oncogenes (divide excessively)  Tumor-suppressor genes: stop division If mutated to be non-functional, cell divides without control

Causes of Cancer (example) p53 = tumor-suppressor gene  if p53 mutated, p53 protein won’t function Won’t stop division if DNA bad  Allow cell to make more cells with same mutated DNA that will make more cells! = CANCER So, what type of gene?

Curing Cancer Conventional treatments:  Surgery (remove tumor) – hard to remove ALL mestases (every little single cell)  Chemotherapy/Radiation – to kill cancer cells (but will also kill good cells) Newer treatments  Focus on fixing the gene or protein that was damaged/mutated that resulted in cancer  cure for p53 cancer? Different cancers damage diff. genes