1. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.

2.  Proteins within the cell control the cell cycle  Signals affecting critical checkpoints determine whether the cell will divide (cyclins, kinases) G 1 checkpoint M checkpoint G 2 checkpoint Control system Figure 8.9A

3. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  In laboratory cultures, normal cells divide only when attached to a surface = anchorage dependent Anchorage, cell density, and chemical growth factors affect cell division

4. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  Cells continue dividing until they touch one another = density-dependent inhibition Cells anchor to dish surface and divide. Figure 8.8A When cells have formed a complete single layer, they stop dividing (density-dependent inhibition). If some cells are scraped away, the remaining cells divide to fill the dish with a single layer and then stop (density-dependent inhibition).

5. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  Growth factors = proteins secreted by cells that stimulate other cells to divide After forming a single layer, cells have stopped dividing. Figure 8.8B Providing an additional supply of growth factors stimulates further cell division.

6. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  Cancer cells have abnormal cell cycles  divide excessively and form tumors

7. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  Breast cancer cell  Dysplasia - altered morphology Figure 8.10x1

8. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Traits of cancer cells  1. Independent of GROW signal from other cells often, oncogenes  2. Ignores STOP signal defective damage control, so problems not corrected. Often, tumor suppressor genes. Ex. p53

9. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings.  Growth factors bind to specific receptors on the plasma membrane to trigger cell division Growth factor Figure 8.8B Cell cycle control system Plasma membrane Receptor protein Signal transduction pathway G 1 checkpoint Relay proteins

10. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Traits of cancer cells, continued  3. No cell suicide (apoptosis) If this occurs, treatments which damage dividing cells may not work.  4. No limit to cell divisions telomeres rebuilt on ends of xsomes new treatment target: telomerase

11. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Traits of cancer cells, continued  5. Angiogenesis - formation of blood vessels new drugs to block this trait  6. Metastasis - ability to move to other tissues  benign: do not move from tumor site  malignant: invasive cells, can travel in blood and lymph system

12. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Malignant Tumor Development Figure 18.2

13. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. How do normal cells become cancerous? Selection within tumor for “most cancerous” cells

14. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Factors Contributing to Cancer  Genetics - 10%  Viruses  Molds and bacteria  Chemicals in the environment  Tobacco  Radiation  Dietary factors  Alcohol use

15. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Advances in Diagnosis: Early Detection  Tumor imaging: X-rays, PET, MRI  Enzyme tests for cancer markers: screening large numbers of people  Genetic testing to identify mutated genes  privacy and treatment issues

16. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Cancer Treatments  Conventional treatments: surgery, radiation, and chemotherapy  Delivery mechanisms: coated metal beads, light-sensitive drugs  Immunotherapy: promotes the immune response  Starving cancers: inhibits angiogenesis  Molecular treatments: target oncogenes  Vaccine - anti-HPV

17. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Most Common Cancers  Skin cancer: three major types  Prostate cancer: most common after age 50 in males  Breast cancer: almost exclusively in women  Lung cancer: smoking is the leading risk factor  Cancers of colon and rectum: early detection has increased survival rates to 62%

18. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Most Common Cancers (cont.)  Lymphoma: related to altered immune function  Urinary bladder cancer: surgery needed early  Cancer of the uterus: includes cervical cancer and cancer of the endometrium  Kidney cancer: found in renal related problems  Leukemia: chemotherapy often effective  Cancers of mouth and pharynx: tobacco major risk

19. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Table 18.3

20. Copyright © 2006 Pearson Education, Inc. publishing as Benjamin Cummings. Most Cancers are Preventable  Know family history  Get regular medical screenings  Learn self-examination techniques  Avoid direct sunlight 10 a.m. to 4 p.m., avoid sunlamps and tanning salons  Watch diet and weight  Don’t smoke  Drink in moderation, if at all  Be informed