Question

1. Damaged DNA is discovered during the G1 checkpoint. How does p53 react, and what are the possible results?

2. If S phase checkpoints detect nucleotides deficit, what happens to the dividing cell and the cell cycle?

3. What three conditions may be detected during the G2 checkpoints, and what are the two possible results if there is inadequate DNA or spindle fibers?

4. What two conditions are checked during the metaphase checkpoint? What happens if the cell “passes” the checkpoints?

5. What role do cyclins play in cell cycle regulation? What happens to the cells and the body if the cell cycles do not complete their cycles?

6. What defines cancer, and what are the two types of tumors that may result?

8a. How do benign masses disrupt normal body function?

8b. How do malignant cancers cause damage and disease in the body?

9. Compare normal cells to cancer cells in the table below.

Normal cells vs Cancer cells

size

shape

ploidy

Anchorage

Contact inhibition

# of nuclei

Cell cycle checkpoint control

Telomere “clock”

angiogenesis

Response to apoptosis signals

other

10. Compare oncogenes to mutated tumor suppressor genes.

11a. What is the normal function of the BRCA gene?

11b. What are the famous mutations to the BRCA gene called and what are the results of those mutations?

12. Compare mutagens and carcinogens. Give examples of both in our environments. How can we reduce our risk of developing cancers with regard to mutagens/carcinogens?

13. Is cancer genetic/inherited? Why or why not? How do people acquire mutations associated with cancer?

14. List 5 ways of detecting cancer.

15. List 3 types of cancer treatment. Can you find mention of any “alternative” or “natural” cancer treatments? Are they used instead of the “usual” types of treatments or along with those treatments?

16. Skin cancer is very common. Name the three most common types and what causes them. Describe how to recognize melanoma and what to do should you suspect you or someone you know has one?

Answer 1

1. p53 is a tumor suppressor gene. It checks the uncontrolled cell division. When there is DNA damage then p53 is activated and produces a Cdk inhibitor. This inhibitor then binds to the Cdk-G1/S cyclin complex and inactivates it. This halts the cell in G1 and prevents it from entering the S phase, allowing time for the DNA damage to be fixed.