Assignment:
1. List three (3) of the hallmarks of cancer.
2. Explain, in basic terms, what "sustained proliferative signaling" means.
3. In ____________ proliferative stimulation, cancer cells themselves produce the chemical(s) that they then also respond to; a type of so-called "self-signaling."
4. Explain how elevating/increasing the number of receptor proteins displayed on the surface of a cancer cell would lead to its sustained proliferative signaling. (i.e. how are the receptors linked to sustained cell replication?)
5. The Rb protein is the product of a(n) oncogene / tumor suppressor gene (circle one).
6. Rb / TP53 (circle one) receives inputs exclusively from the cell's intracellular operating systems and can trigger apoptosis.
7. Explain what the concept of "contact inhibition" means and what loss of that inhibition leads to.
8. What is the name of the cytoplasmic NF2 gene product? What is the main role of this protein?
9. What is apoptosis? List one function of this process in embryonic development and one function of this process in adults.
10. During the process of apoptosis, the targeted cell emits signals to attract ______________, a type of immune cell that can recognize cell parts and remove them from the body.
11. Apoptosis can be induced by signals/factors originating outside of the cell (extrinsic) or from within the cell (intrinsic). Currently, the extrinsic / intrinsic (choose one) apoptotic program is more widely implicated as a barrier to cancer pathogenesis.
12. List one (1) antiapoptotic regulator whose expression is often increased in cancer cells.
13. List two (2) proapoptotic factors whose expression is often downregulated in cancer cells.
14. Normal/healthy cells can pass through only a limited number of successive cell growth-and-division cycles. This limitation isassociated with two distinct barriers to proliferation: 1) _______________ and 2) _________________________.
15. One of the hallmark characteristics of cancer cells is the trait of being immortalized; explain what it means if cells are immortalized.
16. What are telomeres? How are telomeres different over time in normal cells versus cancer cells and how is this difference linked to being immortalized?
17. What takes place during the process of angiogenesis?
18. In adults, the vasculature becomes quiescent and, with the exception of wound healing and female reproductive cycling, does not continue to replicate and expand. Explain how this differs in tumors and what causes this difference?
19. List two activators of angiogenesis and two inhibitors.
20. Increased expression of ______________, a key cell-to-cell adhesion molecule, is well established as an antagonist of invasion and metastasis.
21. In Grade ___ tumors, the cells and tissue are somewhat abnormal and are called moderately differentiated.
22. What information does a cancer's stage provide?
23. In the TNM system of cancer staging, what do the T, N, and M stand for?