Offner Cancer

Question 1

Cancer progression from hyperplasia

Answer 1

Normal -> Hyperplasia -> Dysplasia -> Carcinoma in Situ -> Invasive carcinoma

Question 2

Proto-oncogene

Answer 2

normal gene that can become an oncogene due to mutations or increased expression
- typically code for proteins involved in cell growth and differentiation

Question 3

Oncogene

Answer 3

Encodes a protein which if deregulated participates in the onset/development of cancer
- activate in cancer cells

Question 4

Tumor supressor genes

Answer 4

Inactivates in cancer cells

Question 5

2-hit hypothesis

Answer 5

Both copies of genes need to be suppressed in order for a phenotypic change to take place

Question 6

What results from Microsatellite Instability in colon cancer

Answer 6

Increase in number of growth factors

Question 7

What results from the chromosomal instability pathway in colon cancer?

Answer 7

loss of tumor suppressor genes -> increase in oncogene expression -> loss of more tumor suppression

Question 8

TP53

Answer 8

50% of all tumors have defective p53
- low levels in normal cells
- in cells with DNA damage, p53 levels increase
- p53 arrests cells until they repair themselves or undergo apoptosis

Question 9

Li-Fraumeni syndrome

Answer 9

Inheritance of one mutated copy of p53

Question 10

Relation between Rb and p53

Answer 10

Rb is a tumor supressor gene which functions by binding E2F to inhibit transcription
- if phosphorylated, E2F is released
- an increase in p53 will prevent phosphorylation of Rb (via inhibition of CyclinD/CDK4,6)

Question 11

In normal conditions, how is p53 regulated

Answer 11

MDM2 keeps p53 low, and p53 promotes production of MDM2

Question 12

In cell stress conditions, how is p53 regulated

Answer 12

PTMs to MDM2 cause it to dissociate from p53
- allows concentration of p53 to increase

Question 13

In cancer, how is p53 regulated

Answer 13

MDM2 is upregulated, leading to more degradation of p53