White: Cancer 1&2

Question 1

Properties of cancer cells

Answer 1

Become self-sustaining, do not need signals to grow
release autocrine growth factor signals
Ignore apoptosis signals and anti-growth signals
Reproduce in defiance of normal restraints on cell growth
Invade areas normally reserved for other cells

Question 2

Carcinomas come from

Answer 2

Epithelial cells

Question 3

Sarcomas come from

Answer 3

Connective tissue and muscle tissue

Question 4

Leukemia/lymphoma come from

Answer 4

WBCs and their precursors

Question 5

Overactivity mutations

Answer 5

Gain of function- oncogenes

Involves single mutation event and activation of gene causing proliferation

Question 6

Underactivity mutations

Answer 6

Loss of function - tumor suppressor genes
Involves genes that inhibit growth
One mutation event- no effect
Second mutation causes problems (recessive)

Question 7

Two major categories of tumor suppressor genes

Answer 7

Proteins that normally restrict cell growth and proliferation
Proteins that maintain integrity of the genome

Question 8

Proteins that normally restrict cell growth and proliferation

Answer 8

Proteins that inhibit progression through G1/S in cell cycle (Rb, CKI)
Receptors or components of a signaling pathway that inhibit cell proliferation
Proteins that promote apoptosis

Question 9

Proteins that maintain integrity of the genome

Answer 9

Checkpoint control proteins (ATM, ATR)

DNA repair enzymes or pathways

Question 10

Hereditary retinoblastoma

Answer 10

Loss of function or deletion of one copy of Rb in every cell
Predisposed to cancer w/one copy destroyed already
Somatic event occurs-other copy destroyed, tumor forms

Question 11

Sporadic retinoblastoma

Answer 11

Start with all normal cells

Must have mutation introduced into both copies of Rb-more rare

Question 12

E2F binds

Answer 12

Promotors of G1/S cyclin and S cyclin genes, as well as to DNA synthesis protein genes, inducing gene expression

Question 13

E2F inhibited by

Answer 13

Interaction with Rb protein

If Rb is inactive, E2F will be overactive, causing proliferation

Question 14

Oncogenes role in retinoblastoma

Answer 14

Cyclin or Cdk genes could be oncogenes
Overproduction of them can overcome amount of CKIs
Phosphorylate Rb so it cannot stop E2F
Leads to uncontrolled growth & cancer

Question 15

Tumor suppressor genes in retinoblastoma

Answer 15

CKI or Rb- tumor suppressor genes
CKI/Rb could be lost- leads to cancer
No CKI- no control of Cdk-cyclins
No Rb- no suppression of E2F and entry into cell division

Question 16

If you lose p53, you also lose what functions

Answer 16

Loss of checkpoint control in cell cycle
Loss of cell cycle arrest in response to DNA damage
Loss of DNA repair activities
Loss of apoptosis in response to DNA damage

Question 17

p53 functions

Answer 17

Stimulates transcription of gene encoding CKI called p21
p21 binds to G2/S-Cdk and S-Cdk to stop cell cycle
P53 also activates expression of pro apoptotic proteins BH123 and BH-3

Question 18

Viral proteins of papilloma virus

Answer 18

E6 and E7- responsible for malignancy

These bind to tumor suppressor genes Rb and p53

Question 19

Bcl2 mutation does what

Answer 19

Stops apoptosis

Question 20

Colorectal cancer

Answer 20

One of the most preventable cancers
Arises in epithelial lining of large intestine
Slow disease progression-10 years
Inactivation of Apc (tumor suppressor gene) can cause colorectal cancer

Question 21

Bcr-Abl

Answer 21

Abl is a tyrosine kinase
N-terminus Bcr makes it hyperactive
Causes cell proliferation leading to CML
Treated with Gleevec which inhibits tyrosine kinase activity

Question 22

Gleevec method of operation

Answer 22

Takes place of ATP on Bcr-Abl complex