Tumor Cell Biology

Question 1

Retinoblastoma caused by

Answer 1

(RB genes)

Question 2

Familial adenomatous polyposis caused by

Answer 2

APC gene

this is colon cancer

Question 3

HNP*CC caused by

Answer 3

Mismatch repair genes

Question 4

Melanoma caused by

Answer 4

p15/INK4

Question 5

Inherited breast cancer caused by

Answer 5

BRCA 1/2

Question 6

Neurofibromatosis caused by

Answer 6

NF 1/2

Question 7

Wilm’s Tumor caused by

Answer 7

WT1

Question 8

BRCA + Breast Cancer

Answer 8

• BRCA promotes DNA repair
• You have one mutated and one un-mutated BRCA gene
• Eventually this functional copy will become mutated and you will have no DNA repair regulation so cancer develops
• This breast cancer can then move to the ovaries and the uterus

Question 9

C-myc

Answer 9

is a oncogene that function as a transcription factor

Question 10

Chronic Myelogenous Leukemia (CML) Drug

Answer 10

 STI-571 (gleevec, imatinib) is a kinase that binds only to the Bcr-ABl tyrosine kinase to completely knock out CML

Question 11

Ras Protein

Answer 11

o Exists in a GDP bound (inactive) and a GTP bound (active)
o Cancer Ras are found trapped in their GTP bound form causing abnormal activation of MAPK pathway → always stimulating proliferation

Question 12

G1 Cyclins/CDK

Answer 12

Cyclin D

CDK4

Question 13

G1 → S Cyclins/CDK

Answer 13

Cyclin E

CDK2

Question 14

S Cyclins/CDK

Answer 14

CyclinA

CDK2

Question 15

G2 → M Cyclins/CDK

Answer 15

cyclin B/CDK1

Question 16

G1 Check Point

Answer 16

• 12 hours long
• DNA damage → cell will not go to the S phase because it doesn’t want to replicate the damaged DNA to the daughter cells
• G1 cell cylce arrest: cell tries to repair the damage and if it can, DNA moves on

Question 17

M Phase Checkpoint

Answer 17

If the DNA hasn’t aligned properly, the cell will undergo M cell cycle arrest

Question 18

Cancer + Checkpoints

Answer 18

• Gene amplification of cyclins of CDKs → cell cycle progression faster
• Genes for CDK inhibitors are deleted → cell cycle abnormal and faster
• Check points proteins are mutated → no check points
• NET RESULT: increased proliferation

Question 19

p53 function

Answer 19

 “Guardian of the genome”
 Activated by DNA damage
 Elicits cell cycle arrest to enable DNA repair, if damage is excessive orchestrates cell death

Question 20

Retinoblastoma Protein (Rb) function

Answer 20

 Controls cell cycle moving past G1 checkpoints to the S phase
 Binds regulatory transcription factor E2F which is required for synthesis of replication enzymes (E2F + Rb = no transcription/replication)
 Active G1 CDK/cyclin kinase phosphorylates RB which leasds to release of E2F leading to S phase

Question 21

Process of apoptosis

Answer 21

During apoptosis, the genome will fragment, the cell will shrink and the cell will disintegrate into smaller apoptotic bodies

Question 22

Extrinsic Pathway of Apoptosis

Answer 22

 Death receptors bind to the death ligand and activate the caspases

Question 23

Intrinsic Pathway of Apoptosis

Answer 23

 Disruption of mitochondrial permeability leads to release of cytochrome C which causes Bax levels to increases → apoptosis

Question 24

Types of Caspases

Answer 24

 Inhibitors: need to dimerize to become active

 Executioner: need to be proteolytically cleaved to become activated

Question 25

Targets of executioners

Answer 25

 An inhibitor of DNAse → fragmentation of DNA
 Nuclear lamins → fragmentation of DNA
 Other cytoskeletal associated proteins → disruption of cytoskeleton and cell fragmentation