cell cycle apoptosis and cancer

Question 1

restriction point

Answer 1

growth factor independence (G1 phase)

Question 2

G1 checkpoint

Answer 2

correct any DNA damage (chemical modifications) before continuing

Question 3

G2 checkpoint

Answer 3

verify completeness of complete genomic duplication

Question 4

metaphase checkpoint

Answer 4

ensures chromosomes are attached to mitotic spindle

Question 5

G1 Cyclin D

Answer 5

helps passage of cells through the restriction point in late G1 phase. makes cyclin D-CDK4 and cyclin D-CDK6 complexes

Question 6

G1/S Cyclin E

Answer 6

helps the cells commit to replication and enter S phase. Forms cyclin E-CDK2 complex

Question 7

S phase Cyclin A

Answer 7

initiation of DNA synthesis. Forms cyclin A-CDK2 complex

Question 8

M phase cyclin A and B

Answer 8

nuclear division during mitosis. Forms cyclin A-CDK1 and cyclin B-CDK1 complexes

Question 9

Wee1

Answer 9

inhibits Cdk by phosphorylating roof site

Question 10

Cdc25

Answer 10

dephosphorylates roof site to increase Cdk activity

Question 11

CDK-activating kinase (CAK)

Answer 11

fully activates Cyclin-CDK complex

Question 12

CDK inhibitors (CKIs)

Answer 12

CIP/KIP family. binds to cyclin-CDK complex to inactivate kinase activity of CDK. example-p27

Question 13

APC/C

Answer 13

anaphase-promoting complex or cyclosome. targets cyclins for destruction and inactivates most Cdks.

Question 14

p53

Answer 14

tumor suppressor. help captive by MDM2. When phosphorated p53 released and increases transcription of p21, a CKI. Causes cell cycle to arrest

Question 15

proto-oncogenes

Answer 15

encode proteins that promote cell growth and divsion

Question 16

oncogenes

Answer 16

proto-oncogenes mutated via gain of function mutations

Question 17

oncoproteins

Answer 17

the gene product that causes cell proliferation. (the protein that is transcribed)

Question 18

p53

Answer 18

tumor suppressor gene. observed in >50% of all human tumors. CHR17

Question 19

RB

Answer 19

tupor suppressor gene. retinoblastoma. CHR13

Question 20

APC

Answer 20

tupor suppressor gene. colon cancer. CHR5

Question 21

BRCA1 or 2

Answer 21

tupor suppressor gene. breast cancer. CHR17

Question 22

NF-1

Answer 22

tupor suppressor gene. neurofibromatosis. CHR 17

Question 23

permanent

Answer 23

remain in Go. cannot be regenerated

cardiac muscle, neurons, rbcs

Question 24

Stable (quiescent)

Answer 24

may exit Go to G1 when stimulated by GF
regeneration of damaged tissues
hepatocyte, epithelial cells of kidney tubules

Question 25

Labile

Answer 25

cells never enter Go.
constantly dividing to replace populations
gut epithelium, skin, hair follicles and bone marrow

Question 26

CIP/KIP

Answer 26

alter active site of G1 and S pahse cyclin CDK complexes

p21, p27, p57

Question 27

INK 4

Answer 27

G1 only
bind CDK 4 & 6 and block binding to cyclin D
p15, p16, p18, p19

Question 28

RAS

Answer 28

protooncogene. point mutation glycine to valine. 25% of all cancers. Perpetually active

Question 29

HER2

Answer 29

protooncogene. point mutation changes valine to glutamine. Oncoprotein NEU. Breast cancer. Can also be caused by gene amplification.

Question 30

EGF receptor

Answer 30

deletion in part of gene. active receptor without ligand binding. glioblastoma.

Question 31

ABL

Answer 31

protooncogene. translocation between 9 and 22 generated philadelphia chromosome. Generates BCR-ABL fusion oncoprotein. Causes CML (chronic myelogenous leukemia)

Question 32

c-myc

Answer 32

protooncogene. translocation between 8 and 14. Burkitt lymphoma

Question 33

N-myc

Answer 33

protooncogene. neuroblastoma. gene amplification.