cell cycle & cancer - exam 2

Question 1

checkpoints

Answer 1

regulatory molecules at each checkpoint “decide” if division should proceed

Question 2

G1 checkpoint

Answer 2

is growth factor present

is cell big enough

is dna undamaged

Question 3

G2 checkpoint

Answer 3

is dna replication complete

is dna intact

Question 4

M checkpoint

Answer 4

are chromosomes attached to kinetochore MTs

Question 5

normal cell division

Answer 5

cell cycle control working correctly

problem –> fixed –> cell continues dividing

problem –> not fixed –> apoptosis

Question 6

apoptosis

Answer 6

cell suicide pathway

Question 7

unregulated cell division

Answer 7

problem –> not fixed –> goes past checkpoint anyway

proliferating cancer cells form a tumor - cells can be immortal

Question 8

properties of normal cells

Answer 8

cells start & stop reproducing at the right time

each growth factor has a specific receptor

exhibit anchorage dependence & contact inhibition

Question 9

anchorage dependence

Answer 9

cells need to be anchored to something to divide

cells can be adhered to other cells, extracellular matrix, or tissue culture

Question 10

contact inhibition

Answer 10

crowded cells stop dividing

Question 11

properties of cancer cells

Answer 11

cells divide w/ no growth factor

cells ignore contact inhibition

cells ignore anchorage dependence

Question 12

signal transduction

Answer 12

needs specific shape to bind, sends message, & eventually you get a response

external, internal, external

Question 13

reception

Answer 13

signal binds to receptor

receptor is activated

receptor changes shape

Question 14

transduction

Answer 14

stimulates relay molecules (different proteins)

Question 15

response

Answer 15

activation of cellular response

regulation of cell cycle

Question 16

proto-oncogenes

Answer 16

genes that encode signals, receptors, signaling molecules, control proteins

Question 17

oncogenes

Answer 17

mutated proto-oncogenes

cancer-causing genes

Question 18

tumor suppressors

Answer 18

shut down cell division if something goes wrong

good

security gaurds

Question 19

what happens if tumor suppressors are mutated

Answer 19

cell cycle checkpoints ignored

damaged cells continue to proliferate

form a tumor

Question 20

BRCA

Answer 20

work to protect the genome from double stranded DNA damage during DNA replication

Question 21

what happens if BRCA is damaged

Answer 21

damaged DNA would still go through mitosis

G2 checkpoint

Question 22

p53

Answer 22

boss of all security guards

dna damage or cell cycle abnormalities
p53 activated - works at G1 checkpoint
fixes or apoptosis

Question 23

E6 protein

Answer 23

binds to p53

cell kills p53 because it thinks it’s E6

p53 destroyeed

Question 24

what happens if p53 is mutated

Answer 24

damaged DNA goes through mitosis

G1 checkpoint

Question 25

how can human papilloma virus lead to cancer

Answer 25

p53 is degraded & a cell w/ DNA damage would be allowed to pass through G1 checkpoint

damaged cells would build up & lead to cancer

Question 26

hyper-methylated tumor suppressor

Answer 26

too many methyl groups

gene off because it’s too crowded – suffocating

no tumor suppressor made

Question 27

demethylation

Answer 27

gets ride of methyl groups

makes too much telomerase

all cells now express telomerase – bad

Question 28

role of telomerase in cancer

Answer 28

cells that over express telomerase are immortal

telomerase activity in almost all human tumors

Question 29

antisense moleule

Answer 29

complementary to telomerase mRNA

binds to telomerase mRNA & stops demethylization

Question 30

chemotherapy

Answer 30

injection of chemicals into blood stream to stop mitosis

prevents kinetochore MTs from shortening

non selective

Question 31

radiation therapy

Answer 31

high energy particles damage DNA –> cells destroyed/injured

non selective

Question 32

why is cancer not usually caused by just 1 mutation

Answer 32

cells have backup systems

gets through 1 checkpoint, it will probably get stopped at a later one