cell cycle & cancer - exam 2 Flashcards
checkpoints
regulatory molecules at each checkpoint “decide” if division should proceed
G1 checkpoint
is growth factor present
is cell big enough
is dna undamaged
G2 checkpoint
is dna replication complete
is dna intact
M checkpoint
are chromosomes attached to kinetochore MTs
normal cell division
cell cycle control working correctly
problem –> fixed –> cell continues dividing
problem –> not fixed –> apoptosis
apoptosis
cell suicide pathway
unregulated cell division
problem –> not fixed –> goes past checkpoint anyway
proliferating cancer cells form a tumor - cells can be immortal
properties of normal cells
cells start & stop reproducing at the right time
each growth factor has a specific receptor
exhibit anchorage dependence & contact inhibition
anchorage dependence
cells need to be anchored to something to divide
cells can be adhered to other cells, extracellular matrix, or tissue culture
contact inhibition
crowded cells stop dividing
properties of cancer cells
cells divide w/ no growth factor
cells ignore contact inhibition
cells ignore anchorage dependence
signal transduction
needs specific shape to bind, sends message, & eventually you get a response
external, internal, external
reception
signal binds to receptor
receptor is activated
receptor changes shape
transduction
stimulates relay molecules (different proteins)
response
activation of cellular response
regulation of cell cycle
proto-oncogenes
genes that encode signals, receptors, signaling molecules, control proteins
oncogenes
mutated proto-oncogenes
cancer-causing genes
tumor suppressors
shut down cell division if something goes wrong
good
security gaurds
what happens if tumor suppressors are mutated
cell cycle checkpoints ignored
damaged cells continue to proliferate
form a tumor
BRCA
work to protect the genome from double stranded DNA damage during DNA replication
what happens if BRCA is damaged
damaged DNA would still go through mitosis
G2 checkpoint
p53
boss of all security guards
dna damage or cell cycle abnormalities
p53 activated - works at G1 checkpoint
fixes or apoptosis
E6 protein
binds to p53
cell kills p53 because it thinks it’s E6
p53 destroyeed
what happens if p53 is mutated
damaged DNA goes through mitosis
G1 checkpoint
how can human papilloma virus lead to cancer
p53 is degraded & a cell w/ DNA damage would be allowed to pass through G1 checkpoint
damaged cells would build up & lead to cancer
hyper-methylated tumor suppressor
too many methyl groups
gene off because it’s too crowded – suffocating
no tumor suppressor made
demethylation
gets ride of methyl groups
makes too much telomerase
all cells now express telomerase – bad
role of telomerase in cancer
cells that over express telomerase are immortal
telomerase activity in almost all human tumors
antisense moleule
complementary to telomerase mRNA
binds to telomerase mRNA & stops demethylization
chemotherapy
injection of chemicals into blood stream to stop mitosis
prevents kinetochore MTs from shortening
non selective
radiation therapy
high energy particles damage DNA –> cells destroyed/injured
non selective
why is cancer not usually caused by just 1 mutation
cells have backup systems
gets through 1 checkpoint, it will probably get stopped at a later one
