oncogenes and oncoproteins quiz Flashcards
what are the six hallmarks
- proliferative signaling
- evading growth suppressors
- resisting cell death
- enabling replicative immortality
- inducing angiogenisis
- activating angiogenesis
to be cancerous must undergo…
some genetic changes that it to show each of the hallmarks of cancer
the genetic changes that cause cancer that occur on or around genes are sorted into what 2 categories
oncogenes and tumor suppressor genes
oncogene
gene that has the power to cause cancer when turned “on” or “up”
oncoprotein
the protein coded for by an oncogene
oncogenes and oncoproteins usually
don’t cause cancer, only do when there is some kind of mutation
before they mutate, oncogenes are called
proto-oncogenes
how can proto-oncogenes be activated
gene duplication , error with regulatory protein, error with regulatory DNA , chromosomal translocation
gene duplication
the gene is accidentally copied, resulting in more expression of the protein
result of gene duplication
genes have an extra copy and will expressed at higher rates
error with regulatory protein
the protein that would turn a gene off can no longer do so
(thinking of regulation) almost all genes have
promoters and operator just upstream of the gene
upstream
in front
example of a promoter
where RNA polymerase binds to turn DNA into mRNA
example of an operator
where regulatory proteins bind to alter expression of the gene
activators
turn expression up
repressor
turn expression down
so with an error with regulatory protein…. there is a
repressor that does not work
error with regulatory DNA
the DNA in the operato mutates so that regulatory proteins cannot bind there anymore
chromosomal translocation
the gene “moves” during DNA replication and has a new operator
things that causes the activation of oncoproteins
hypermorphic mutation
failure of on/off switch
failure of ubiquitination
hypermorphic mutation
mutation in protein structure makes it work faster
failure of on/off switch
kinase, phosphatase, or other on/ off switch fails to turn off oncoprotein
failure of ubiquitination
failure to destroy a protein leads to higher levels of them
examples of oncogenes
RAS
BCL-2
Telomerase
ubiquitination is the
systematic and selective destruction of a protein
RAS genes have over
150 products
the most common RAS genes are
H-ras, N-ras, K-ras
H-ras is found on
chromosome 11
N-ras is found on
chromosome 1
K-ras is found on
chromosome 12
each one of the RAS genes is responsible for
turning on or off various proteins that turn on proteins,
RAS genes are one of first steps starts a cascade
that will ultimately turn on genes that often lead to more cell division
RAS proteins themslves can be
turned on of off
mutant RAS is found in
30% of cancer, 90% of pancreatic cancers
each RAS protein can be turned “on” or “off” by a system v
very similar to phosphorylation
in the case of RAS proteins being turned on or off, RAS proteins will either be bound to
GDP
GTP
GDP
guanidine diphosphate
when RAS proteins binds to GDP
it will be off
GTP
guanidine triphosphate
when RAS proteins binds to GTP
it will be on
RAS proteins are almost always located
very close to a receptor protein on a cell’s membrane
when a receptor protein on the cell membrane is activated by RAS
a cascade will cause a GDP to be removed from RAS and a GTP to be added to it, causing RAS to become active
when other things happen, RAS is turned off by having
the third phosphate group cut off ( becomes GDP)
while all 150 RAS proteins are somewhat different
the begininng amino acid sequences are the same
Almost all mutations affecting the ____codon of any RAS protein have
affecting the 61st codon, have been shown to inhibit the conversion of GTP to GDP
mutations to RAS proteins inhibiting the conversion of GTP to GPD causes
the RAS proteins to be always on and cells are always told to grow `
RAS would be an example of which of the 6 hallmarks
proliferative signalling
BCL-2 is
a protein involved in the apoptosis pathway
BCl-2 usually orks to
PREVNT apoptosis
in some cases, BCL-2
is turned up too high, which stops p53 and its friends form initiating apoptosis
when BCL-2 stops p53 and friends from iniitiating apoptosis
allows cancerous cells to proliferate
shutting off the overexpression of BCL-2 is crucial to
helping anti-cancer medications work, so we can let to body cure itself by committing apoptosis instead f killing it ourselves
genasense
an antisense drug
genasense is
perfectly complementary to mRNA strand that carries instructions to produce BCL-2
soooo genasense can
stop ribosomes from reading the mRNA and making the protein
which hallmark is the BCL-2 . protein
Resisting cell death
Every chromomsome has a
'’cap’’ on both end of the same 6 bases
every chromomsome has a “cap” on both ends of which of the same bases
TTAGGG
TTAGGG are repeated how many times
2500 times per chromosome in new cells
each time a chromosome replicates and the cell divides
part of the telomere is lost and the chromosome shortens
after the telomere is entirely lost…..
chromosome replication and cells division stops completely
Hayflick limit was by
Leonard Hayflick in the 1960s
what did Hayflick discover
that human cells are only capable of replicating a certain number of times
human cells can only replicate about how many times
50-70
telomerase is an enzyme
that lengthens the telomeres
telomerase is almost
almost always off in somatic human cells,
exception of a ew cell types where telomerase is off
stem cells, white blood cells, sperm cells, skin cells, etc
does every cell have the gene to make telomerase
yes
why is telomerase considered an oncoprotein
because without it, cancer cells would have a limited number of replications because they couldn’t replicate anymore
what hallmark is the telomerase pathway
enabling replicative immortality
