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pathophysiology > oncogenes and oncoproteins quiz > Flashcards

oncogenes and oncoproteins quiz Flashcards

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1
Q

what are the six hallmarks

A
  • proliferative signaling
  • evading growth suppressors
  • resisting cell death
  • enabling replicative immortality
  • inducing angiogenisis
  • activating angiogenesis
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2
Q

to be cancerous must undergo…

A

some genetic changes that it to show each of the hallmarks of cancer

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3
Q

the genetic changes that cause cancer that occur on or around genes are sorted into what 2 categories

A

oncogenes and tumor suppressor genes

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4
Q

oncogene

A

gene that has the power to cause cancer when turned “on” or “up”

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5
Q

oncoprotein

A

the protein coded for by an oncogene

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6
Q

oncogenes and oncoproteins usually

A

don’t cause cancer, only do when there is some kind of mutation

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7
Q

before they mutate, oncogenes are called

A

proto-oncogenes

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8
Q

how can proto-oncogenes be activated

A

gene duplication , error with regulatory protein, error with regulatory DNA , chromosomal translocation

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9
Q

gene duplication

A

the gene is accidentally copied, resulting in more expression of the protein

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10
Q

result of gene duplication

A

genes have an extra copy and will expressed at higher rates

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11
Q

error with regulatory protein

A

the protein that would turn a gene off can no longer do so

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12
Q

(thinking of regulation) almost all genes have

A

promoters and operator just upstream of the gene

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13
Q

upstream

A

in front

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14
Q

example of a promoter

A

where RNA polymerase binds to turn DNA into mRNA

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15
Q

example of an operator

A

where regulatory proteins bind to alter expression of the gene

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16
Q

activators

A

turn expression up

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17
Q

repressor

A

turn expression down

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18
Q

so with an error with regulatory protein…. there is a

A

repressor that does not work

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19
Q

error with regulatory DNA

A

the DNA in the operato mutates so that regulatory proteins cannot bind there anymore

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20
Q

chromosomal translocation

A

the gene “moves” during DNA replication and has a new operator

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21
Q

things that causes the activation of oncoproteins

A

hypermorphic mutation
failure of on/off switch
failure of ubiquitination

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22
Q

hypermorphic mutation

A

mutation in protein structure makes it work faster

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23
Q

failure of on/off switch

A

kinase, phosphatase, or other on/ off switch fails to turn off oncoprotein

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24
Q

failure of ubiquitination

A

failure to destroy a protein leads to higher levels of them

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25
examples of oncogenes
RAS BCL-2 Telomerase
26
ubiquitination is the
systematic and selective destruction of a protein
27
RAS genes have over
150 products
28
the most common RAS genes are
H-ras, N-ras, K-ras
29
H-ras is found on
chromosome 11
30
N-ras is found on
chromosome 1
31
K-ras is found on
chromosome 12
32
each one of the RAS genes is responsible for
turning on or off various proteins that turn on proteins,
33
RAS genes are one of first steps starts a cascade
that will ultimately turn on genes that often lead to more cell division
34
RAS proteins themslves can be
turned on of off
35
mutant RAS is found in
30% of cancer, 90% of pancreatic cancers
36
each RAS protein can be turned "on" or "off" by a system v
very similar to phosphorylation
37
in the case of RAS proteins being turned on or off, RAS proteins will either be bound to
GDP | GTP
38
GDP
guanidine diphosphate
39
when RAS proteins binds to GDP
it will be off
40
GTP
guanidine triphosphate
41
when RAS proteins binds to GTP
it will be on
42
RAS proteins are almost always located
very close to a receptor protein on a cell's membrane
43
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
44
when other things happen, RAS is turned off by having
the third phosphate group cut off ( becomes GDP)
45
while all 150 RAS proteins are somewhat different
the begininng amino acid sequences are the same
46
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
47
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 `
48
RAS would be an example of which of the 6 hallmarks
proliferative signalling
49
BCL-2 is
a protein involved in the apoptosis pathway
50
BCl-2 usually orks to
PREVNT apoptosis
51
in some cases, BCL-2
is turned up too high, which stops p53 and its friends form initiating apoptosis
52
when BCL-2 stops p53 and friends from iniitiating apoptosis
allows cancerous cells to proliferate
53
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
54
genasense
an antisense drug
55
genasense is
perfectly complementary to mRNA strand that carries instructions to produce BCL-2
56
soooo genasense can
stop ribosomes from reading the mRNA and making the protein
57
which hallmark is the BCL-2 . protein
Resisting cell death
58
Every chromomsome has a
''cap'' on both end of the same 6 bases
59
every chromomsome has a "cap" on both ends of which of the same bases
TTAGGG
60
TTAGGG are repeated how many times
2500 times per chromosome in new cells
61
each time a chromosome replicates and the cell divides
part of the telomere is lost and the chromosome shortens
62
after the telomere is entirely lost.....
chromosome replication and cells division stops completely
63
Hayflick limit was by
Leonard Hayflick in the 1960s
64
what did Hayflick discover
that human cells are only capable of replicating a certain number of times
65
human cells can only replicate about how many times
50-70
66
telomerase is an enzyme
that lengthens the telomeres
67
telomerase is almost
almost always off in somatic human cells,
68
exception of a ew cell types where telomerase is off
stem cells, white blood cells, sperm cells, skin cells, etc
69
does every cell have the gene to make telomerase
yes
70
why is telomerase considered an oncoprotein
because without it, cancer cells would have a limited number of replications because they couldn't replicate anymore
71
what hallmark is the telomerase pathway
enabling replicative immortality

pathophysiology (24 decks)

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