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pathophysiology > oncogenes and oncoproteins quiz > Flashcards

oncogenes and oncoproteins quiz Flashcards

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
Q

examples of oncogenes

A

RAS
BCL-2
Telomerase

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26
Q

ubiquitination is the

A

systematic and selective destruction of a protein

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27
Q

RAS genes have over

A

150 products

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28
Q

the most common RAS genes are

A

H-ras, N-ras, K-ras

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29
Q

H-ras is found on

A

chromosome 11

30
Q

N-ras is found on

A

chromosome 1

31
Q

K-ras is found on

A

chromosome 12

32
Q

each one of the RAS genes is responsible for

A

turning on or off various proteins that turn on proteins,

33
Q

RAS genes are one of first steps starts a cascade

A

that will ultimately turn on genes that often lead to more cell division

34
Q

RAS proteins themslves can be

A

turned on of off

35
Q

mutant RAS is found in

A

30% of cancer, 90% of pancreatic cancers

36
Q

each RAS protein can be turned “on” or “off” by a system v

A

very similar to phosphorylation

37
Q

in the case of RAS proteins being turned on or off, RAS proteins will either be bound to

A

GDP

GTP

38
Q

GDP

A

guanidine diphosphate

39
Q

when RAS proteins binds to GDP

A

it will be off

40
Q

GTP

A

guanidine triphosphate

41
Q

when RAS proteins binds to GTP

A

it will be on

42
Q

RAS proteins are almost always located

A

very close to a receptor protein on a cell’s membrane

43
Q

when a receptor protein on the cell membrane is activated by RAS

A

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
Q

when other things happen, RAS is turned off by having

A

the third phosphate group cut off ( becomes GDP)

45
Q

while all 150 RAS proteins are somewhat different

A

the begininng amino acid sequences are the same

46
Q

Almost all mutations affecting the ____codon of any RAS protein have

A

affecting the 61st codon, have been shown to inhibit the conversion of GTP to GDP

47
Q

mutations to RAS proteins inhibiting the conversion of GTP to GPD causes

A

the RAS proteins to be always on and cells are always told to grow `

48
Q

RAS would be an example of which of the 6 hallmarks

A

proliferative signalling

49
Q

BCL-2 is

A

a protein involved in the apoptosis pathway

50
Q

BCl-2 usually orks to

A

PREVNT apoptosis

51
Q

in some cases, BCL-2

A

is turned up too high, which stops p53 and its friends form initiating apoptosis

52
Q

when BCL-2 stops p53 and friends from iniitiating apoptosis

A

allows cancerous cells to proliferate

53
Q

shutting off the overexpression of BCL-2 is crucial to

A

helping anti-cancer medications work, so we can let to body cure itself by committing apoptosis instead f killing it ourselves

54
Q

genasense

A

an antisense drug

55
Q

genasense is

A

perfectly complementary to mRNA strand that carries instructions to produce BCL-2

56
Q

soooo genasense can

A

stop ribosomes from reading the mRNA and making the protein

57
Q

which hallmark is the BCL-2 . protein

A

Resisting cell death

58
Q

Every chromomsome has a

A

'’cap’’ on both end of the same 6 bases

59
Q

every chromomsome has a “cap” on both ends of which of the same bases

A

TTAGGG

60
Q

TTAGGG are repeated how many times

A

2500 times per chromosome in new cells

61
Q

each time a chromosome replicates and the cell divides

A

part of the telomere is lost and the chromosome shortens

62
Q

after the telomere is entirely lost…..

A

chromosome replication and cells division stops completely

63
Q

Hayflick limit was by

A

Leonard Hayflick in the 1960s

64
Q

what did Hayflick discover

A

that human cells are only capable of replicating a certain number of times

65
Q

human cells can only replicate about how many times

A

50-70

66
Q

telomerase is an enzyme

A

that lengthens the telomeres

67
Q

telomerase is almost

A

almost always off in somatic human cells,

68
Q

exception of a ew cell types where telomerase is off

A

stem cells, white blood cells, sperm cells, skin cells, etc

69
Q

does every cell have the gene to make telomerase

A

yes

70
Q

why is telomerase considered an oncoprotein

A

because without it, cancer cells would have a limited number of replications because they couldn’t replicate anymore

71
Q

what hallmark is the telomerase pathway

A

enabling replicative immortality

pathophysiology (24 decks)

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