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CAN > L05: Oncogenes > Flashcards

L05: Oncogenes Flashcards

1
Q

What is an oncogene

A

A gene that has the potential to cause cancer when mutated or overexpressed

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2
Q

What are oncogenes derived from

A

Proto-oncogene

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3
Q

What is a proto-oncogenes

A

Normal cellular gene that opromotes normal cell growth and proliferation in a regulated matter

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4
Q

How does a photo-oncogene become a oncogene

A

Gene mutation

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5
Q

What are the products of oncogenes

A

Growth factor receptors
Signal transuction molecules
Transcription factors

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6
Q

For a proto-oncogene to become an oncogene how many alleles need to be mutated

A

One allele (dominant allele)

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7
Q

Can oncogenes become involved in the hallmarks of cancer

A

Yes

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8
Q

What are the 4 ways in which oncogenes become activated

A

1) point mutations introduced to the gene
2) amplification of gene that includes proto-oncogene
3) chromosome translocation that brings proto-oncogene under the control of a different promoter
4) chromosome translocation that brings 2 genes together

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9
Q

What does point mutation to a a gene result in

A

Altering the characteristic of a protein

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10
Q

What does amplification of a gene that includes proto-oncogene lead to

A

Overexpression of a gene products

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11
Q

What does chromosome translocation that brings proto-oncogene under the control of a promoter lead to

A

Protein expression

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12
Q

What does translocation that brings 2 genes together result in

A

A protein with novel characteristics

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13
Q

In a normal cell what happens to DNA

A

Transcribed into RNA

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14
Q

In a cell what happens to RNA

A

Translated into protein

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15
Q

Name an example of a gene that undergoes point mutation which alters characteristic of the protein

A

RAS

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16
Q

Which 3 genes encode for RAS

A

KRAS
NRAS
HRAS

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17
Q

If there is a point mutation for RAS what happens to RAS

A

Permanently switched on

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18
Q

What is the role of activated RAS

A

Pass on the signal from a tyrosine kinase receptor for gene expression

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19
Q

What are the 3 amino acids of RAS

A

G12
G13
Q61

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20
Q

If there is a mutation of the RAS gene how many amino acids are mainly affected

A

1 out of the 3

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21
Q

What causes the activation of a normal ras protein

A

Converting GDP (found in inactive RAS) to GTP

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22
Q

How does the mutations of RAS allow it to become acitvated

A

It changes the amino acids and therefore the binding of GTP

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23
Q

Normally what removes GTP from ras to switch it off

A

GAP

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24
Q

If there is an oncogenic RAS mutation what happens to GAP

A

GAP becomes blocked

25
Q

Apart from directly giving mutation to the RAS gene what are the other ways of activating RAS permanently

A

Mutating the RTK (receptor tyrosine kinase) permanently so it signals to RAS permanently

26
Q

Name an exmaple of a RTK that causes the permanent activation of itself and RAS

A

Egfr

27
Q

Name 2 examples of amplification of piece of gene that includes a proto-oncogene

A

MYCN

EGFR

28
Q

What type of cancer is MYCN amplification most common in

A

Neuroblastoma

29
Q

In a normal cell how many copies of MYCN are there

A

2

30
Q

What are the 2 ways of amplification MYCN

A

1) many copies of MYCN (more than 2) become present on normal chromosome and extra chromosomal
2) MYCN has multiple copies on a single chromosome

31
Q

What does amplification of MYCN lead to

A

Overexpression of MYCN protein

32
Q

Name 2 examples of where chromosome translocation bring proto-oncogene under the control of a promoter

A

C-MYC

BCL-2

33
Q

What type of cancer is c-MYC a hallmark of

A

Burkitt lymphoma

34
Q

Which chromosome is the translocation of c-MYC found on in burkitt lymphoma

A

Chromosome 8 and 1 immunoglobulin loci

35
Q

What leads to c-MYC expression

A

IGH enhancer

36
Q

What does too much c-MYC lead to

A

Cell growth
Proliferation
Ribosomal synthesis
Protein synthesis

37
Q

Which cancer is BCL-2 involved in

A

Follicular lymphoma

38
Q

What does translocation occur between

A

Chromosome 18 and iGH on chromosome 14

39
Q

What is BCL2

A

A pro survival gene that counteracts apoptosis

40
Q

Name an example of when a chronometer translocation brings 2 genes together

A

BCR-ABL

41
Q

What cancer is BCR-ABL found in

A

Chronic myeloid leukemia

42
Q

Between what 2 chromosome does translocation occur

A

22 and 9

43
Q

What does BCR-ABL lead to

A

Increased cell survival

Increased proliferation

44
Q

What medicine can block the fusion of BCR-ABL

A

Imatinib

45
Q

What is the role of imatinib

A

Inhibits tyrosine kinase by prevent ATP binding

46
Q

What causes the activation of tyrosine kinase receptors EGFR

A

Phosphorylation of tyrosine resides

47
Q

How do tyrosine residues become activated

A

When ATP bind to the packed in tyrosine kinase receptor

48
Q

How can we block the acitvation of Tyrosine kinase receptors so

A

Tyrosine kinase receptors

49
Q

Name a first generation tyrosine kinase inhibitor

A

Gefitinib

50
Q

How does gefitinib work

A

Prevent ATP binding by competing with ATP

51
Q

What is a risk of using 1st generation tyrosine kinase inhibits

A

Drugs resistance

52
Q

If we get drug resistance what is the other option of treatmetn

A

Using 2nd generation tyrosine kinase inhibitor

53
Q

Name an example of a second generation TKI

A

Afatinib

54
Q

How does afatinib work

A

Irreversible binding to atp pocket in the tyrosine kinase receptor

55
Q

Name an example of a 3rd generation TKI

A

Asimertinib

56
Q

What is the role of asimertinib

A

Bind to mutated EGFR that have become drug resistant

57
Q

What are the ways we can target EGFR/RAS/MAPK pathway

A

Target the proteins within the pathway

58
Q

Name a drug that is used to target RAF

A

Vermurafenib

Dabrafenib

59
Q

Name a drug that is used to target MEK protein

A

Trametinib

CAN (25 decks)

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