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Molecular Basis Of Disease/ Microbiology And Immunology > Oncogenes And Tumour Suppressor Genes > Flashcards

Oncogenes And Tumour Suppressor Genes Flashcards

1
Q

What are the major functional changes in cancer?

A

Increased growth
Failure to undergo apoptosis or senescence
Loss of differentiation
Failure to repair DNA damage

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2
Q

How does increased growth happen in cancer?

A

Loss of regulation and stimulation of environment promoting growth

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3
Q

What do oncogenes cause?

A

Gain of function- making cells divide

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4
Q

What are oncogenes?

A

Altered gene whos product can act in a dominant fashion to help make a cell cancerous

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5
Q

What is the normal version of oncogenes?

A

Protoconcogenes

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6
Q

What do tumour supressor genes cause?

A

Loss of function- normal activity prevents cancer formation

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7
Q

What is Rous’s protocol for inducing sarcoma in chickens?

A

Remove sarcoma and break up into small tissue chunks
Grind up with sand
Filter and collect filtrate through a fine-pore filter
Inject filtrate into young chickens
Observe sarcoma in injected chickens

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8
Q

How is c-src captured by retrovirus?

A

The virus can acquire fragments of genes from the host at integration sites

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9
Q

What is the c-src oncogene product?

A

60 kDa intracellular tyrosine kinase

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10
Q

What can the C-Src oncogene do?

A

Phosphorylate cellular proteins and affect growth

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11
Q

What are the ways to become an active oncogene?

A

Mutation/deletion
Gene duplication/amplification
Translocation

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12
Q

What do gene duplications/amplifications do for oncogenes?

A

Increase synthesis of encoded proteins

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13
Q

What are the four types of protein involved in the growth signal transduction pathway?

A

Growth factors
Growth factor receptors
Intracellular signal transducers
Nuclear transcription factors

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14
Q

What do the majority of oncogene proteins function as?

A

Elements of the signalling pathways that regulate cell proliferation and surivival in response to growth factor stimulation

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15
Q

What do the majority of oncogene proteins function as?

A

Growth factors, growth backer receptors and intracellular signalling molecules

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16
Q

What were RAS oncogenes identified from?

A

Studies of two cancer causing cell lines

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17
Q

What are RAS oncogenes?

A

Small GTPases that are normally bound to GDP in a neutral state

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18
Q

What proportion of oncogenic activation of RAS is seen in human cancer?

A

30%

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19
Q

What codons are the mutations in on RAS oncogenes?

A

12, 13 and 61

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20
Q

What do the point mutations lead to in RAS oncogenes?

A

Loss of GTPase acting on the RAS protein that is normally used to inactivate the RAS GDP

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21
Q

How do the RAS oncogene intracellular signal transducers work?

A

Binding of extracellular growth factor signal

  • > Promotes recruitment of RAS proteins to the receptor complex
  • > recruitment promotes RAS to exchange GDP for GTP (activates RAS)
  • > activated RAS then initiates the remainder of the signalling cascade (mitogen activated protein kinases)
  • > kinases ultimately phosphorylate targets such as transcription factor to promote expression of genes important for growth and survival
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22
Q

What does the MYC oncogene family consist of?

A

C-MYC
MYCN
MYCL

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23
Q

Where was the MYC oncogene family originally identified?

A

In avian myelocytomatosis virus

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24
Q

What are MYC oncoproteins?

A

Transcription factors

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25
Q

How much of the genome do the MYC oncogenes transcribe?

A

15%

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26
Q

What are the major downstream effectors of MYC?

A 
Those involved in:
Ribosome biogenesis
Protein translocation
Cell cycle progression and metabolism
Cell proliferation, differentiation, survival and immune surveillance
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27
Q

What proportion of human cancers are affected by overexpression of MYC?

A

40%

28
Q

What does MYC encode?

A

Helix-loop-helix leucine zipper transcription factor

29
Q

How does MYC transactivate gene expression?

A

Dimerises with MAX (its partner protein)

30
Q

When is MYC activated (generally)?

A

Comes under the control of foreign transcriptional promotors

31
Q

What does activated MYC lead to?

A

Deregulation of the oncogene that drives proliferation as a result of chromosomal translocation

32
Q

What is burkitts lymphoma?

A

High grade lymphoma

33
Q

Who is affected by burkitts lymphoma?

A

Children aged 2-16

34
Q

Where do the chromosomal translocations occur in the MYC gene?

A

Parts of chromosomes 2, 14 and 22 attach themselves to chromosome 8

35
Q

Which accounts for 15-20% of leukaemia?

A

Chronic myelogenous leukaemia

36
Q

What proportion of chronic myelogenous leukaemia patients carry the philadelphia chromosome?

A

95%

37
Q

What is the result of the philadelphia chromosome generation?

A

Tyrosine kinase activity of the oncogene ABL leading to abnormal proliferation

38
Q

What are tumour supressor genes usually regulators of?

A

Cell cycle checkpoints, differentiation or DNA repair

39
Q

What does loss of tumour supressor gene function require?

A

Inactivation of both alleles of the gene

40
Q

Are tumour supressor genes dominant or recessive?

A

Recessive

41
Q

When do retinoblastomas occur?

A

When immature retinoblasts continue to grow very fast and do not turn into mature retinal cells

42
Q

How can you see retinoblastomas?

A

Tumour will reflect light back in a white colour

43
Q

What is leukocoria?

A

When the tumour reflects light back in a white colour

44
Q

What are the two forms of retinoblastoma?

A

Familial

Sporadic

45
Q

Where is the hereditary mutation in retinoblastoma?

A

chromosome 13

46
Q

What does the Rb gene family include?

A

Three members collectively known as pocket proteins

47
Q

How many binding partners does prb have?

A

Over 100

48
Q

What is the main function of the RB protein?

A

Regulate the cell cycle by inhibiting G1-S phase transition

49
Q

Which is the first cyclin to be synthesised?

A

Cyclin D

50
Q

What does Cyclin D do?

A

Drives progression through G1 with CDK 4/6

51
Q

What does the g1 checkpoint lead to if the DNA is damaged?

A

Arrest of the cell cycle

52
Q

What is a key substrate for cyclin D?

A

RB protein

53
Q

What is the main binding factor?

A

E2F transcription factor

54
Q

What is Rb activity regulated by?

A

Phosphorylation

55
Q

What happens when the Rb tumour suppressor is active?

A

Inhibits cell proliferation

56
Q

What happens when RB is dephosphorylated?

A

Active and remains bound to E2F

57
Q

What happens when RB is phosphorylated?

A

E2F is released and migrates to the nucleus to induce transcription

58
Q

What can RB be inactivated by?

A

Phosphorylation, mutation or viral oncoprotein binding

59
Q

How does viral inactivation in small DNA tumours mainly work?

A

Dirupting ELF binding or destabalisation of RB

60
Q

What was the first tumour supressor gene to be identified?

A

P53

61
Q

what is the prevelance of p53 mutation in cancers?

A

30-50%

62
Q

What does frequent mutation of p53 in tumour cell genomes suggest?

A

Tumour cells try to eliminate p53 function before they can thrive

63
Q

What are p53 levels kept low by?

A

MDM 2 protein

64
Q

What is the MDM2 protein made from?

A

Oncogene-ubiquitin ligase

65
Q

What happens in normal unstressed cells with MDM2 and p53?

A

Move between the nucleus and cytosol

66
Q

What happens with MDM2 and p53 in the nucleus?

A

Bind to form a complex where MDM modifies the carboxyl terminus of p53 and targets it for degredation by the proteasome

67
Q

What activates p53?

A

Stress signals

Molecular Basis Of Disease/ Microbiology And Immunology (57 decks)

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