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Dysfunction > OTSG > Flashcards

OTSG Flashcards

1
Q

What are the major functional changes in cancer?

A

→increased growth
→failure
→loss of differentiation
→failure to repair DNA damage

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2
Q

What are oncogenes normally components of?

A

→growth factor signalling pathways that when mutated produce products in higher quantities

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3
Q

What do tumour suppressor gene act as?

A

→a stop signal to uncontrolled growth, may inhibit the cell cycle or trigger apoptosis

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4
Q

What was the discovery of Rous’ protocol?

A

→sarcoma was transmissible through viruses-

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5
Q

What was found in Rous’ extra gene?

A

→there is an extra gene

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6
Q

Explain the oncogene hypothesis

A

→some genes of cancer causing viruses were mutated forms of the cellular gene not viral genes

→Rous sarcoma viral gene was in fact a host gene that had
been ‘kidnapped’ by the virus (and ‘transformed’ into an oncogene

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7
Q

What is the oncogene characterised by in c-src and how does it exert its effect?

A

→60kDa intracellular tyrosine kinase

→Can phosphorylate cellular proteins and effect growth

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8
Q

What are some agents that can turn proto-oncogenes to oncogenes?

A

→Chemicals
→Physical
→Viruses

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9
Q

What percentage of cancers are caused by oncoviruses?

A

→15-20%

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10
Q

How do DNA viruses exert their cancerous effect?

A

→cause lytic infection leading to the death of the cellular host

→can replicate their DNA along with that of the
host and promote neoplastic transformation

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11
Q

How do RNA viruses exert their cancerous effect?

A 
→Integrate DNA copies of their genomes
into the genome of the host cell 
→these contain transforming oncogenes 
they induce cancerous transformation 
of the host
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12
Q

What are ways oncogenes are activated?

A

→Mutation

→Amplification/duplication

→Translocation

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13
Q

What are the 4 types of proteins involved in the transduction of growth signals?

A

→Growth factors
→Growth factor receptors
→Intracellular signal transducers
→Nuclear transcription factors

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14
Q

Where in the cell is Ras and Raf found?

A

→intracellular

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15
Q

How is Ras and Raf involved in oncogenic transcriptional regulatory proteins?

A

→ERK MAP kinase pathway

→induction of additional genes

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16
Q

Which studies was ras genes identified in?

A

→Harvey sarcoma virus

→Kirsten sarcoma virus

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17
Q

What are Ras proteins?

A

→small GTPases that are normally bound to GDP in a neutral state

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18
Q

What percentage of human cancer involve Ras oncogenic activation?

A

→30%

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19
Q

What mutations lead to Ras oncogenic activation?

A

→Point mutations in codons 12, 13 and 61

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20
Q

What is the amino acid change in Ras oncogenic activation leading to bladder carcinoma?

A

→Glycine to valine

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21
Q

What is the amino acid change in Ras oncogenic activation leading to lung cancer?

A

→Glycine to cysteine

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22
Q

Describe the transduction pathway of Ras proteins

A

→Binding of extracellular growth factor signal

  1. Promotes recruitment of RAS proteins to the receptor complex
  2. Recruitment promotes Ras to exchange GDP (inactive
    Ras) with GTP (active Ras)
4. Activated Ras then initiates the remainder of the 
signalling cascade (mitogen activated protein kinases)
  1. These kinases ultimately phosphorylate targets, such as
    transcription factor to promote expression of genes
    important for growth and survival

Ras hydrolyzes GTP to GDP fairly quickly, turning itself “off”

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23
Q

What does mutation in the RAS protein lead to?

A

→loss of GTPase activity of the RAS protein
normally required to return active RAS to
the inactive RAS GDP

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24
Q

What are the three members of the MYC oncogene family?

A

→ C-MYC,
→MYCN,
→MYCL,
→which encode c-Myc, N-Myc, and L-Myc, respectively

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25
Q

What family do the MYC oncoproteins belong to?

A

→family of transcription factors

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26
Q

What are the major downstream effectors of MYC?

A

→ribosome biogenesis,
→protein translation,
→cell-cycle progression

→metabolism

27
Q

What virus was MYC proteins first identified in?

A

→avian myelocytomatosis virus

28
Q

What does MYC encode?

A

→helix-loop-helix leucine zipper transcription factor

29
Q

What does the helix loop helix zipper dimerise with?

A

→Max, to transactivate gene expression

30
Q

What can be the result of deregulation of MYC?

A

→chromosomal translocation

31
Q

What lymphoma is EBV associated with?

A

→Burkitt’s lymphoma

32
Q

Describe Burkitt’s lymphoma

A

→BL is a high grade lymphoma

→can effect children from the age of 2 to 16 years

33
Q

What do all cases of Burkitt’s lymphoma carry?

A

→chromosomal translocations that place the MYC gene under the regulation of the Ig heavy chain
→c-myc expression is deregulated

34
Q

What is classical African or endemic BL?

A

→children with chronic malaria infections have a reduced resistance to the virus

35
Q

What are the three distinct alternative chromosomal translocations and what do they fuse with?

A

→chromosome 2,14,22

→form one of these three chromosomes is fused to a section of chromosome 8

36
Q

WHat percentage of chronic myelogenous leukaemia carry Philadelphia?

A

→95%

37
Q

What fusion does Philadelphia chromosomes involve?

A

→BCR-ABL fusion protein
→tyrosine kinase activity
of the oncogene ABL is constitutive

38
Q

What is inhibited in Imainib therapy for CML?

A

→tyrosine kinase inhibitor

39
Q

What are some intrinsic tumour suppressor pathways?

A

→RB
→p53
→TAp73

40
Q

What does loss of tumour suppressor gene function require?

A

→requires inactivation of both alleles of the gene

→recessive genes

41
Q

What are three functions of suppressor genes?

A

→regulators of cell cycle checkpoints (e.g. RB1),
→differentiation (e.g. APC)
→DNA repair (e.g. BRCA1)

42
Q

Why does retinoblastoma occur?

A

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

43
Q

What is characteristic about a retinoblastoma eye?

A

→reflect light back in a white colour

44
Q

What are the two forms of retinoblastoma?

A

→familial (40%) and sporadic (60%)

45
Q

Which chromosome is affected in retinoblastoma?

A

→on chromosome 13 (13q14),

the retinoblastoma 1 (Rb1) gene along with BRCA2

46
Q

What is the retinoblastoma two-hit hypothesis?

A

→the loss of both of the functional copies of the Rb gen

47
Q

What are the Rb proteins known as?

A

→pocket proteins

48
Q

What does RB mainly bind to?

A

→E2F transcription factor

49
Q

What is the function of the G1 checkpoint?

A

→leads to the arrest of the cell cycle in response to DNA damage

50
Q

What is a substrate of RB in the cell cycle?

A

→cyclin D

51
Q

WHat is RB phosphorylated by?

A

→Cyclin D and E families and their cdk

52
Q

What happens when RB is hyperphosphorylated?

A

→becomes inactive
→E2F is released and migrates to the nucleus to induce transcription
→progression from G1 to S occurs

53
Q

Which three viruses have been found to destabilise Rb?

A

→Adenovirus - E1A
→Papilloma - E7
→Polyoma – Large T antigen

54
Q

Describe p53 structure?

A

→an amino transactivation domain,
→a central DNA binding domain,
→a tetramerization domain
→a carboxyl regulatory domain

55
Q

How are p53 levels kept low?

A

→by MDM2 protein

56
Q

What is the MDM2 protein function?

A

→a ubiquitin ligase (also an oncogene)-

→targets for proteosome for degradation

57
Q

How does MDM target p53 for proteasome?

A

→MDM2 binds p535 to form a complex in the nucleus

→ modifies the carboxyl terminus of p53 MDM modifies the carboxyl terminus of p53

58
Q

What is the half life of p53?

A

→20 min half life

59
Q

What does phosphorylation of p53 lead to?

A

→disrupts the interaction between it and

MDM2

60
Q

What does PRIMA-1 do to muatant p53?

A

→ Restores mutant p53 by modifying the thiol groups in the core domain of the protein

61
Q

What is nutilin?

A

→a potent MDM2 antagonist

62
Q

How is RITA a p53 therapeutic?

A

→binds to p53
→increases half life of p53,
→prevents export of p53 to proteosome

63
Q

What does inhibition of CRM1 lead to?

A

→nuclear

accumulation of p53

Dysfunction (29 decks)

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