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Cancer Y2 > Oncogenes and Tumour Suppressor Genes > Flashcards

Oncogenes and Tumour Suppressor Genes Flashcards

1
Q

What are the 6 hallmarks of cancer

A
  • Disregard of signals to stop proliferating
  • Disregard of signals to differentiate
  • Capacity for sustained proliferation
  • Evasion of apoptosis
  • Ability to invade
  • Ability to promote angiogenesis
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2
Q

What does a cell cycle checkpoint do and why

A

Arrest growth to ensure genetic fidelity by allowing the cell to check that everything is okay

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3
Q

What can permanent activation of a cyclin do

A

Drive a cell through a cell cycle checkpoint

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4
Q

What is the role of a proto-oncogene (7)

A

Code for essential proteins involved in the maintenance of cell growth, division and differentiation such as:

  • Growth factors
  • Growth factor receptors
  • Intracellular transducers (signaling proteins)
  • Intracellular receptors
  • Transcription factors
  • Cell cycle regulatory proteins
  • Cell death regulators
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5
Q

What is the difference between a proto-oncogene and an oncogene

A

A single mutation which means the protein product no longer responds to control influences, can be single base mutation

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6
Q

Give 4 examples of proto-oncogenes that can be converted to oncogenes

A

SRC, MYC, Ki-RAS, Ha-RAS

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7
Q

What 4 mechanisms can convert a proto-oncogene to oncogenes

A

Mutation in the coding sequence, gene amplification, chromosomal translocation, insertional mutagenesis

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8
Q

What is gene amplification and what does it cause

A

Overproduction of normal protein because of multiple gene copies

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9
Q

What does a mutation in the coding sequence cause, what are examples of mutations in the coding sequence

A

Point mutations or deletions, causes an aberrantly active protein

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10
Q

What is a chromosomal translocation and what does it do? Give an example of a disease it causes

A

Chimaeric genes, its a strong enhancer that increases normal protein levels

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11
Q

What is an insertional mutagenesis? How can you get one? Example

A

A fusion to actively transcribed genes that overproduces proteins or a fusion protein that is hyperactive, can get one through viral infection, e.g. Philadelphia chromosome

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12
Q

How many copies of a proto-oncogene need to be damaged to give oncogenic properties

A

1

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13
Q

SRC: function, mechanism of activation, location, associated cancers?

A

Tyrosine kinase, over expression/C terminal deletion, cytoplasmic, breast/colon/lung

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14
Q

MYC: function, mechanism of activation, location, associated cancers?

A

Transcription factor, translocation, nuclear, Burkitt’s lymphoma

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15
Q

JUN: function, mechanism of activation, location, associated cancers?

A

Transcription factor, over expression/deletion, nuclear, lung

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16
Q

Ha-RAS: function, mechanism of activation, location, associated cancers?

A

G-protein, point mutation, cytoplasmic, bladder

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17
Q

Ki-RAS: function, mechanism of activation, location, associated cancers?

A

G-protein, point mutation, cytoplasmic, colon/lung

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18
Q

How does RAS become activated and deactivated

A

Binds GTP to make RAS active, then dephosphorylation to GDP makes it inactive

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19
Q

What cell activity are RAS proteins central to

A

MAPK cascade (mitogen activated protein kinase)

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20
Q

Which tumour are RAS oncogenes common in and rare in

A

Rare in breast cancer and found in 95% of pancreatic cancers

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21
Q

Which codon mutations inhibit GTP hydrolysis

A

12 (Gly), 59 (Ala) and 61 (Gln)

22
Q

What is different about proto-oncogenes and tumour suppressor genes? What is the exception

A

Mutations are required in both copies of TSG to promote oncogenic activity rather than the one, p53 gene is the exception

23
Q

What features are there of inherited cancers (6)

A
  • Family history of related cancers
  • Unusually early age of onset
  • Bilateral tumours in paired organs
  • Synchronous or successive tumours
  • Tumours in different organ systems in same individual
  • Mutations inherited through the germline
24
Q

What mutation incurs retinoblastoma (gene, type of gene, chromosome)

A

RB1 TSG mutation on 13q14

25
Q

How can you tell the difference between sporadic retinoblastoma and hereditary

A 
Sporadic = usually only one eye
Hereditary = can be unilateral, bilateral or multifocal
26
Q

What does RB1 encode

A

A nuclear protein that is involved in regulating cell cycle in developing retinal cells

27
Q

What are the functional classes of TSGs (8)

A
  • Regulate cell proliferation
  • Maintain cellular integrity
  • Regulate cell growth
  • Regulate the cell cycle
  • Nuclear transcription factors
  • DNA repair proteins
  • Cell adhesion molecules
  • Cell death regulators
28
Q

What is Knudsons 2 hit hypothesis regarding inherited and sporadic TSG cancer

A

Inherited TSG cancers usually mean that people are born with one mutant TSG allele and acquire the other one, sporadic means they acquire both e.g. through smoking

29
Q

p53: function, location, associated cancers?

A

Cell cycle regulator, nuclear, many (colon, breast, bladder, lung, etc)

30
Q

BRCA1: function, location, associated cancers?

A

Cell cycle regulator, nuclear, breast, ovarian and prostate

31
Q

PTEN: function, location, associated cancers?

A

Tyrosine and lipid phosphatase, cytoplasmic, prostate, glioblastoma

32
Q

APC: function, location, associated cancers?

A

Cell signalling, cytoplasmic, colon

33
Q

p16-INK4a: function, location, associated cancers?

A

Cell cycle regulator, nuclear, colon and others

34
Q

MLH1: function, location, associated cancers?

A

Mismatch repair, nuclear, colon, gastric

35
Q

What is special about p53 (bad thing)

A

A mutation in a single copy is sufficient to get dysregulation of activity

36
Q

What does p53 guard (list) (6)

A 
Metabolic homeostasis
Antioxidant defence
DNA repair
Growth Arrest
Senescence
Apoptosis
37
Q

What activates/stabilises p53?Examples?

A

DNA damaging agents, e.g. chemicals or UV

38
Q

When activated what does p53 activate (3)

A

p21 (Waf1), MDM2 (hDM2), BAX

39
Q

What p21(Waf1) do

A

Binds and inhibits cyclin dependent kinases and cyclins to arrest cell cycle

40
Q

What MDM2 (hDM2) do

A

Binds to and inactivates p53 (autoregulatory loop)

41
Q

What BAX do

A

Promotes apoptosis

42
Q

What family does BAX belong to

A

BCl-2

43
Q

What is the function of p53 (words)

A

Tries to repair cells that have undergone damage- if this doesn’t happen, p53 commits the cell to apoptosis

44
Q

What happens to cells in which both the cell and p53 is damaged

A

Division goes forward- these cells are the ones that often continue to cancer, but sometimes to die because damage is too great

45
Q

What is the most commonly mutated gene in human cancer? How many cancers is this present in

A

p53, over 50%

46
Q

What domain do 98% of p53 transforming mutations occur

A

DNA binding domain

47
Q

What mutation and which chromosome results in APC, what does the mutation do

A

Deletion in 5q21, results in loss of APC TSG gene

48
Q

What does APC gene do, what does it control?

A

Involved in inhibiting transcriptional up regulation in the nucleus, it controls beta catenin

49
Q

What does beta catenin do

A

Drives proliferation via the upregulation of transcription

50
Q

What disease does loss of APC gene result in

A

FAP - familial adenomatous polyposis

51
Q

Differences between oncogenes and TSGs (6)

A

Gene active in tumour vs inactive in tumour
Specific translocations/point mutations vs deletions or mutations
Mutations rarely hereditary vs mutations can be inherited
Dominant at cell level vs recessive at cell level
Broad tissue specificity vs considerable tumour specificity
Leukaemia and lymphoma vs solid tumours

52
Q

Describe the development of colorectal cancer, from normal epithelium to metastasis and the three mutations/stages in between

A

normal epithelium -> APC mutation -> hyper proliferative epithelium -> Ki-Ras mutation -> adenoma -> p53 -> carcinoma -> metastasis

Cancer Y2 (15 decks)

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