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CAN > L01: What Is Cancer > Flashcards

L01: What Is Cancer Flashcards

1
Q

What is the definition of cancer

A

Uncontrolled growth of abnormal cells in a tissue, invasive and spreading

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2
Q

Is there a difference between malignant and benign tumours

A

Yes

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3
Q

What do majority of cancer originate from

A

Epithelium

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4
Q

What is the difference between benign and malignant tumour

A

Benign do not spread to other tissues

Malignant metastases to different organs

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5
Q

What are tumours that are in the epithelium called

A

Squamous cell carcinoma and adenocarcinoma

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6
Q

What does sacromas arise from

A

Mesenchymal cells

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7
Q

What does leukaemia and lymphoid myeloid tumours arise from

A

Hamatopoetic tissue and immune system

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8
Q

What does neuro ectodermal tumours arise from

A

Central and peripheral nervous sytem

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9
Q

What is the first significant mutation that lead to dramatic change in the cell called

A

Gate keeping mutation / initiation driving mutation

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10
Q

What are the 2 places mutations can occur to cause cancer

A

1) Germ line

2) somatic cells

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11
Q

What do normal genes that are not mutated control

A 
Growth 
Passing signals form outside the cell across cytoplasm to the nucleus 
Apoptosis 
Cell cycle 
Stemness 
DNA repair
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12
Q

What are the 3 ways mutations can occur

A

Copying errors i.e replication errors
Spontaneous depurination
Exposure to agents e.g uv light

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13
Q

What is a tumour that originates from one type of cell called

A

Monoclonal

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14
Q

What is a tumour that originates from a collection of different cell types called

A

Polyclonal tumour

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15
Q

Overall are tumours monoclonal or polyclonal as research has confirmed

A

Monoclonal

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16
Q

Name 2 examples of monoclonal cancer

A

Breast cancer

Colon cancer

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17
Q

What can happen to monoclonal cells that leads to them becoming heterogenous

A

Continues mutations of alleles due to genetic instability

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18
Q

How many genetic steps does cancer go through

A

3 stages

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19
Q

What are the 3 stages of the genetic steps for forming cancer known as

A

Stage 1: initiation
Stage 2: clonal expansion
Stage 3: introduction to foreign micro environments

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20
Q

What occurs in stage 1 (initiation)

A

Normal cells have an initiating mutation

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21
Q

If a initiating mutation occurs in a cell what usually occurs to the cell

A

Apoptosis or senescence

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22
Q

If apoptosis or senescence of a cell with a initiating mutation fails what happens to the cell

A

1) Escapes from immunosupression and senescence

2) continuous to fixation of initiating mutation due to its survival

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23
Q

What happens in stage 2 (clonal expansion)

A

1) The cell with the initiating mutation divides to form population
2) the population grows and requires additional driver mutations that increase the clonal heterogeneity

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24
Q

What occurs in stage 3 (intro to foreign micro environments)

A

1) ongoing clonal expansion leads to a population fo cells breaking the basement membrane so it enters the stroma
2) genetic events signals are produced by the stroma
3) immune cells infiltrate that provide further stimulation by secreting growth factors
4) growth factors provide selective forces that shape the tumour
5) some cells after breaking basement membrane go onto metastasis

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25
Q

What is a tumour suppressor gene

A

A protein that stops the growth of tumours by stopping the cell cycle

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26
Q

In cancer what can happen to tumour supressor genes

A

Function can be lost

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27
Q

For tumour supressor genes to lose their function how many alleles does it have to lose

A

2 alleles (reccessive)

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28
Q

What are oncogenes

A

Positive regulators of cell growth (opposite of tumour supressor genes)

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29
Q

When are oncogenes activated

A

When their Regulator controls weakens

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30
Q

How many alleles of oncogenes have to be lost/mutated for oncogene to become active

A

1 allele (dominant)

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31
Q

Overall in terms of tumour supressor genes and oncogenes what happens to them in cancer

A

Tumour suppressor gene is silenced

Oncogenes is activated

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32
Q

What are the 6 hallmarks of cancer

A

1) sustaining proliferative signalling
2) evading growth suppressors
3) resisting cell death
4) enabling replicative immortality
5) inducing angiogenesis
6) acitvating invasion and metastasis

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33
Q

What are the hallmarks of cancer

A

Hallmarks that allow tumour growth

34
Q

What is hallmark 1:sustaining proliferative signalling about

A

Gaining independence from the external signals which provide ability for uncontrolled proliferation

35
Q

What happens in normal cells when there are extracellular signals

A

Intracellular pathways become activated

36
Q

How do cancer cells acquire hallmark 1

A

Altering the signalling cascade

37
Q

What signalling cascade does cancer cells alter

A

Extracellular growth signal
Transmembrane transducer of growth signal
Intracellular circuits that translate the signals

38
Q

In normal cells where doe growth factors bind to

A

Growth factor receptors in the plasma membrane of the cell

39
Q

When the growth factor binds to its growth factor receptor what becomes activated

A

Intracellular signals

40
Q

In cancer what can happen to the receptor

A

Mutated

41
Q

If the growth factor receptor is mutated what can it lead to

A

Ligand independent signalling

42
Q

What is ligand independent signalling

A

Activation of intracellular signals without the need of a ligand binding to the receptor

43
Q

If the receptor is mutated what is not required

A

Extracellular growth signal

44
Q

What is the other way the cancer cell can acitvate its receptor

A

Secrete its own growth factor

45
Q

What is the secretion of growth factor from the cancer cell called

A

Autocrine signalling

46
Q

Which major protein is involved in the intracellular signal i.e the signal created when the receptor is activated

A

Ras protein

47
Q

What can happen to ras protein in cancer that changes the intracellular signal

A

Become mutated

48
Q

What is hallmark 2: evading growth supressors about

A

Silencing tumour suppressor genes

49
Q

Which tumour suppressor gene is likely to be suppressed

A

Prb

50
Q

Where does prb usually act

A

In the cell cycle in the restriction point between g1 to s phase

51
Q

In cancer what happens to prb

A

Mutated

52
Q

What is hallmark 3: resisting cell death about

A

Downregulating apoptosis

53
Q

In a normal cell what happens to a cell if there is damage

A

Apoptosis

54
Q

Which common protein carries out apoptosis

A

P53

55
Q

In cancer what happens to p53

A

Mutated or downregulated

56
Q

What is the action of P53

A

DNA repair
Cell cycle arrest
Block angiogenesis
Apoptosis

57
Q

What activates p53

A 
UV radiation 
Lack of nucleotides 
Ionizing radiation 
Oncogene signalling 
Hypoxia 
Blockage of transcription
58
Q

What is hallmark 4: enabling replicative immortality about

A

Limitless replicative potential

59
Q

In a normal cells what does DNA have in terms of replication

A

A limited potential to replicate

60
Q

After the normal cell dna replicates where does the cell leave and into

A

Leaves the cell cycle and enters senescence

61
Q

What regulates the cell leaving cell cycle and entering senescence

A

Telomeres

62
Q

Where are telomeres found

A

At the tip of DNA

63
Q

What are telomeres

A

6 base sequence that prevent/protect the chromosome from deterioration or fusion with a neighbour chromosome

64
Q

What does lack of telomeres lead to

A

Chromosomal fusion and apoptosis

65
Q

What is the role of the enzyme telomerase

A

Add repeats to DNA

66
Q

What happens in cancer cells to escape senescence

A

Increase in levels of enzyme telomerase

67
Q

What is hallmark 5: inducing angiogenesis about

A

Formation of new blood vessels around the cancer cells

68
Q

What is angiogenesis important

A

For supplying oxygen and nutrients and taking waste away from growing tumour cells

69
Q

What simulates angiogenesis in cancer

A

Angiotensin switch: Dow regulation of angiogenic inhibitors

Increase in pro-angiogenic induces

70
Q

What is hallmark 6: activating invasion and metastasis about

A

Invading other sites in the body

71
Q

What does hallmark 6 cause in cancer cells

A

Epithelial to mesenchymal transition

Change in expression of adhesion receptors

72
Q

How many cells are able to metastases the secondary site

A

A few cells

73
Q

What are the other 2 emerging hallmarks

A

Deregulating cellular energetic

Avoiding immune destruction

74
Q

What are the 2 hallmarks that enable characteristic

A

Genome instability and mutation

Tumour promoting inflammation

75
Q

What do hallmarks of enabling characteristic give rise to

A

Fast life
Or
Slow life history selection

76
Q

What type of environment gives a fast like history selection

A

Unstable environments

77
Q

What type of environment gives rise to slow life

A

Stable environment with limited resources

78
Q

Which hallmarks are associated with fast life history selection

A 
Evading growth suppressor 
Activating invasion and metastasis
Sustaining proliferative signal 
Genome instability and mutation 
Enabling replicative immortality
79
Q

Which hallmarks are associated with slow life history selection

A

Inducing angiogenesis
Evading immune destruction
Resisting cell death

80
Q

Which hallmarks are associated with both fast and slow life history selection

A

Deregulating cellular energetic

Tumour promoting inflammation

CAN (25 decks)

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