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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
What is a tumour suppressor gene
A protein that stops the growth of tumours by stopping the cell cycle
26
In cancer what can happen to tumour supressor genes
Function can be lost
27
For tumour supressor genes to lose their function how many alleles does it have to lose
2 alleles (reccessive)
28
What are oncogenes
Positive regulators of cell growth (opposite of tumour supressor genes)
29
When are oncogenes activated
When their Regulator controls weakens
30
How many alleles of oncogenes have to be lost/mutated for oncogene to become active
1 allele (dominant)
31
Overall in terms of tumour supressor genes and oncogenes what happens to them in cancer
Tumour suppressor gene is silenced | Oncogenes is activated
32
What are the 6 hallmarks of cancer
1) sustaining proliferative signalling 2) evading growth suppressors 3) resisting cell death 4) enabling replicative immortality 5) inducing angiogenesis 6) acitvating invasion and metastasis
33
What are the hallmarks of cancer
Hallmarks that allow tumour growth
34
What is hallmark 1:sustaining proliferative signalling about
Gaining independence from the external signals which provide ability for uncontrolled proliferation
35
What happens in normal cells when there are extracellular signals
Intracellular pathways become activated
36
How do cancer cells acquire hallmark 1
Altering the signalling cascade
37
What signalling cascade does cancer cells alter
Extracellular growth signal Transmembrane transducer of growth signal Intracellular circuits that translate the signals
38
In normal cells where doe growth factors bind to
Growth factor receptors in the plasma membrane of the cell
39
When the growth factor binds to its growth factor receptor what becomes activated
Intracellular signals
40
In cancer what can happen to the receptor
Mutated
41
If the growth factor receptor is mutated what can it lead to
Ligand independent signalling
42
What is ligand independent signalling
Activation of intracellular signals without the need of a ligand binding to the receptor
43
If the receptor is mutated what is not required
Extracellular growth signal
44
What is the other way the cancer cell can acitvate its receptor
Secrete its own growth factor
45
What is the secretion of growth factor from the cancer cell called
Autocrine signalling
46
Which major protein is involved in the intracellular signal i.e the signal created when the receptor is activated
Ras protein
47
What can happen to ras protein in cancer that changes the intracellular signal
Become mutated
48
What is hallmark 2: evading growth supressors about
Silencing tumour suppressor genes
49
Which tumour suppressor gene is likely to be suppressed
Prb
50
Where does prb usually act
In the cell cycle in the restriction point between g1 to s phase
51
In cancer what happens to prb
Mutated
52
What is hallmark 3: resisting cell death about
Downregulating apoptosis
53
In a normal cell what happens to a cell if there is damage
Apoptosis
54
Which common protein carries out apoptosis
P53
55
In cancer what happens to p53
Mutated or downregulated
56
What is the action of P53
DNA repair Cell cycle arrest Block angiogenesis Apoptosis
57
What activates p53
``` UV radiation Lack of nucleotides Ionizing radiation Oncogene signalling Hypoxia Blockage of transcription ```
58
What is hallmark 4: enabling replicative immortality about
Limitless replicative potential
59
In a normal cells what does DNA have in terms of replication
A limited potential to replicate
60
After the normal cell dna replicates where does the cell leave and into
Leaves the cell cycle and enters senescence
61
What regulates the cell leaving cell cycle and entering senescence
Telomeres
62
Where are telomeres found
At the tip of DNA
63
What are telomeres
6 base sequence that prevent/protect the chromosome from deterioration or fusion with a neighbour chromosome
64
What does lack of telomeres lead to
Chromosomal fusion and apoptosis
65
What is the role of the enzyme telomerase
Add repeats to DNA
66
What happens in cancer cells to escape senescence
Increase in levels of enzyme telomerase
67
What is hallmark 5: inducing angiogenesis about
Formation of new blood vessels around the cancer cells
68
What is angiogenesis important
For supplying oxygen and nutrients and taking waste away from growing tumour cells
69
What simulates angiogenesis in cancer
Angiotensin switch: Dow regulation of angiogenic inhibitors | Increase in pro-angiogenic induces
70
What is hallmark 6: activating invasion and metastasis about
Invading other sites in the body
71
What does hallmark 6 cause in cancer cells
Epithelial to mesenchymal transition | Change in expression of adhesion receptors
72
How many cells are able to metastases the secondary site
A few cells
73
What are the other 2 emerging hallmarks
Deregulating cellular energetic | Avoiding immune destruction
74
What are the 2 hallmarks that enable characteristic
Genome instability and mutation | Tumour promoting inflammation
75
What do hallmarks of enabling characteristic give rise to
Fast life Or Slow life history selection
76
What type of environment gives a fast like history selection
Unstable environments
77
What type of environment gives rise to slow life
Stable environment with limited resources
78
Which hallmarks are associated with fast life history selection
``` Evading growth suppressor Activating invasion and metastasis Sustaining proliferative signal Genome instability and mutation Enabling replicative immortality ```
79
Which hallmarks are associated with slow life history selection
Inducing angiogenesis Evading immune destruction Resisting cell death
80
Which hallmarks are associated with both fast and slow life history selection
Deregulating cellular energetic | Tumour promoting inflammation

CAN (25 decks)

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