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Cancer Biology > The Evolution of Cancer > Flashcards

The Evolution of Cancer Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

How error prone is asexual division of cells?

A

1-10 mutations per division

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2
Q

How is tumour diversity limited?

A

Mutations alone lead to less variation than sexual reproduction

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3
Q

What 3 factors impact the ability for somatic mutations to evolve?

A

Rate of mutation
Population turnover
Population size

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4
Q

Name 3 similarities between single cell organismal evolution and somatic evolution

A

Asexual reproduction
Large population sizes
Short generation times

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5
Q

What are the key differences between organismal evolution and somatic evolution?

A

Single celled organisms have typically already evolved to peak fitness, therefore most mutations will be deleted
In multicellular organisms, they have evolved for the fitness of the organism, not the cell

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6
Q

What are synonymous mutations (dS)?

A

They do not change the amino acid

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7
Q

What are non-synonymous mutations (dN)?

A

They do change the amino acid

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8
Q

What does it mean if there is more dN than dS?

A

There has been positive selection

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9
Q

What does it mean if there is more dS than dN?

A

There has been negative selection

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10
Q

What drives tumourigenesis?

A

When positive selection occurs (dN is higher than dS)

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11
Q

In terms of selection, what are most cancer mutations?

A

Neutral

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12
Q

Why is metastasis hard to detect?

A

Since we can only detect formed tumours

It may be moving through the blood or lymphatics but isn’t seen

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13
Q

As you get older what do you develop, even in healthy patients?

A

More and bigger clones

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14
Q

What are the 3 types of genetic diversity?

A

Mutation
Copy number changes
Structural aberrations

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15
Q

Give 2 examples of genes which undergo copy number changes in cancer?

A

Myc and Her2

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16
Q

What are the two types of structural aberrations?

A

Chromosomal translocations

Chromosomal deletions

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17
Q

Give an example of a chromosomal translocation

A

9:22 in CML (BCR:Abl)

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18
Q

Give an example of a chromosomal deletion

A

8p in breast and other cancers

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19
Q

What does whole genome copy number changes do?

A

The genes double their genome

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20
Q

What 3 ways can you measure genetic diversity in a tumour?

A

Deep sequencing
Single cell sequencing
Multi-region sequencing

21
Q

What is deep sequencing?

A

Uses next generation sequencing to measure mutant allele frequencies and copy number variations
You take one sample from the tumour

22
Q

What is the issue with deep sequencing?

A

Cannot locate where the different mutations are

23
Q

What is multi-region sequencing?

A

Next generation sequencing of different geographical regions of the tumour

24
Q

Advantage of deep sequencing

A

Cheep and quick

25
Q

What is the issue of multi-region sequencing?

A

Still cannot locate the exact location of the different mutations

26
Q

What is single cell sequencing?

A

Whole-genome amplification from a single cell and sequence it
Means you know which cell it came from
Ideally use lots of cells

27
Q

What is the issue with single cell sequencing?

A

It is expensive, however, is getting cheeper

28
Q

How does intra-tumour heterogeneity help detect evolutionary history?

A

If there is a group of cells, and most of them have one or two mutations which are the same, these are typically the starter mutations

29
Q

What are trunk mutations?

A

The mutations which are present in all of the samples

30
Q

What are branch mutations?

A

The mutations which are present in some but not all cells

31
Q

What are the 4 different models of tumour evolution?

A

Linear evolution
Branched evolution
Neutral evolution
Punctuated evolution

32
Q

What is linear evolution?

A

Where a driver mutation provides a selection advantage and forms mutations in a chain

33
Q

Give the first model of tumour evolution

A

CRC progression

APC mutation -> K-Ras mutation -> Loss DCC -> Loss p53 -> other alterations

34
Q

What is branched evolution?

A

Clones diverge from a common ancestor and these subclones evolve in parallel because they offer increased fitness

35
Q

Why may multiple clones exist?

A

Cooperative interactions

Lack of competition

36
Q

Why do clones coexist?

A

They both have an advantage and therefore they aren’t outcompeting each other

37
Q

What do fewer branches and longer trunks cause?

A

Better chemotherapy outcome

38
Q

How does neoadjuvant chemotherapy effect tumour landscape?

A

Provides the selective pressure for further evolution

39
Q

What is natural evolution?

A

There is an extreme case of branching evolution, but there is no fitness benefit in subclones during the life of the tumour

40
Q

What two pieces of evidence argue against neutral evolution?

A

Subclonal driver mutations

Convergent evolution

41
Q

What is convergent evolution?

A

The same mutation being selected in more than one subclone

42
Q

What is punctuated evolution?

A

Rapid bursts of change followed by stable clonal expansions

Huge genetic diversity allows complex karyotypes to be selected

43
Q

How is punctuated evolution different from linear or branched evolution?

A

Linear and branched are more associated around point mutations
Punctuated evolution is more associated with copy number aberrations or chromosomal structural rearrangements

44
Q

4 factors which can cause punctuated evolution

A

Genome doubling
Failed mitosis
Chromothrypsis
DNA replication error

45
Q

How does genome doubling induce punctuated evolution?

A

Failed cytokineses or endoreplication

46
Q

How does mitosis induce punctuated evolution?

A

Chromosomal gain/ loss/ rearrangement

47
Q

How does chromothrypsis induce punctuated evolution?

A

Chromosomes are shattered and repaired in a random order

48
Q

What is lower numbers of copy numbers associated with?

A

Disease free survival

A better prognosis

Cancer Biology (13 decks)

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