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Cancer Lectures > Epigenetic Mechanisms in Cancer > Flashcards

Epigenetic Mechanisms in Cancer Flashcards

1
Q

Define genetics

A

The study of the genetic material which determine the properties of inheritance and phenotype

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2
Q

Define epigenetics

A

The study of modifications that alter phenotype without altering the genotype

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3
Q

If there is low DNA methylation and histone acetylation, is the gene turned on or off?

A

On

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4
Q

If there is high DNA methylation and H3-K27me3, is the gene turned on or off?

A

Off

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5
Q

If there is low DNA methylation and histone acetylation, is the the gene turned on or off?

A

On

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6
Q

What is the best described epigenetic mechanism?

A

DNA methylation at CpG dinucleotides

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7
Q

What is DNA methylation regulated by?

A

Dnmt1

Dnmt3a/3b

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8
Q

All cells in a organism are genetically identical so why can’t liver cells for example become stem cells again, or skin cells?

A

Due to cell identity

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9
Q

Define cell identity

A

A unique transcriptional programme which is locked into place by epigenetic modifications

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10
Q

There is parallel usage of the terms epigenome and epigenetic code, but what are these terms used to describe?

A

The set of epigenetic features that create different phenotypes in different cells

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11
Q

Are epigenetics heritable?

A

Yes over rounds of cell division and sometimes transgenerationally

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12
Q

In the context of epigenetics, what does epi- imply?

A

Features that are ‘on top of’ or ‘in addition to’ genetics

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13
Q

How can DNA be epigenetically modified?

A

By methylation

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14
Q

How can chromatin be epigenetically modified?

A 
By:
Phosphorylation
Acetylation
Methylation
Ubiquitination
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15
Q

Where does DNA methylation occur in prokaryotes?

A

On adenine residues

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16
Q

Where does DNA methylation occur in eukaryotes?

A

On cytosine residues

Only at CpG dinucleotides

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17
Q

What is the principle role of DNA methylation?

A

To switch off transcription long-term

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18
Q

What are the two different kinds of DNA methyltransferase?

A

Replication dependent: Dnmt1

De novo: Dnmt3a/3b

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19
Q

What does DNA methylation maintain?

A

Genomic stability of transposons, endogenous retroviruses, repetitive elements etc.

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20
Q

What does DNA methylation do to junk DNA?

A

It keeps the junk DNA quiet

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21
Q

How does the cytosine analogue 5-azacytidine act as evidence that DNA methylation maintains genomic instability?

A

It cannot be methylated and when added to cells it dilutes DNA methylation through each round of cell division. Loss of DNA methylation leads to reactivation of endogenous retroviruses

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22
Q

How do Dnmt1 knockout mice act as evidence that DNA methylation maintains genomic instability?

A

Mice containing a mutation in the Dnmt1 gene retain only 10% of normal activity and develop aggressive T cell tumours due to trisomy of chromosome 15

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23
Q

Which is a common trait of cancer cells, hypermethylation or hypomethylation of DNA?

A

Hypomethylation

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24
Q

How does DNA methylation lead to long-term silencing?

A

It functions by recruiting histone modifying enzymes

25
Q

In which cell types does the conversion of 5-methyl cytosine to 5-hydroxymethyl cytosine predominantly happen?

A

In the brain and stem cells

26
Q

DNA demethylation does NOT generally occur in mammalian cells. Give one of the very few specific exceptions to this rule

A

Except in embryonic development

27
Q

What are the two theories for why 5-methyl cytosine is converted to 5-hydroxymethyl cytosine?

A

Theory 1: the product prevents the binding of methylated-DNA binding proteins
Theory 2: the product is a stable intermediate in the DNA demethylation process

28
Q

What are histone tails thought to interact with?

A

The PO4- backbone of DNA

29
Q

How is the eukaryotic genome packaged?

A

Into chromatin

30
Q

Describe the transcriptional status of relaxed and condensed chromatin

A

Relaxed is transcriptionally active

Condensed is transcriptionally silent

31
Q

Describe the structure of a histone molecule

A

Have a globular domain and an unstructured, long N-terminal tail rich in Lys+ and Arg+

32
Q

Describe the structure of a nucleosome

A

147 base pairs of DNA wrapped twice around a histone octamer

33
Q

What type of polymer is a histone?

A 
An octamer consisting of 8 monomers
2x H2A
2x H2B
2x H3
2x H4
34
Q

What is the histone code hypothesis?

A

Histone modifications associated with a gene predict whether a gene is on, off, or might be on at sometime in the future

35
Q

What does Lys acetylation in a histone tail suggest about the transcription status of the gene?

A

The gene is always on

36
Q

What does Lys methylation in a histone tail suggest about the transcription status of the gene?

A

It is context dependent

37
Q

What does Lys methylation of H3K4 in a histone tail suggest about the transcription status of the gene?

A

It is on

38
Q

What does Lys methylation of H3K27 in a histone tail suggest about the transcription status of the gene?

A

It is off

39
Q

What does a healthy epigenome suggest about the genome?

A

That it is healthy

40
Q

Where might DNA methylation be low?

A

Where there is euchromatin

41
Q

Where might DNA methylation be high?

A

Where there is heterochromatin

42
Q

What has ChIP-seq been used to monitor in respect to epigenetics?

A

Histone modifications

43
Q

What families can post-translational modifications be sorted into?

A

Readers, writers, erasers

44
Q

Where is euchromatin found?

A

Active genes

Recombination sites

45
Q

Where is heterochromatin found?

A 
Centromeres
Telomeres
Repetitive elements
Tissue specific genes
Intergenic regions
Inactive X-chromosomes
46
Q

What is ChIP-Seq?

A

ChIP and next generation sequencing

47
Q

What is the ENCODE project?

A

The encyclopedia of DNA elements

48
Q

How many data sets are there in the ENCODE project?

A

1640

49
Q

How many different cell types are there in the ENCODE project?

A

147

50
Q

There are a number of different DNA-binding proteins and a number of RNA polymerase components in 72 cell types using ChIP-Seq. How many are there?

A

119

51
Q

How is epigenetics altered in cancer?

A

Massive global genomic hypomethylation
Transcriptional silencing of tumour suppressor genes by CpG island promoter hypermethylation, e.g. p16INK4a, p14ARF etc.
Human tumours undergo an overall loss of H4K16Ac and H4K20me3

52
Q

What are patients with germline mutations in DNMT3b-ICF known to have?

A

Numerous chromosome aberrations

53
Q

What does ICF stand for?

A

Immunodeficiency-centromeric region instability-facial anomalies

54
Q

Give examples of classical autoimmune diseases that are characterised by massive genomic hypomethylation

A

Systemic lupus erythematosus

Rheumatoid arthritis

55
Q

Most human disease have an epigenetic cause. What happens to the perfect control of our cells by DNA methylation, histone modifications, chromatin-remodelling and microRNAs in sick cells?

A

The control becomes dramatically distorted

56
Q

What are tumour suppressors inactivated by?

A

DNA hyper-methylation

57
Q

Histone modifications are often described as epigenetic, but what might they just reflect?

A

Transcription

58
Q

Summarise the significant alterations to the epigenome in cancer cells

A

Global genomic hypomethylation with hypermethylation of tumour suppressor promoters, e.g. p16

Cancer Lectures (24 decks)

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