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My MCBG > DNA Repair And Cancer > Flashcards

DNA Repair And Cancer Flashcards

1
Q

Ataxia Telangiectasia

A

Neurodegenerative disease of cerebellum
Normal DNA Repair Pathway disrupted
Increased risk of cancer (radiation sensitivity0

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2
Q

Types of DNA Damage/Breaks

A

Single Stranded Breaks
Double Stranded Breaks

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3
Q

Single stranded breaks repairability

A

Easier too repair than double stranded breaks
Template strand still present to make complementary copy

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4
Q

Double stranded breaks repairability

A

Harder to repair
Template strand not present to repair coding strand

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5
Q

2 Sources for DNA damage

A

-Exogenous
-Endogenous

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6
Q

Exogenous sources of DNA Damage

A

-Ionising radiation (X-Rays)
-Alkylating agents (Add alkyl group to base G meaning correct bonding can’t happen strand. Breaks
-Mutagenic chemicals
-Anti-cancer drugs
-Free radicals

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7
Q

2 Types of DNA damage that lead to need for Base Excision Repair and Nucleotide Excision Repair Respectively

A

-Deamination ( Cytosine converted to Uracil)
-Dimerisation (Forms between 2 similar bases, Thymine when exposed to UV light)

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8
Q

How can DNA Replication errors damage DNA?

A

Wrong DNA nucleotide/base pairs may be incorporated by DNA Polymerase enzyme

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9
Q

Replication fork

A

The point at which DNA Helicase has unwound the DNA and DNA Polymerase has bound to start incorporating new nucleotides

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10
Q

DNA Exonuclease

A

Proof reads newly replicated DNA
Cuts out incorrect base pairs at the end of the DNA strands

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11
Q

Fork Slippage

A

When wrong number of repetitive sequence is copied (Extra nucleotide added onto new strand or template strand loops out so 1 nucleotide is missing in new strand)

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12
Q

Diseases caused by fork slippage

A

Huntington Disease (Autosomal DOminant Inheritance)
Fragile X Syndrome

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13
Q

Huntington’s disease

A

Polyglutamine (CAG) repeats in protein too many times triggering Huntingtons

CAG repeats cause neural degeneration of Basal Ganglia affecting movement

Short Tandem Repeats

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14
Q

DNA Replication stress

A

Inefficient replication where rep fork slows, stalls , breaks

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15
Q

General DNA Damage response mechanism

A

Damage DNA activates signal
Detected by sensors
Sensors activated transducers
Transducers activate effectors which try and correct the damage

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16
Q

G2 Checkpoint importance

A

Temporarily halts cell to check if DNA has been replicated correctly and make any repairs

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17
Q

Types of single strand break repair

A

-Nucelotide excision repair
-Base excision repair
-Mismatch repair

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18
Q

Base Excision Repair Process

A

Deamination of C to U
Base removed from nucleotide
Baseless nucleotide removed from DNA Backbone
DNA Polymerase fills hole with correct nuclreotide
Gap sealed by DNA Ligase

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19
Q

Nucleotide Excision Repair (Single Stranded break repairs) Main Problem that it tries to repair and the process

A

UV forming a Thymine dimer
Surrounding DNA opens to form bubble
Enzymes cut out damaged region from bubble
Polymerase replaces excised DNA
Lipase seals backbone

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20
Q

Mismatch repair (singles stranded breaks)

A

MIsmatched base detected e.g G to T
Mispaired nucelotide and its neighbours cut out from new strand
Polymerase replaces new strand
Lipase seals gap in DNA Backbone

21
Q

The 2 Double Strand Break Repair mechanisms

A

-Non-Homologous End Joining
-Homology-directed repair

22
Q

What is the process of Non-Homologus End Joining (Double Stranded break repair)?

What is the problem with it?

A

Proteins recognise and bind to broken strands
Other proteins remove extra nucleotides that may be damaged (resection)
DNA Lipase seals DNA backbone (phosphodiester bonds)

Repaired DNA might not be identical to original DNA

23
Q

Homolgy Directed repair (Double strand break repair)

A

Protein complex removes DNA on either side of break (RESECTION)
Heteroduplex forms
D loop forms
Polymerase and ligase repairs the break

24
Q

What DNA repair process fails causing Lynch Syndrome?

A

Mutations in mismatch repair genes
Autosomal dominant inheritance
High risk of - colorectal, endometrial, gastric and ovarian cancer

25
Q

Xeroderma Pigmentosa (XP)

A

Inherited condition
Genes involved in producing key proteins needed in DNA Repair pathway of Nucleotide Excision Repair
People very vulnerable to UV radiation (UV Causes Thymine dimer to form)

26
Q

Xeroderma Pigmentosa cancer risk factor

A

Cells unable to repair damaged DNA so cancerous cells more likely to proliferate

27
Q

Intratumour Heterogenity

A

Not all cells in tumour are the same
Different sections of cells in tumour called sub clones

28
Q

Intertumour heterogenity

A

Differences between different tumours

29
Q

Chemotherapy effectiveness against cancer

A

Tumours have intratumour heterogeneity
Chemotherapy may work effectively against all but 1 of the sub clones (so tumour not fully killed)

Chemo may cause a sub clones to mutate become a drug resistant sub clone (could be more aggressive)

30
Q

Problem with Non-Homologous End Joining Repair

A

If more than 2 DNA ends are near each other wrong ends could be joined together

Short sequence of DNA often lost from broken ends changing gene sequence

31
Q

Genetic Redundancy

A

More than 1 gene has the same function
E.g: Gene A and Gene B = same

32
Q

Synthetic lethality Strategies

A

Utilise Genetic Redundancy to target only cancer cells

33
Q

Synthetic lethality strategy mechanism

A

Chemicals in chemo target the healthy gene to destroy the healthy gene. The healthy cells have other healthy gene so will be fine. Cancerous cells will only have mutated gene left so cell is undergoes apoptosis

34
Q

PARP inhibitors and breast cancer

A

Utilises Genetic redundancy
Either BRCA1or BRCA2 is mutated so the PARP inhibitor targets the healthy BRCA gene so cancer cells enter apoptosis

35
Q

What type of failed DNA repair mechanism causes Ataxia Telangiectasia?

A

Failed Homolgy Directed repair (double strand repair)

Patients sensitive to UV

36
Q

What is the cell cycle?

A

A series of events that a cell undergoes while it grows and divides

37
Q

Interphase

A

G1, S, G2
Where a cell spends most of It’s time

38
Q

G1 (Growth Stage 1)

A

Cell prepares for DNA Replication
Grows in size and makes more organelles, enzymes and proteins needed for new cells

39
Q

S (synthesis)

A

Where DNA replication takes place
Ensures 46 Pairs of chromosomes are present/96 chromatids so when mitosis carried out cells are diploid

40
Q

G2 (Growth stage 2)

A

More growth
Cell forms material to form the spindle

41
Q

Mitosis, Meiosis

A

Mitosis produces 2 genetically identical diploid daughter cells

Meiosis produce 4 non genetically identical haploid daughter cells

42
Q

Cytokinesis

A

Cleaving of a cell to produce 2 new separate cells

43
Q

Cell cycle stages

A

G1, S, G2, Mitosis/Meiosis, Cytokinesis

44
Q

Cell cycle checkpoints

A

Regulate the stages of the cell cycle

45
Q

3 Cell cycle checkpoints

A

G1 Checkpoint
G2 Checkpoint
M (Metaphase) Checkpoint

46
Q

G1 Checkpoint

A

Are conditions appropriate for replication (S/SYnthesis)

47
Q

G2 Checkpoint

A

Checks if DNA has been correctly replicated

48
Q

M (Metaphase checkpoint)

A

Checks if spindle fibres correctly join at centromeres of chromosomes

My MCBG (2 decks)

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