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Cancer Biology > Chapter Two > Flashcards

Chapter Two Flashcards

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1
Q

What does accumulation of mutations in DNA lead to?

A

carcinogenesis

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2
Q

What is a Kataegis?

A

It is a localized area of hypermutation in the genome.

Ex. Maybe when replication was taking place DNA Poly kept making horrible mistakes.

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3
Q

What is chromothripsis?

A

A cellular crisis when a singular cell shatters chromosomes (because of many erros) that results in many genomic rearrangements.

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4
Q

What is the regulatory region of a gene?

A

The region 5’ end of a gene that contains the promoter region and enhancers that are further from the coding region.

Left to Right just like in genetics.

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5
Q

What is the coding region of a gene?

A

The actual meat of the gene where nucleotides are transcribed into RNA usually downstream of the promoter.

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6
Q

How does the promoter region act in a regulatory fashion?

A

It is influenced by transcription factors to turn on/off.

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7
Q

What is the TATA box?
What binds to it?

A

a nucleotide sequence TATAAAA found near the transcription site.

TATA box binding protein binds to this region to initiate transcription.

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8
Q

What is the response element within a promoter

A

It is a short DNA sequence that is recognized by a specific protein/hormone that contributes to regulation of expression.

Back to the hormone therapy we talked about in chapter one where certain hormones are brought to lower levels and expression isn’t seen of that protein.

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9
Q

What are the enhancer elements

A

They are the upstream DNA sequences like CATT or GC that you’ve learned about in genetics that are involved in tissue and stage specific expression.

Super enhancers are clusters of enhancer elements

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10
Q

What can happen when there are mutations within the regulatory region of DNA?

A

If there are mutations within the regulatory regions, stuff could stop being made, or made to much.

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11
Q

What about when mutations happen within the coding region?

A

You could get a protein with incorrect function, or one that doesn’t function at all.

If p53 isn’t functioning correctly, mutations won’t get fixed and oncogenes can pop up.

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12
Q

Explain the mutation of transition simply.

A

When a purine is substituted with a purine or pyrimidine is replaced with another pyrimidine.

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13
Q

Explain the mutation of transversion simply.

A

When a purine is substituted with a pyrimidine or vice versa.

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14
Q

Explain the mutation of insertion simply.

A

When a nucleotide is inserted (added) it causes a frame shift within that gene - stuff gets pushed over and it reads it as such.

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15
Q

Explain the mutation of deletion simply.

A

When a nucleotide is deleted, it also causes a frameshift, where stuff becomes pushed over and it is read as such.

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16
Q

Explain the mutation of translocation.

A

When a part of a different chromosome, or the same one, gets translocated, which messes with how things are read as well.

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17
Q

Describe gene amplification.

A

The number of a specific gene copies is increased.

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18
Q

In relation to mutations in cancer, what is a driver mutation and what is a mutator phenotype?

A

Driver mutations are mutations in known cancer genes that gives them a growth advantage. (usually need 20+ but sometimes only 5-7)

A mutator phenotype is a mutation that gives rise to cells that have an increased rate of mutation.

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19
Q

What are passenger mutations?

A

They confer no growth advantage, but they exist nonetheless.

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20
Q

What is radiation?

What are the two types of particles that we talked about?

A

It is energy that is traveling in waves or in a stream of atomic particles.

Alpha particles have two protons and two neutrons

Beta particles have electrons

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21
Q

What is all included in energy waves?

A
  1. The visible spectrum
  2. Gamma rays (super short)
  3. X-rays (also short waves)
  4. UV radiation
  5. IR rays
  6. Radio waves
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22
Q

What are the three types of UV radiation?

A
  1. UVA
  2. UVB - most effective carcinogen because it causes cyclo-butane pyrimidine dimers and pyrimidine-pyrimidone
  3. UVC - ozone blocks.
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23
Q

What are cyclo-butane pyrimidine dimers?

What do they do to the DNA?

A

It forms a four membered ring between the two adjacent bases.

It bends the helix and makes it look like a purine to DNA Poly, so during replication, an A is read.

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24
Q

What are pyrimidine-pyrimidones?

What does it look like to DNA Poly?

Are they as frequent as the previously mentioned dimers and are they more serious?

A

They are when a pyrimidine binds at one site with another and an alcohol group is created one group away from the old ketone.

It looks like a site on the DNA where there is no bases.

They are less frequent and easily repaired by DNA.

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25
Q

What is ionizing radiation?

A

It is radiation that is made of both type of particles as well as pure gamma rays.

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26
Q

What is the effect of ionizing radiation on DNA?

How does it damage it directly and indirectly?

A

It makes molecules within DNA ions, by displacement of electrons.

Damage:

Direct - making stuff ions is bad

Indirect - it impacts normal water to create reactive oxygen species - radiolysis

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27
Q

What type of research has been done on ionizing radiation and cancer?

A

Victims of atomic bombings were looked at and leukemia is the most prevalent.

Children exposed were the most susceptible.

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28
Q

What happens in radiolysis of water?

A

There is a loss of an electron which makes reactive free radical species.

29
Q

What is a free radical?

A

It is any species capable of existing independently that only contains one or more unpaired electrons.

30
Q

What are ROS’s?

A

They are reactive intermediates of oxygen.

free radicals including O2.- and OH.-

They also include non radicals like H2O2.

31
Q

Why is H2O2 more harmful to DNA than other radicals that are more reactive?

What happens when it gets to the nucleus?

A

Because it has time to travel to the nucleus and can oxidize (steal an electron) from DNA

the example that was shown is the oxidation of guanine to oxoguanine which is then read by DNA poly as T and then paired with A

32
Q

Some mutations are detrimental to cells, but others have no effect. Define degeneracy and wobble.

A

Degeneracy is the redundancy of genetic code.

Wobble is when there is no specificity at the third base in a codon, meaning that there can be three different codons (that all code for the same amino acid) yet have different tRNAs

33
Q

Chemical carcinogens are normally what?

They attack the nucleophilic site of purines and pyrimidines rings.

A

They are normally electrophilic.

34
Q

What do chemical carcinogens do to DNA with their nucleophilic attack?

A

They covalently add functional groups to the DNA.

35
Q

What is a DNA adduct?

A

It is a base within the DNA that has been chemically modified.

36
Q

Are chemical carcinogens carcinogenic before they are metabolized?

A

Yes they can, but some also need to be metabolized before they become the ultimate carcinogens.

37
Q

What are PAH’s?

A

poly aromatic hydrocarbons

they are formed during the burning of tobacco, coal, gas, and garbage.

When they are metabolized to their ultimate carcinogens they will lead to G to T transversions.

What will happen is that G will be interpreted as as a T and A will be added, and when another replication happens the A will pair with a T.

38
Q

What are heterocyclic amines?

A

They are carcinogens that are produced by cooking meat.

39
Q

What are nitrosamines and nitrosamides?

A

They are found in tobacco and are formed when preservative nitrates react with amines during the smoking of fish and meat.

40
Q

What do nitrosamines and nitrosamides do to guanine?

A

They methylate it.

41
Q

What are alkylating agents?

What is the example we talked about and why is it unique?

A

They add alkyl groups to the DNA

Mustard gas, it has two reactive groups. It can form cross links between the strands (inter) or within them (intra).

42
Q

DNA tumor viruses are one type of oncogenic virus. What do they do? What are some examples?

A

They encode for viral proteins that block tumor suppressor genes.

Examples are HPV and EBV that replicate within episomes in the host cell.

43
Q

Retroviruses are another type of oncogenic virus. What do they do? What are some examples?

A

They are RNA viruses that are reverse transcribed into DNA and then incorporated into the host DNA

Examples include HIV and Human T cell Leukemia Virus.

44
Q

What is helicobacter pylori and what can it cause?

A

It is a spiral bacterium that has no cell wall.

It can cause chronic infection and ulcers in the stomach, and is associated with gastric cancer.

45
Q

What is S Typhi?

A

It is a typhoid pathogen that can cause chronic infection of the gallbladder.

Associated with gallbladder carcinoma.

46
Q

What are endogenous carcinogens?

A

They are things that our own body produces that can be carcinogenic.

This being things that metabolism produces like H2O2.

Completely separate from radiation and it produces less reactive radicals at specific locations.

47
Q

What is an endogenous carcinogen that no one thinks of?

A

Replication errors!

48
Q

What is one-step repair? How does it work?

A

It is repair that takes place when alkylating agents add methyl groups to stuff - we gotta get that off!

Alkyltransferase is an enzyme that works to transfer a alkyl group from the O6 atom of guanine.

When the methyl is transferred, the enzyme gets deactivated.

49
Q

What is nucleotide excision repair?

A

This is when helix distorters like dimers and adducts are removed.

50
Q

What are the two sub pathways of NER?

A
  1. Global Genome NER - the whole genome is surveyed for helix distortion
  2. Transcription coupled NER - when damaged active genes that interfere with transcription are located
51
Q

What is the mechanism of NER?

A

Endonuclease cleaves the lesion as well as 30 adjacent nucleotides.

Then proliferating cell nuclear antigen encircles the damaged region.

Finally DNA Poly fills the gaps

52
Q

What is base excision repair?

A

This is when chemically altered bases like 8-oxoguanine caused by endogenous mechanisms are removed.

53
Q

What is the mechanism for BER?

A

glycolyses scan the DNA for oxoguanine, and once located it is flipped outside the helix and cleaved.

This leaves the abasic site. Then endonuclease cleaves the DNA backbone at this site and DNA poly fixes it.

Importantly PARP interacts with the single strand break and recruits other repair proteins.

54
Q

What the heck is PARP?

What do it do?

A

PARP - Poly (ADP-ribose) polymerase

It interacts with single strand breaks and recruits other repair proteins.

55
Q

What is mismatch repair?

A

It is a DNA repair mechanism that fixes errors that are missed by DNA polymerase during replication.

Fixes things like insertions, deletions, slippage errors and mismatches.

56
Q

Generally speaking, what is recombinational repair?

A

It is the repair of double stranded DNA breaks.

57
Q

What is non-homologous recombination repair?

What are the downsides of this repair mechanism?

A

Again this is the repair that takes place because of a double strand break, and involves non-homologous ends are joined.

It is very error prone and can lead to translocations - incorrect chromosome being put together.

58
Q

Explain the repair mechanism of homologous recombination.

A
  1. When a double strand break happens, ATM kinase is activated.
  2. ATM kinase activates RAD 50 complex, which creates clean 3’ ends that have overhang, which is important in later steps.
  3. Then BRCA 1/2 will transport RAD 51 to the nucleus which, with the help of RAD 52 will bind to the exposed overhung ends.
  4. Then, the RAD 51 attached single strands will invade the duplicate sister chromatid and exchange the homologous sequence. The sequence from the sister chromatid acts as a template for repair.
  5. Now, with the additional repaired sequence on each single strand from the initial break, other enzymes called resolvases will restore the junctions that were made.
  6. This leaves two copies of intact DNA at the end of the process.
59
Q

Tell me about Radiation Therapy.

A

Lots of people with cancer receive it.

What happens is the ionizing radiation reacts with water to create ROS that will cause DNA damage and hopefully apoptosis.

60
Q

When does radiation therapy typically work better?

A

It does its job to create more double strand breaks when it is in the presence of more oxygen

Big tumors are typically pretty hypoxic, so it doesn’t work as well.

61
Q

What are the different types of chemotherapy we talked about and what do they each do?

A
  1. Alkylating agents - forms DNA adducts by covalent bonds with an alkyl group
  2. Platinum based drugs - uses chlorine on platinum to create platinum-nitrogen bonds that create irreparable cross links
  3. Antimetabolites - these are things that are structurally similar to other endogenous compounds so when they bind they inhibit nucleic acid synthesis
  4. Organic molecules - these weave their way into the DNA and don’t allow for replication
62
Q

What does ADME stand for?

A

Absorption
Distribution
Metabolism
Excretion

63
Q

T/F
Tumor cells receive the same dose for a given treatment

A

F

64
Q

How does extrinsic/acquired resistance go against typical darwinian evolution?

A

Normally, the ones with the adaptations survive. But cancer cells will change and adapt to survive singularly.

65
Q

What is the most brutal part of cancer drugs to you?

A

That the drugs add a strong selective pressure.

66
Q

What are the different mechanisms for drug resistance?

A
  1. Decreasing influx - the cell down regulates the receptor proteins used
  2. Increasing efflux - the P-glycoprotein works to push stuff out right as it gets into the cell
  3. There is a change in metabolism - shutting off certain pathways that are required for the drug to work
  4. Gene amplification - protein x is being made too much and making it difficult for the drug to work
  5. DNA repair increased - find ways to ultimately avoid apoptosis and live
67
Q

What are synthetic lethal strategies?

A

inhibits function of one gene that is only cytotoxic in the presence of an additional mutation

68
Q

Explain the genius idea of the PARP inhibitors.

A

Because if you inhibit PARP, which is crucial for BER to work, then double strand breaks start to accumulate.

Then, DS breaks which are best repaired by homologous recombination, are stopped because many breast cancers have BRCA 1/2 mutations which is also needed to bring RAD 51 to the nucleus.

Cancer Biology (10 decks)

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