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Biology of Cancer SSC > Carcinogenesis > Flashcards

Carcinogenesis Flashcards

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1
Q

What is a benign cancer?

A

A cancer that grows slowly, is non invasive, and does not metastasise.

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2
Q

What is a malignant cancer?

A

A cancer that grows rapidly, is invasive, and has the potential for metastasis.

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3
Q

What is carcinogenesis?

A

The process of transformation of a normal cell to a cancer cell

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4
Q

What is initiation?

A

Initial mutation due to carcinogenic initiator

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5
Q

What is promotion

A

The induction of cell division that confers a selective advantage over other cells within the tissue

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6
Q

What is progression?

A

Clonal expansion of tumour cells via conversion, propagation, and dedifferentiation

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7
Q

What is transformation?

A

Potential for regression

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8
Q

What is evolution?

A

Formation of a drug resistant clinical tumour

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9
Q

What is metastasis?

A

Spread of transformed cells

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10
Q

In colorectal carcinogenesis, what is often the first “hit”?

A

APC gene mutation leading to inactivation

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11
Q

What does APC gene inactivation lead to?

A

Change in frequency of division leading to an increase in stem cells.

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12
Q

What does the APC gene normally do?

A

Code for the tumour suppressor APC protein which helps control how often the cell divides and checks how many chromosomes it has after cell division.

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13
Q

What does a higher rate of proliferation mean?

A

Higher mutational risk for a “second hit”

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14
Q

Give examples of what the subsequent “hits” may be

A
  • Ras mutation -> activation

- p53 inactivation

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15
Q

What is mutagenesis?

A

When the genetic information of an organism is changed in a stable way, resulting in mutation

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16
Q

What are the 2 stimuli for mutagenesis?

A
  • Environmental stimuli

- Intracellular stimuli

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17
Q

Give 3 examples of how environmental stimuli can cause mutagenesis

A
  • Ultimate carcinogens (bind to DNA and alter sequence)
  • Ionising radiation/UV (strand breaks, cross links)
  • DNA translocation to transcriptionally active regions
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18
Q

Give 3 examples of how intracellular stimuli can cause mutagenesis

A
  • Misinterpretation of code
  • Polymerase slippage/base malalignment
  • Ineffective repair
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19
Q

Give 6 examples of initiating stimuli

A 
Chemical carcinogens
Oncogenic viruses
Radiation
UV light
Oxygen-free radicals
Replication errors
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20
Q

Give 2 examples of direct acting carcinogens

A
  • Alkylating/Acylating agents

- Weak carcinogens (cytotoxic drugs)

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21
Q

Name 3 alkylating/acylating agents

A
  • Dimethylsulphate
  • Chlorambucil
  • Dichloromethane
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22
Q

What is a procarcinogen?

A

A precursor to a carcinogen - it does not cause cancer itself but can be converted to a carcinogen by enzymatic action

23
Q

Give 2 examples of common procarcinogen groups

A
  • Polycyclic aromatic amines

- Combustion of organic compounds (coal, petrol, cooked foods, tobacco smoke)

24
Q

Name 3 polycyclic aromatic amines

A
  • benz(a)anthracene
  • dimethylbenzanthracene
  • benzopyrene
25
Q

What is aflatoxin?

A

A procarcinogen produced by a certain type of fungi that grows on maize, tree nuts, cottonseeds and peanuts, especially in warm and humid regions.

26
Q

How is aflatoxin carcinogenic once it has been metabolised?

A

Forms a DNA adduct

27
Q

What is aflatoxin exposure linked with?

A

High liver cancer incidence

28
Q

Why don’t we all get cancer all the time?

A
  • Repair mechanisms in place
  • mismatch and excision repair
  • p53
29
Q

Which is harder for a cell to deal with - single or double stranded DNA breaks?

A

Double stranded

30
Q

How many base changes result in permanent mutation?

A

Fewer than 1 in 1000

31
Q

What is a transition single point mutation?

A

Purine->purine or pyramidine->pyramidine

32
Q

What is a transversion single point mutation?

A

Purine->pyramidine or pyramidine->purine

33
Q

Where on DNA nucleotides are there nucleophilic binding sites with potential for mutagenesis?

A

On N, NH2, and O group, especially in Adenine and Guanine

34
Q

What are the 4 outcomes of DNA changes?

A
  • Excision repair
  • Error prone repair
  • Mismatch repair
  • Defects in DNA replication
35
Q

How does excision repair work?

A

For base or nucleotide repair. Modified bases/nucleotides removed error-free by base excision by DNA glycosylases. Nucleotide excision removes bases with bulky adducts.

36
Q

How does error-prone repair work?

A

Low fidelity DNA polymerases respond to severe DNA damage - recognise specific lesions and restore original sequence.

37
Q

How does mismatch repair work?

A

Exonuclease part of DNA polymerase proof-reads and corrects mismatched bases in the new strand of DNA during replication.

38
Q

What defects in DNA replication can occur?

A
  • Genome rearrangements

- Chromosome loss

39
Q

Give 4 example of promoting agents

A
  • Chemical promoters
  • Hormones
  • Inflammation
  • Microbial infection
40
Q

Give 4 example of chemical promoters

A

-Phorbol esters
-Phenols (tobacco tar)
-Xenoestrogens (phenobarbital, insecticides)
Saccharin

41
Q

What can cause chronic irritation as a promoter?

A

Pipe smoking

42
Q

What endoparasite can be an infectious promoter?

A

Schistosoma haematobium (bladder cancer)

43
Q

What bacterial infection can be an infectious promoter?

A

Helicobacter pylori (gastric cancer)

44
Q

Give an example of treatment for cancer targeting sustained proliferative signalling
(Hallmarks of Cancer)

A

EGFR inhibitors

45
Q

Give an example of treatment for cancer targeting the evasion of growth suppressors
(Hallmarks of Cancer)

A

Cyclin-dependant kinase inhibitors

46
Q

Give an example of treatment for cancer targeting the avoidance of immune destruction
(Hallmarks of Cancer)

A

Immune activating anti-CTLA4 mAb (CTLA-4 inhibits T cells, so overall this treatment enhances immune responses)

47
Q

Give an example of treatment for cancer targeting replicative immortality
(Hallmarks of Cancer)

A

Telomerase inhibitos

48
Q

Give an example of treatment for cancer targeting tumour-promoting inflammation
(Hallmarks of Cancer)

A

Selective anti-inflammatory drugs

49
Q

Give an example of treatment for cancer targeting activation of invasion and metastasis
(Hallmarks of Cancer)

A

Inhibitors of HGF/c-Met

50
Q

Give an example of treatment for cancer targeting angiogenesis induction
(Hallmarks of Cancer)

A

Inhibitors of VEGF signalling

51
Q

Give an example of treatment for cancer targeting genome instability and mutation
(Hallmarks of Cancer)

A

PARP inhibitos

52
Q

Give an example of treatment for cancer targeting resistance to cell death
(Hallmarks of Cancer)

A

Proapoptotic BH3 mimetics

53
Q

Give an example of treatment for cancer targeting deregulation of cellular energetics
(Hallmarks of Cancer)

A

Anaerobic glycolysis inhibitors

Biology of Cancer SSC (16 decks)

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