2.7: cancer Flashcards

1
Q

(causative factors) genetics

A

defective alleles inherited from parents

increased predispositions to cancer

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2
Q

normal RB gene function

A

halts cell cycle in absence of growth factors

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3
Q

mutated RB gene

A

loss or RB activity

allows proliferation in absence of growth factors

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4
Q

normal p53 gene function

A

prevents cells with dmg DNA from proliferating

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5
Q

mutated p53 gene

A

damaged cells continue to divide

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6
Q

normal BRCA1, BRCA2 gene function

A

repair of DNA double strand breaks

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7
Q

mutated BRCA1, BRCA2 gene

A

inability to repair breaks

increased risk of ovarian and breast cancer

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8
Q

types of chemical carcinogens

A

tar, EtBr

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9
Q

how do chemical carcinogens cause cancer

A
  1. covalent bonds w DNA -> DNA-carcinogen complex
  2. distorts DNA double helix
  3. replication errors
  4. removing nucleotides
  5. DNA strand breakage
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10
Q

types of ionising radiation

A

X-rays, gamma rays, UV rays

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11
Q

how does ionising radiation cause cancer

A
  1. high energy
  2. breaks in DNA backbone / formation of pyrimidine dimers
  3. permanent base change
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12
Q

types of infectious agents

A

HIV, HPV

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13
Q

how do infectious agents cause cancer

A

1, integrate genetic material into human DNA
2. days regulation of cell cycle checkpoints
3. uncontrolled proliferation of dmg DNA cells

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14
Q

what is a proto oncogene?

A

genes coding for proteins that

promote normal cell growth and division

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15
Q

what is a tumour suppressor gene?

A

genes coding for proteins that

normally inhibit cell division

cell cycle arrest, DNA repair, blocking angiogenesis and apoptosis

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16
Q

what is a gain in function mutation

A

proto-oncogene -> oncogene
- increase in amt of protein produced
- hyperactivity of protein

eg Ras gene

17
Q

how many alleles needed to undergo GOF mutation

A

1

18
Q

loss in function mutation

A
  • accumulation of mutations
  • excessive cell growth and divisions

eg p53 gene

19
Q

how many alleles need to undergo LOF mutation

A

2

20
Q

why is it relatively difficult to develop cancer?

A
  1. proofreading mechanisms check and repair mutations
  2. cells w irreparable mutation undergo apoptosis via p53
  3. only mutations in PO or TSG will lead to cancer
  4. all mutations must occur in a single cell for cancer to form
21
Q

what is the multi step model of cancer?

A
  1. GIF of PO
  2. LOF of TSG
  3. evasion of apoptosis
  4. activation of telomerase gene
  5. angiogenesis
  6. metastasis and tissue invasion
22
Q

activation of telomerase

A
  • cancer cells activate
  • add new copies of telomeric repeat seq
  • telomeres do not shorten
  • cells divide infinitely

limitless replicative potential

23
Q

what is angiogenesis

A

formation of blood vessels

supplies nutrients to cancer cells

remove toxic waste

blood vessels provide a route to the rest of the body for metastasis

24
Q

describe how dysregulation of checkpoints of cell div may result in cancer

A
  1. M checkpoint dysregulation
    - cells enter anaphase despite improper attachment of spindle fibres of chromosomes at metaphase
    - non-disjunction -> daughter cells with extra copies of proto-oncogenes
  2. G1/G2 checkpoint dysregulation
    - unrepaired dmg DNA being passed on to daughter cells

dysregulation allows cells w improper structures to enter next cell cycle phase
replicate = uncontrolled and excessive cell division = cancer