Epi and carcinogenesis Flashcards

1
Q

4 most common CA

A

lung, breast, colon, prostate

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2
Q

how many canadians will get CA and how many will die of itq

A

get - 40%

die - 25%

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3
Q

what is most deadly common CA

A

lung

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4
Q

2 things that CA incidence patterns reflects

A
  1. presence of env. factors

2. primary prevention

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5
Q

2 types of primary prevention

A
  1. lifestyle mod

2. screening

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6
Q

3 things that CA mortality rates reflect

A
  1. effect of screening
  2. natural Hx of Ca
  3. treatments
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7
Q

how is race important (2)

A
  1. may define risk groups

2. may reflect presence of polymorphisms in a pop. that increase thier susceptibilty

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8
Q

3 genetic influnces on CA

A
  1. genomic instability - natural mutations
  2. inherited mutation
  3. acquired mutation
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9
Q

4 ways cells try to prevent accumulation of mutations

A
  1. continuous shedding of certain cells - epithelial stress
  2. defenses against genotoxic injury
  3. DNA damage checkpoints in cell cycle
  4. cellular sensence
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10
Q

what % of CA have a notable genetic component

A

5-10%

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11
Q

2 types of inhertiance patterns

A
  1. specific recognized defect

2. general familial predisposition

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12
Q

2 types of specific recognized defects

A
  1. inherited CA syndromes

2. defective DNA repair syndromes

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13
Q

what is mech. of inherited CA syndrome

A
  1. germline mutation of in one allele of critical gene (usually tumor supressor)
  2. mutation of second allele in somatic cells
  3. dysregulation of cell growth and prolif.
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14
Q

who do inherited syndromes present

A

usually a specific phenotype

- except Li- fraumeni syndrome

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15
Q

what is defective DNA- repair syndrome

A

usually rare and via defects in ability to repair DNA causing subsequent mutations

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16
Q

**how to tell if mutation is due to inherited mutations

A

if sporadic, the mutations will only be in tumour cells

17
Q

characterisitcs of familial predisp. to CA

A

higher freq., but no pattern

  • early age of onset
  • multiple or bilateral tumors
  • no specific marker or transmission pattern
18
Q

what are vast majorty of mutations in CA

A

aquired via env.

19
Q

some env. influences

A

diet, smoking, alcohol, chemiscals, radiation

20
Q

what are 2 types of carcinogens

A

direct - no metabolic activation needed

indirect

21
Q

2 steps in chemical carcinogens

A
  1. initiation - exposure causes mutation
    - not sufficient to cause cancer
  2. promotion - causes damaged cells to prolif
22
Q

what are 2 types of radiation

A
  1. UV - due to formations of crosslinks in DNA

2. ionizing - often leukemias, thyroid, breast colon

23
Q

3 classes of microbial carcinogens and examples

A
  1. RNA viruses
    - HTLV-1
  2. DNA viruses
    - HPV
    - HBV
    - EBV
    - HHV-8
  3. bacteria
    - h. pylori
24
Q

what is cancer and cause of HTLV-1

A

CA - T-cell leukemia - 3-5%

cause - tropism for CD4 - viral integration into genome

25
Q

what is cancer and cause of HPV

A

CA - cervical

cause - 16 and 18 - viral integration causing genomic instability

26
Q

what is cancer and cause of EBV

A

CA - lymphoma

cause -

27
Q

what is cancer and cause of HBV

A

CA - 70-80% hepatocellular carcinoma

cause - immune mediated chronic inflammation

28
Q

what is cancer (2) and cause of pyloori

A

CA - 1. gastric adenocarcinoma 2. gastric lymphoma

cause - 1. CagA gene , 2. gen. reactive T cells - polyclonal B cell proliferation

29
Q

how is age related

A

generally older due to accumulation of mutations and decline in immune competence

30
Q

common CA in children

A

leukemias and blastomas

31
Q

3 other predisposing factors

A
  1. conditions that result in cell prolif (hyper and metaplasias)
  2. chronic inflammatory disorders (UC, h pyloir, hepatitis)
  3. dysplastic lesions - not ALL will progress