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EMS > T5 Tumours > Flashcards

T5 Tumours Flashcards

1
Q

what are the three types of differentiation in tumour?

A
  • well-differentiated
  • moderately
  • poorly
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2
Q

anaplasia

A

poorly differentiated neoplasm; highly pleomorphic

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3
Q

most common cancers in males & females

A
  • (prostate or breast)
  • lung
  • bowel
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4
Q

most mortal cancers in the UK

A
  • pancreas
  • brain
  • lung
  • oesophagus
  • stomach
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5
Q

what are the effects of 1ry tumour?

A
  • bleeding

- obstruction

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6
Q

what are the effects of distant metastases?

A

cancer spreading

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7
Q

what are the causes of paraneoplastic syndromes?

A
  • proteins secreted by tumour

- immune cross reactivity

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8
Q

classification of tumours

A

(see week 5 summary notes)

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9
Q

what effect fo initiators have on DNA

A
  • genotoxic –> chemically modify it
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10
Q

what is the effect of promoters

A

induce proliferation; DNA replication

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11
Q

in a mutation, what causes the gain of function?

A

activation of proto-oncogenes

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12
Q

in a mutation, what causes the loss of function?

A

inactivation of tumour suppressor

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13
Q

how is tumour suppressor gene inactivated?

A
  • methylation

- CpG islands

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14
Q

what are the direct acting chemicals causing mutation?

A
  • free radicals
  • nitrosamines
  • UV light
  • ionising radiation
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15
Q

what do procarcinogens require before ractoing with DNA?

A

enzymatic activation

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16
Q

give examples of procarcinogens

A
  • aromatic amines

- polycyclic aromatic hydrocarbons (PAHs)

17
Q

DNA damage & repair mechanisms

A

check out summary notes

18
Q

what enzyme can detoxify/excrete carcinogen? (might be why not all exposures lead to cancer)

A

glutathione S-transferase

19
Q

what cancers is alcohol associated with?

A
  • oral
  • oesophageal
  • bowel
  • liver
20
Q

what does alcohol casue that can lead to cancer?

A
  • acetyldehyde formation
  • +++ oestrogen & testosterone
  • +++ carcinogens uptake (esp. in GI cells)
  • — folate (needed for accurate DNA replication)
  • kill surface epithelium
21
Q

cancers associated with chronic inflamamtion

A
  • HBV

- HCV

22
Q

why does inflammatory response increase the risk of cancer?

A
  • free radicals –> DNA damage

- growth factor repairing tissues –> promotor

23
Q

sporadic vs inherited cancer in terms of Kundson’s two hit hypothesis

A
  • sporadic: two hits required
  • inherited: one hit required
    (autosomal dominant pattern of inheritence
24
Q

function of gatekeepers

A
  • directly regulate tumour growth
  • monitor & control cell division & death
  • preventing accumulation of mutations
25
Q

function of caretakers

A
  • improve genomic stability: repair mutations
26
Q

function of landscapers

A
  • control surrounding stormal environment
27
Q

examples of TSG

A
  • APC
  • BRCA1/2
  • TP53
  • Rb
28
Q

function of oncogenes

A
  • regulate cell growth /differentiation
29
Q

examples of oncogenes

A
  • growth & signal transduction factors

- RET genes

30
Q

compare the difference between the effect of gain/loss of function on the risk of cancer

A
  • TSG: loss of function –> +++ cancer risk

- onco: gain of function –> +++ cancer risk

31
Q

examples of autosomal recessive conditions

A
  • MUTYH associated polyposis
  • Fanconi anaemia
  • Alaxia telangiectasia
    (can increase risk of sporadic cancer)
32
Q

compare sporadic to familial cancers:

A

sporadic: old onset; one cancer in individual; unaffected fam; rarely genetic cancers
familial: young onset; multiple cancers; fam affected; genetic cancers

33
Q

diagnostic vs predictive testing

A
  • diagnostic: DNA from affected relative to identify mutation
  • predictive: testing for mutation in affecetd individuals’ relatives
34
Q

what cancer is associated with Lynch syndrome

A
  • bowel
  • endometrial
  • ovarian
  • stomach
  • urinary tract
35
Q

what is the inheritance pattern for breast cancer and lynch syndrome

A

AD

36
Q

which mismatch repair genes are affected in Lynch syndrome

A
  • MLH1
  • MLH2
  • MLH6
  • MLH2

EMS (10 decks)

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