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BDS Module 4 > OC 10 - pathogenesis of HNC 1+2 > Flashcards

OC 10 - pathogenesis of HNC 1+2 Flashcards

1
Q

What types of cancer does the term ‘head and neck cancer’ cover?

A

cancers of the mouth, oropharynx, nasopharynx, hypopharynx, nose, paranasal sinuses, larynx, salivary glands, ear

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2
Q

What are the majority of head and neck cancers?

A

squamous cell carcinomas (SCC)

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3
Q

What does SCC arise from?

A

lining mucosa

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4
Q

What is rhabdomysosaecoma?

A

a malignant skeletal muscle cancer

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5
Q

What is meant by saying neoplasia is a genetic disease?

A
  • tumour cells usually show nuclear abnormalities
  • nearly all carcinogens are mutagens
  • altered DNA content (aneuploidy) is common in tumour cells
  • chromosomes from tumour cells show structural abnormalities, some being characteristic of specific tumour types
  • some tumours are clearly inherited and tumours can run in families
  • mutations exist in genes that regulate cell behaviour
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6
Q

What are the (simplified) steps of carcinogenesis?

A
  1. initiation - DNA damage and mutation
  2. promotion - clonal expansion of abnormal cells leading to cancer
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7
Q

What are the components of a neoplasm?

A
  • neoplastic cells
  • blood vessels
  • inflammatory cells
    • (macrophages, lymphocytes, polymorphs)
  • fibroblasts
  • stroma
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8
Q

What are the key elements in cancer development?

A
  • tumour growth
  • invasive growth
  • angiogenesis
  • metastasis
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9
Q

What are the key elements of tumour growth?

A
  • replication
  • escape from senescence
  • evasion of apoptosis
  • limitless replicative potential
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10
Q

If a tumour is monoclonal, what does this mean?

A

All the cells in a tumour appear to arise from one parent cell which has undergone a genetic change. This is then passed on to all the progeny.

most tumours are monoclonal

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11
Q

In tumour cells, what happens in further genetic change develops in the progeny cells?

A

tumour becomes heterogenous

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12
Q

What are the stages of tumour progression?

A

normal cell—>transformed cell—>clonal expansion—> tumour progression—>further tumour progression

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13
Q

What 3 things happen in invasive growth?

A
  • reduction in cell-cell adhesion (between tumour cells)
  • invasion of basement membrane and stroma
  • tumour cells need to be motile
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14
Q

What causes reduction in cell-cell adhesion?

A

reduced/loss of E-cadherin

E-cadherin - a transmembrane glycoprotein important in cell-cell adhesion

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15
Q

What happens during invasion of basement membrane and stroma?

A
  • tumour cell attached to BM via integrins and matrix proteins
  • tumour cells produce proteolytic enzymes e.g. collagenases, matrix metalloproteases which break up the matrix
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16
Q

What happens for tumour cells to become motile?

A

Extrude pseudopodia which attach to stromal proteins. Actin cytoskeleton enables movement

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17
Q

Where do groups of cells that display invasive growth predominate?

A

in well differentiated carcinomas e.g. SCC

18
Q

What do groups of cells that display invasive growth have high levels of?

A

high levels of autocrine pro-migratory factors and of proteolytic enzymes

19
Q

What is protected when tumour cells invade in groups?

A

inner cells protected from immunological assault

20
Q

What properties are required for a tumour cell to invade?

A
  • adhesion molecules
  • receptors for connective tissues e.g. laminin
  • proteolytic enzymes e.g. collagenases, cathepsin
  • altered cell division and apoptosis - produces pressure of growth
  • amoeboid movement
21
Q

What is angiogenesis?

A

formation of new blood vessels

22
Q

What is the angiogenic switch?

A

angiogenesis is usually under tight physiological control however control is lost in tumours —> development of rich blood supply around tumours

23
Q

How are new blood vessels formed during angiogenesis?

A

new blood vessels formed by outgrowth of endothelial cells from post capillary venules into tumour mass

24
Q

What is a critical step in progression of a small localised tumour to a bigger one with metastatic potential?

A

angiogenesis

25
Q

What stimulates angiogenesis?

A

increased production of factors by tumour cells e.g. VEGF and angiogenin

26
Q

What does VEGF stand for?

A

vascular endothelial growth factor

27
Q

What is often a pre-requisition for tumour progression?

A

angiogenesis

28
Q

Do tumours require more, less or the same oxygen and metabolites as normal cells?

A

tumours require less oxygen and metabolites than normal cells

29
Q

How does density of tumour micro vasculature correlate with prognosis?

A

it does not need to correlate

30
Q

What are metastasis?

A

tumour implants that are discontinuous with the primary lesion - “secondaries”

31
Q

What effects/implications can the presence of metastasis have?

A

affects tumour stage and has prognosis implications

32
Q

What are the common sites of metastatic disease?

A
  • regional lymph nodes
  • liver
  • lung
  • bone
  • brain
  • skin
  • unusual sites - think of renal cancer, thyroid cancer, melanoma
33
Q

What are the routes of metastasis?

A
  • lymphatic
  • haematogenous
  • across body cavities
  • across serous cavities
  • across meninges/ventricles/spinal canal
  • direct implantation
34
Q

What type of cancer is lymphatic spread frequently seen in?

A

carcinomas

35
Q

What type of cancer is haematogenous spread frequently seen in?

A

sarcomas

36
Q

How does metastasis occur?

A
  • tumour cells breach the basement membrane of vessel and enter vessel lumen
  • tumour cells carried to site of metastasis
  • bind to endothelial cells, penetrate BM, move out of vessel
  • establishment of metastasis, cell proliferation, angiogenesis
  • complex molecular interactions involved in these stages
37
Q

What accounts for common metastatic profiles?

A

circulatory patterns

38
Q

Why are the lung and liver common sites of metastasis?

A

lung and liver are very effective at arresting circulating cancer cells
- allows tumour cells to stop and grow at a site

39
Q

What is the ‘seed and soil hypothesis’?

A
  • the seed (cancer cell) is dependant on some property of the soil (the metastatic site)
  • deliver of cancer cells to a potential metastatic site is primarily mechanical - but the growth of metastatic deposit is is dependent upon compatibility with the “soil”

explained by target tissues possessing appropriate extracellular matrix and cell adhesion molecules to allow tumour cells to stop and grow at a site

40
Q

Some benign tumours can progress to become malignant - what does this give evidence of?

A

the multiple step theory of carcinogenesis

41
Q

What is the most common type of salivary gland tumour?

A

pleomorphic adenoma

BDS Module 4 (65 decks)

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