Pathogenesis of head and neck cancer

What are the variable aetiology for head and neck cancers

tobacco, alcohol, high risk HPV infection, EBV

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What is the progeny of tumour cells

tumour cells indicating inheritance of properties

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what is aneuploidy

altered DNA content

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due to what processes do tumours grow

replication, evasion apoptosis, limitless replicative potential , escape from senescence

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what are the key elements in cancer development

tumour growth, angiogenesis, invasion and metastasis

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what is angiogenesis

the development/formation of new blood vessels

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what do monoclonal tumours mean

it means that all cells in a tumour appear to arise from one parent cells which has undergone a genetic change. this is then passed on to all the progeny

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what is the marked genetic heterogeneity shown by head and neck SCC

loss of function in tumour suppressor genes- p53 and activation of oncogenes - EGFR

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What is a heterogenous tumour

when further genetic changes develop in the progeny

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what are some of the things shown by transformed cells

- altered nuclear/cytoplasmic ratio- this is increased in nuclear size, altered and variable nuclear morphology (pleomorphism)- look bigger, altered nuclear staining (hyperchromasia)- nuclear looks darker than normal, altered DNA content (aneuploidy)

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part 2

molecular alterations in key regulatory genes , reduced requirements for growth factors (or serum) when grown in vitro, altered antigen expression, altered surface charge, altered surface. carbohydrate expression, growth at very low cell densities in

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part 3

in vitro, loss of contact inhibition, growth in an anchorage independent manner, immortality, tumourigenesis, cancer cells have invasive properties and the potential to metastasise

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what are carcinogens

environmental factors- chemical, radiation, viruses,

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what are the risk factors for oral cavity/lip

tobacco, alcohol, betel quid/pan/, previous oral cancer, exposure to UV light, poor diet, immune suppression, genetics, social deprivation, HPV- oropharyngeal cancer

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what is epithelial dysplasia

a pre- malignant process

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Atypical epithelial alterations are limited to ....

the surface squamous epithelium

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where do some of the alterations happen:

in architecture, maturation, differentiation

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what are the histological features of epithelial dysplasia/ cellular atypia

1. nuclear and cellular pleomorphism 2. alterations in nuclear/ cytoplasmic ratio (invariably an increase), nuclear hyperchromatism, prominent nucleoli, increased and abnormal mitosis

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continued

6. loss of polarity of basal cells 7. basal cell hyperplasia, drop shaped rate pegs - wider at their deepest part, irregular epithelial stratification or disturbed maturation, abnormal keratinisation, loss/reduction of intercellular adhesion

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what is the grading of epithelial dysplasia

mild, moderate, severe also low/high grade

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the more severe/ higher grade of dysplasia the ....... the risk of malignancy

the greater

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what are some of the oral potentially malignant disorders

lichen planus, discoid lupus erythematosus, chronic hyperplastic candidosis, dyskeratosis congenita, tertiary syphilis, oral submucosa fibrosis, leukoplakia inc proliferative verrucous leukoplakia

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what is the management of epithelial dysplasia

modify risk factors, high risk sites, anti fungal treatment, excision/ co2 laser excision, topical agents, close clinical review, rebiopsy

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in invasive growth, what are the 3 things that need to happen

reduction in cell-cell adhesion, invasion of basement membrane and stroma, tumour cells need to be motile

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what happens when basement membrane and stroma are invaded

tumour cell attaches to BM via integrins and matrix proteins, tumour cells produce proteolytic enzymes- collagenase, matrix metalloproteases which break up the matrix

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when tumour cells need to be motile, they extrude .... and why? and what cytoskeleton enables movement

they extrude pseudopodia which attach to stroll proteins. actin cytoskeleton enables moment

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what is the angiogenetic switch

development of rich blood supply around tumour

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

angiogenesis

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what are the new blood cells formed by in angiogenesis

by outgrowth of endothelial cells from post capillary venules into tumour mass.

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what is stimlulus . give examples

increased production of angiogenic factors by tumour cells - VEGF, FGF, ANGIOGENIN , inhibition of angiogenesis potential anticancer therapy area

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does density of tumour microvasculature correlate with prognosis

no. it doesn't need to correlate

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what are the common sites for metastatic disease in head and neck cancer

regional lymph nodes , lung

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what are the routes of metastasis ? and give the specific name

lymphatic - carcinoma. Haematogenous (blood)- sarcoma, across body cavities- serous cavities, meninges, ventricles, spinal canal. direct implantation

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describe metastatic disease

1. Tumour cells breach the basement membrane of newly formed vessels and enter vessel lumen. 2. Tumour cells carried to site of metastasis 3. Bind to endothelial cells, penetrate BM, move out of vessel

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continued

4. Establishment of metastasis- cell proliferation, angiogenesis 5. Complex molecular interactions involved in these stages

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give an example of a bening tumour that can progress to become malignant

pleomorphic adenoma - carcinoma ex pleomorphic adenoma

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Pathogenesis of head and neck cancer

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