Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M4: Oral cancer > Pathogenesis of the Head and neck 1 > Flashcards

Pathogenesis of the Head and neck 1 Flashcards

1
Q

What are the most common head and neck cancers?

A

Squamous cell carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Other common head and neck cancers aside from SCC?

A

Salivary glands e.g. polymorphous adenocarcinoma
Odontogenic epithelium e.g ameloblastic carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Less frequent malignant tumour example

A

rhabdomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Main aetiological factors for head and neck cancers

A

tobacco, alcohol, high risk HPV infection, EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aetiology of most salivary gland tumours

A

Unknown.

Molecular alterations identified in some e.g. MAML2 rearrangements in mucoepidermoid carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Neoplasia

A

Genetic disease

Tumour cells breed true (parent cells were already tumour cells meaning this has been inherited).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How would you describe the development of a cancer?

A

Multistep, progressive, cumulative process.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Multistep theory of carcinogenesis

A
  1. Initiation - DNA damage and mutation
  2. Promotion - clonal expansion of abnormal cells leading to cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Components of neoplasm

A
  1. Neoplastic cells
  2. Blood vessels
  3. Inflammatory cells (macrophages, lymphocytes, polymorphs)
  4. Fibroblasts
  5. Stroma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A
  1. Tumour growth (replication, escape from senescence, evasion of apoptosis, limitless replicative potential)
  2. Invasive growth
  3. Angiogenesis
  4. Metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Key elements in cancer development (4)

A
  1. Tumour growth (replication, escape from senescence, evasion of apoptosis, limitless replicative potential)
  2. Invasive growth
  3. Angiogenesis
  4. Metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tumour growth

A

Commonly tumours are monoclonal (i.e. stem from one parent cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is tumour heterogeny?

A

When there are differences of the same type of tumour shown in different patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What occurs during invasive growth?

A
  1. Reduction in cell-cell adhesion (e.g. reduced/loss of E-cadherin)
  2. Invasion of basement membrane and stroma (tumour cell attaches to BM and produce proteolytic enzymes to break up matrix)
  3. Tumour cells need to be motile (extrude pseudopodia which attach to stroll proteins, actin cytoskeleton enables movement).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do groups of cells display invasive growth?

A
  1. Require cell-cell adhesion and communication
  2. Predominates in well differentiated carcinomas
  3. Inner cells protected from immunological assault
  4. High levels of autocrine pro-migratory factors and of proteolytic enzymes
  5. Heterogenous sets of cells invade together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Angiogenesis (5)

A

“formation of new blood vessels”

  1. Usually under tight physiological control however control is lost in tumours - the angiogenic switch - development of rich blood supply around tumour.
  2. Vessels formed are abnormal
  3. New blood vessels formed by outgrowth of endothelial cells from post capillary venules into tumour mass.
  4. Critical step in progression of small localised tumour into a bigger one with metastatic potential.
  5. Stimulus is increased production of factors by tumour cells; VEGF, angiogenic, inhibition of angiogenesis anticancer therapy area
17
Q

Does the dentist of tumour microvasculature correlate with prognosis?

A

No

18
Q

What is often a pre-requisite for tumour progression?

A

angiogenesis

19
Q

Metastasis

A

“cancer spread to other sites”

  1. Tumour implants that are discontinuous with the primary lesion “secondaries”
  2. Sinister event
  3. Non-random
  4. Affects tumour stage and has prognostic implications
20
Q

Common sites of metastatic disease (7)

A
  1. Regional lymph nodes
  2. liver
  3. lung
  4. bone
  5. brain
  6. skin
  7. Unusual sites: renal cancer, thyroid cancer, melanoma
21
Q

Routes of metastasis

A
  1. Lymphatics (carcinomas)
  2. Haematogenous (sarcomas)
  3. Across body cavities (serous cavities/meninges/ventricles/spinal canal)
  4. Direct implantation
22
Q

Process of metastasis

A
  1. Tumour cells breach the basement membrane of vessel and enter vessel lumen
  2. Tumour cells carried to site of metastasis
  3. Bind to endothelial cells, penetrate BM, move out of vessel
  4. Establishment of metastasis, cell proliferation, angiogenesis
  5. Complex molecular interactions involved in these stages.
23
Q

Describe metastatic disease profile

A

Circulatory patterns account for common metastatic profiles.
Lung and liver very effective at arresting circulating cancer cells.

24
Q

What is the “seed and soil hypothesis” in metastasis?

A

The seed (cancer cell) is dependent on some property of the soil (the metastatic site).

Delivery of cancer cells to a potential metastatic site is primarily mechanical - but the growth of metastatic deposits is dependent upon compatibility with the “soil”.

Explained by target tissues possess appropriate extracellular matrix and cell adhesion molecules to allow tumour cells to stop and grow at a site.

M4: Oral cancer (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions