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MBD/MI (Wothaya) > Tumour Angiogenesis, Invasion And Metastasis > Flashcards

Tumour Angiogenesis, Invasion And Metastasis Flashcards

1
Q

What are the characteristics of malignant tumours?

A

Growth
Invasiveness
Metastasis

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2
Q

What is the growth potential of a malignant tumour?

A

Unlimited as long as adequate blood supply is available

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3
Q

What is the invasiveness characteristic of a malignant tumour?

A

Migration of tumour cells into the surrounding stroma where they disseminate

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4
Q

What is the metastatic characteristic of a malignant tumour?

A

Spread of tumour cells from the primary site to form secondary tumours at other sites in the body

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5
Q

What are the key steps in cancer progression?

A

Transformation
Angiogenesis
Motility and invasion
Metastasis

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6
Q

What is transformation of a cancer?

A

Extensive mutagenic and epigenetic changes followed by clonal selection

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7
Q

What is angiogenesis?

A

New blood vessel formation from pre-existing vessels

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8
Q

What is vasculogenesis?

A

Formation of new blood vessels from progenitors

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9
Q

What are the types of angiogenesis?

A

Developmental (vasculogenesis)
Normal angiogenesis
Pathological angiogenesis

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10
Q

What is pathological angiogenesis?

A

Tumour angiogenesis

Seen in ocular and inflammatory disorders

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11
Q

When does normal angiogenesis occur?

A

Wound repair
Placenta furing pregnancy
Cycling ovary

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12
Q

What is the max. Size of a tumour without their own blood supply?

A

1-2mm^3 without their own organ blood supply

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13
Q

What are the steps in tumour angiogenesis?

A

Small tumour gets big enough to need its own blood supply
Tumour switches on expression of angiogenic genes/factors
New blood vessels grow in and around the tumour, increasing the delivery of oxygen

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14
Q

What is a strong stimulus for tumour angiogenesis?

A

Hypoxia

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15
Q

What genes are involved in angiogenesis?

A

Vascular endothelial growth
Glucose transporter 1
Urokinase plasminogen activator receptor
Plasminogen activator inhibitor 1

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16
Q

What does plasminogen activator 1 cause?

A

Invasion and metastasis

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17
Q

What factors stimulate the directional growth of endothelial cells (angiogenic factors)?

A

Vascular endothelial growth factor
Fibroblast growth factor 2
Placental growth factor
Angiopoietin 2

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18
Q

What are the angiogenic factors secreted by?

A

Tumour cells or components of the extracellular matrix

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19
Q

What does VEGF do?

A

activates cell survival, vascular permeability, gene expression and cell proliferation

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20
Q

What do you loose in the epithelial-mesenchymal transition?

A

Epithelial shape and polarity
Cytokeratin intermediate filament expression
Epithelial adherens junction position

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21
Q

What do you gain in the epithelial-mesenchymal transition?

A 
Fibroblast-like shape and motility
Invasiveness
Vimentin intermediate filament expression
Mesenchymal gene expression 
Protease secretion
22
Q

What proteases are secreted in the epithelial-mesenchymal transition?

A

MMP-2 and MMP-9

23
Q

What causes the loss of epithelial shape and cell polarity in the epithelial-mesenchymal transition?

A

Beta-catenin and cloudin-1

24
Q

What causes the loss of epithelial adherens junction position in the epithelial-mesenchymal transition?

A

E-cadherin

25
Q

What increases the gain of mesenchymal gene expression in the epithelial-mesenchymal transition?

A

Fibronectin, PDGF receptor, alpha 5 beta 6 integrin

26
Q

What are E-cadherins?

A

Homotypic adhesion molecules

27
Q

What are E-cadherins dependant on?

A

Calcium

28
Q

What do E-cadherins inhibit?

A

Invasiveness

29
Q

What does E-cadherin bind to?

A

Beta-katenin

30
Q

What is contact inhibition?

A

Once cells have bound to other cells with the same cadherin, it signals for them not to migrate or proliferate

31
Q

What forms a tumour mass?

A

When E-cadherin is lost in tumours, so you loose contact inhibition and cells grow on top of each other and proliferate

32
Q

What factors are released by stromal cells?

A

Angiogenic factors, growth factors, cytokines and proteases

33
Q

What does the tumour activation of urokinase-type plasminogen activator result in?

A

Plasmin production

34
Q

What does plasmin activate?

A

Matrix metalloproteases

35
Q

What do matrix metalloproteases do?

A

degrade extracellular matrix
release matrix-bound angiogenic factors

Which allows invasion

36
Q

What is an example of a matrix bound angiogenic factor?

A

Transforming growth factor-beta1

37
Q

What are the common sites of metastasis for breast cancer?

A

Lung
Liver
Brain
Bone

38
Q

What are the hypotheses for pattern of tumour spread?

A

Mechanical hypothesis
Seed and soil hypothesis
Genetic alterations acquired during disease progression

39
Q

What is the mechanical hypothesis for tumour spread?

A

Anatomical considerations like blood and lymphatic systems and entrapment in capillary beds

40
Q

What is the seed and soil hypothesis for tumour spread?

A

Specific adhesions between tumour cells and endothelial cells in the target organ, creating a favourable environment in the target organ for colonisation

41
Q

What tumour processes can be targeted to inhibit cancer?

A

Tumour angiogenesis
Cell motility
Invasion

42
Q

What is avastin?

A

Monoclonal antibody drug that targets anti-angiogenesis

43
Q

What types of cancer is avastin approved for?

A

Colorectal, lung, kidney, ovarian

44
Q

How does avastin work?

A

Binds to VEGF and prevents it from binding to VEGF receptors on endothelial cells

45
Q

What are the common sites of metastasis for breast cancer?

A

Lung
Liver
Brain
Bone

46
Q

What are the common sites of metastasis for colorectal cancer?

A

Liver

lung

47
Q

What are the common sites of metastasis for stomach cancer?

A

Oesophagus
Liver
Lung

48
Q

What are the common sites of metastasis for lung cancer (non small-cell)?

A

Adrenal gland
Liver
Bone
Brain

49
Q

What are the common sites of metastasis for pancreatic cancer?

A

Liver

Lung

50
Q

What are the common sites of metastasis for prostate cancer?

A

Bone

MBD/MI (Wothaya) (57 decks)

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