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omgmbd > L23: Tumour Angiogenesis, Invasion & Metastasis > Flashcards

L23: Tumour Angiogenesis, Invasion & Metastasis Flashcards

1
Q

What are the characteristics of malignant tumours?

A

→growth
→invasiveness
→metastasis

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2
Q

What are the key steps in cancer progression?

A

→transformation
→angiogenesis
→motility and invasion
→metastasis

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3
Q

What happens in transformation in cancer progression?

A

→extensive mutagenic
→epigenetic changes
→clonal selection

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4
Q

What happens in angiogenesis of cancer progression?

A

→new blood vessel formation (overcomes limitations imposed by hypoxia

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5
Q

What happens in motility and invasion in cancer progression?

A

→epithelial to mesenchymal transition

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6
Q

What is metastasis?

A

→colonisation of target organs (ability to expand from micrometastases)

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7
Q

What is the difference between angiogenesis and vasculogenesis?

A

→Angiogenesis is the formation of new blood vessels from pre-existing vessels

→Vasculogenesis is the formation of new blood vessels from progenitors

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8
Q

What are the three types of angiogenesis and what does each lead to?

A

→Developmental/ vasculogenesis= organ growth
→Normal
angiogenesis= wound repair, placenta
→Pathological angiogenesis= tumour angiogenesis

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9
Q

What is the maximum size of tumours without their own blood supply?

A

→1-2 mm3

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10
Q

Describe the angiogenic process

A

→Tumour switches on expression of angiogenic genes/factors

→they initiate new blood vessel growth

→New network of blood vessels grows in and around the tumour

→increasing the delivery of oxygen and nutrients
that allows it to increase growth

→provides a route for cells to shed off and spread

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11
Q

What allows directional growth of new vessels toward a tumour?

A

→Chemotaxis signals

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12
Q

What is a strong stimulus for tumour angiogenesis?

A

→hypoxia→

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13
Q

What is hypoxia?

A

→low oxygen tension <1% O2

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14
Q

What genes are activated by hypoxia?→

A

→VEGF
→GLUT-1
→u-PAR
→PAI-1

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15
Q

What are the 4 factors that stimulate the directional growth of endothelial cells?

A

→Vascular Endothelial Growth Factor (VEGF)
→Fibroblast Growth Factor 2 (FGF 2)
→Placental growth factor (PlGF)
→Angiopoietin 2 (Ang 2

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16
Q

How are factors that stimulate directional growth of endothelial cells found in the cells?

A

→stored bound to components of the extracellular matrix

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17
Q

How are factors that stimulate directional growth of endothelial cells activated?

A

→Matrix metalloproteinase 2 (MMP-2)

18
Q

What do matrix metalloproteinase?

A

→proliferation,
→migration
→invasion

19
Q

Describe the signalling of Vascular endothelial growth factor

A

→VEGF binds to VEGF-R2 on endothelial cells

→VEGF/VEGF-R2 dimerizes at the plasma membrane and recruits cofactors

→subsequently activate 3 major signal transduction pathways

20
Q

What are the pathways that VEGF activate?

A

→cell survival,
→vascular permeability,
→gene expression
→cell proliferation

21
Q

What are the three mechanisms of tumour cell motility and invasion?

A

→Increased mechanical pressure caused by rapid cellular proliferation

→Increased motility of the malignant cells (epithelial to mesenchymal transition)

→Increased production of degradative enzymes by both tumour cells and stromal cells

22
Q

What is epithelial mesenchymal transition?

A

→ epithelial cells lose their cell polarity and cell–cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells

23
Q

What do epithelial cells lose in EMT and what do they lead to?

A

→β-catenin, claudin-1=Epithelial shape and cell polarity

→Cytokeratin intermediate filament expression

→E-cadherin= Epithelial adherens junction protein

24
Q

What do epithelial cells acquire during EMT?

A

→Fibroblast-like shape and motility

→Invasiveness

→Vimentin intermediate filament expression

→Mesenchymal gene expression (fibronectin, PDGF receptor, αvβ6 integrin)

→Protease secretion (MMP-2, MMP-9)

25
Q

What are E-cadhedrins?

A

→Homotypic adhesion molecule (adhesion of cells with the same cadherin)

→Calcium-dependent

26
Q

What is the function of E-cadherins?→

A

→Inhibits invasiveness

→Binds β-catenin

27
Q

What does loss of E-cadherins lead to?

A

→disrupted cell-cell adhesion
→loss of contact inhibition
→cells grown on top of each other as opposed to a monolayer

28
Q

What are some factors released by stromal cells?

A

→angiogenic factors,
→growth factors, cytokines,
→proteases
→u-PA

29
Q

What is uPA?

A

→Urokinase-type plasminogen activator

→plasmin production

30
Q

What roles does plasmin play in tumour progression?

A

→activates matrix metalloproteinases (MMPs),

→permit invasion by degrading extracellular matrix

→release matrix-bound angiogenic factors such as transforming growth factor-β1 (TGF-β1)

→ allows cells to migrate

31
Q

What does uPA do to latent cancer cells?

A

→activates latent cancer cells

32
Q

What is the different between intravasation and extravasation?

A

→intravasation= entry of tumor cells into the circulation

→extravasation= exit of tumor cells from the circulation

33
Q

What are common sites of tumour metastasis for breast cancer?

A

→lung
→brain
→liver
→bone

34
Q

What are common sites of tumour metastasis for lung cancer?

A

adrenal gland

35
Q

What are common sites of tumour metastasis for gastric cancer?

A

→oesophagus

→stomach

36
Q

What are common sites of tumour metastasis for prostate cancer?

A

→bone

37
Q

What are the two hypotheses to explain the pattern of tumour spread?

A

→mechanical
→seed and soil
→Genetic alterations acquired during progression allow tumour cells to metastasize

38
Q

What is the mechanical hypothesis of tumour spread pattern?

A

→metastasis is determined by the pattern of blood flow

→entrapment in capillary beds

39
Q

Explain the seed and soil hypothesis of tumour spread pattern

A

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

40
Q

What aspect of cancer progression has been successfully addressed?

A

→tumour angiogenesis

41
Q

What types of cancer is Avastin used for?

A

→colorectal,
→lung, kidney
→ovarian cancersand eye diseases

42
Q

Describe the mechanism of Avastin/ Bevacizumab

A

→a monoclonal antibody
→binds to VEGF

→prevents VEGF binding to VEGF receptors on endothelial cells

omgmbd (29 decks)

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