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Biology Of Cancer > Invasion And Metastasis > Flashcards

Invasion And Metastasis Flashcards

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1
Q

What is metastasis

A

A secondary tumour that grows separate from the primary and has arisen from detached transported cells

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2
Q

What are the two common hits in colorectal cancer?

A

APC gene (a tumour suppressor) by a germline mutation in FAP and a somatic mutation in sporadic CRC

Second hit is a somatic mutation to APC

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3
Q

After the initial two hits in CRC, what other mutations can occur after this?

A

In proto-oncogenes

  • KRas
  • Smad4

p53

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4
Q

What do the initial two hits in CRC cause?

A

Aberrant crypt foci and progression to early adenoma

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5
Q

What are the steps in metastasis?

A

Growth of primary tumour
Local invasion
Transport to different sites
Thrive at a new site

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6
Q

How can cancer cells be transported to different sites?

A

Intravasation
Transport through circulation
Arrest in microvessels of various organs

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7
Q

If metastasis is such an inefficient process, what makes it successful?

A

The huge number of cells

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8
Q

What steps do cells have to do in order to metastasis which makes it inefficient?

A

Intravasate into the vasculature and survive in the bloodstream
Arrive and arrest in secondary sites
Extravasate out of the vasculature into the secondary organ
80% get to this point

Form micrometastases - around 2% initiate growth
Persist to grow into micrometastases - 0.02% manage this

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9
Q

Give an example of what environmental changes can occur to allow metastasis

A

Tumour-associated macrophages promote breast cancer metastasis
-A paracrine loop between tumour cells and macrophages is required for tumour cell migration

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10
Q

How is cell-to-cell adhesion lost?

A

Changes in cadherins such as E-cadherin on the plasma membranes that hold cells together

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11
Q

How can E-cadherin be repressed?

A

Activation of repressors such as

  • SNAIL
  • SLUG
  • ZEB1
  • ZEB2
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12
Q

Which cancer is high expression of ZEB1 and 2 seen in?

A

Bladder cancer - leads to less E-cadherin

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13
Q

What is epithelial to mesenchymal transition?

A

When cells lose their polarity and cell-cell adhesion

Gain migratory and invasive properties to become mesenchymal stem cells

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14
Q

How can epithelial to mesenchymal transition be activated?

A

A number of signalling pathways including

  • E-cadherin and catenins being repressed which are epithelial markers
  • mesenchymal markers induced such as fibronectin and N-Catherine
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15
Q

What are the different types of migration modes cells need to have to metastasise?

A

Mesenchymal transition
Amoeboid transition
Collective migration

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16
Q

Which types of cancer cells use mesenchymal transition?

A

Fibrosarcoma

Glioblastoma

17
Q

What happens to allow mesenchymal transition?

A

Activation of Rac at the leading end allowing formation of new contracts (integrin)
Inhibition of Rho leading to dissolution of adhesions at the other end
Contraction of actin and myosin to promote translocation of the cell

18
Q

How is Rho activated in mesenchymal transition?

A

When a GDP nucleotide is converted to GTP by guanine nucleotide exchange factors

19
Q

What is amoeboid motility?

A

When cancer cells squeeze through matrix barriers without the use of MMPs or integrin engagement

20
Q

Which cells migrate using amoeboid motility?

A

Leukaemia and lymphoma

21
Q

What is collective migration?

A

When a number of cells move together and so retain cell-to-cell adhesion

22
Q

What must be changed about proteolysis of a cell in order to invade?

A

Remodelling of the extracellular matrix - must destruct the basement membrane

Increased proteolytic activity of the cells

23
Q

What are some extracellular matrix degrading proteins?

A 
Matrix metalloproteinases
Serine proteases 
Adamlysin-related membrane proteases 
Bone-morphogenic protein (BMP)-1 type metalloproteinases
Heparanases 
Cathepsins, cysteine proteases
24
Q

Give some examples of serine proteases? (A category of extracellular matrix degrading proteins)

A

Plasminogen activating system
Plasmin
Serpins
Thrombin

25
Q

What are the two types of matrix metalloproteinases (MMPs)?

A

Transmembrane type MT-MMPs
Secreted MMPs
-undergo extracellular cleavage by plasmin
-bind to ECM

26
Q

What do cells form during intravasation and what components are required for this?

A

Invadosome

  • actin regulators
  • signalling/adaptors
  • components of adhesion complexes
  • proteases eg MMP2
  • membrane remodelling
27
Q

How big can a tumour get before it requires blood vessels?

A

2mm

28
Q

How is angiogenesis induced by tumours?

A

Tumour cells secrete VEGF to promote angiogenesis
Endothelial cell release paracrine growth factors
Hypoxia-inducible factors (HIFs) transcription of VEGF
PDGF promotes survival

29
Q

How can tumour vessels be structurally abnormal?

A

Formation of emboli and tumour nests

30
Q

What are some different body cavities that cells can travel via (by direct invasion)

A

In colon cancer - the peritoneum
In lung cancer - pleurae
In brain cancer - the ventricles

31
Q

How do cancer cells exit blood vessels?

A

Similar to macrophages

  • attach to the endothelium
  • roll
  • spread out
  • extravasate through the epithelium into the stroma
32
Q

Describe the mechanism of homing of cancer cells

A

Get selective adhesion to sites on the endothelial cells at the site of organ homing
Selective chemotaxis of circulating tumour cells to the organ producing soluble attribution
Selective growth from the local environment

33
Q

Name the proteins required for the different stages of immigration of tumour cells from lymphatics and blood vessels

A

Attachment and rolling over endothelium - interaction of surface carbohydrates and selectins

Spreading - integrins and actin cytoskeleton

Extravasation - integrins, MMPs, actin, cytoskeleton

34
Q

What are selectins?

A

A family of carbohydrate-building cell adhesion proteins

  • L-selectin
  • P-selectin
  • E-selectin
35
Q

What binds to selectins?

A

Carbohydrate ligands which are covalently linked to mucous and proteoglycans on the surface of tumour cells

36
Q

How is rolling stopped?

A

Selectins trigger biochemical signals that stop the rolling of tumour cells
Get activation of integrins, increased chemokine and MMP production

37
Q

Define invasion

A

Infiltration of local tissue by cancer cells

Biology Of Cancer (13 decks)

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