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People and Illness > Metastasis > Flashcards

Metastasis Flashcards

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1
Q

What is the sequence of events which occurs in metastasis?

A

detachment of tumour cells form their neighbours
invasion of surrounding connective tissue
intravasation into lumen of vessels
evasion of host defence mechanisms
adherence to endothelium at remote location
extravasation of cells from vessel lumen into surrounding tissue
survival and growth in new environment

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2
Q

E-cadherin is expressed in many carcinomas. T/F?

A

True

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3
Q

What proteinases are often over expressed in cancer cells?

A

Matrix metalloproteinases

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4
Q

E-cadherin is calcium dependent and sometimes in cancer cells there is a mutation so that the calcium binding domain of E-Cadherin is missing. What effect does this have?

A

Unfunctional E-cadherin allowing aggressive tumour invasion

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5
Q

What are integrins?

A

Cell-surface molecules that bind to extracellular matrix molecules

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6
Q

Specific integrins seem to promote invasion and metastasis. Describe possible mechanisms by which this occurs

A

Decreased adhesion to the basement membrane surrounding the epithelium
increased migration through stroma
increased adhesion to basement membrane or endothelial cells of blood vessels

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7
Q

Describe the mechanism by which HGF can induce epithelial cells to dissociate and scatter in culture.

A

HGF binds to c-met (a receptor tyrosine kinase) causing increased tyrosine phosphorylation of B-catenin which disrupts E-cadherin mediated adhesion

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8
Q

What type of collagen do matrix metalloproteinases degrade and why is this relevant to metastasis?

A

Type four collagen - which makes up the basement membrane thus allowing tumour to break through the bm

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9
Q

Describe the role of VEGF in metastasis

A

VEGF is expressed by hypoxic cancer cells
VEGF binds to its receptors on nearby endothelial cells causes these cells to migrate towards the tumour and start to form new blood vessels
the newly formed vessels are weak and leaky which allows fibrinogen to leak out and a clot to form
the clot provides a good surface for the endothelium to grow onto

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10
Q

Tumour cells can exploit the abilities of lymphocytes to intravasate and extravasate. T/F?

A

True

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11
Q

What are the ten major characteristics of cancer cells?

A 
Unlimited multiplication
Escape from growth suppressors
Promotion of invasion and metastasis
Resistance of apoptosis
Stimulation of angiogenesis
Maintenance of proliferative signalling
Elimination of cell energy limitations
Evasion of immune destruction
Genome instability and mutation
Tumour enhanced inflammation
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12
Q

Metastasis is the leading cause of cancer related death. How does metastasis cause death?

A

Physical obstructions
Compromised organ function
Competing with healthy tissue for nutrients and oxygen

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13
Q

How do mesenchymal cells differ from epithelial cells?

A 
Loose or no interactions between cells
No cell-cell junctions
No clear apical/basolateral membranes
No apicobasal polarised distribution of organelles and cytoskeleton
Mobile and sometimes invasive
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14
Q

E-cadherin binding is homotypic. What does this mean?

A

E-cadherin on one cell binds to e-cadherin on another cell

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15
Q

What molecules facilitate the binding of E-cadherin to the actin cytoskeleton?

A

alpha and beta catenin

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16
Q

E-cadherin expression can be disrupted in cancer by silencing of the CDH1 promoter. How does this occur?

A

Methylation mutations in proteins which interact with e-cadherin such as beta catenin

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17
Q

What transcription factors normally suppress E-cadherin and can be over-expressed in cancer cells?

A

Slug
Snail
Twist

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18
Q

Integrins exhibit bidirectional signalling. T/F?

A

True

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19
Q

How many possible heterodimers can be formed from integrins?

A

24

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20
Q

Where are integrins found?

A

basal epithelial cells

focal adhesions of migrating cells

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21
Q

In what ways is altered intern expression useful for cancer cells?

A

Supports oncogenic growth factor receptor signalling
Allows cell migration and invasion
Allows extravasation from blood vessels
Causes colonisation of metastatic sites
Allows survival of circulating tumour cells

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22
Q

In metastasis, why cells secrete HGF?

A

Stromal cells

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23
Q

What protein is activated by urokinase plasminogen activator?

A

Plasminogen is activated to plasmin

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24
Q

What is the function of cathepsin K collagenolytic activity?

A

Matrix degradation

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25
Q

What type of cancers commonly spread through the lymphatic system?

A

Carcinomas e.g. breast, colon and lung

26
Q

What type of cancers commonly spread through the blood?

A

Sarcomas

Some carcinomas such as kidney, colorectal and prostate

27
Q

What type of cancers commonly spread through transcoelomic spread?

A

Cancers which originate in the peritoneal cavity such as ovarian and colorectal

28
Q

What steps are involved in intravasation?

A

Attachment
degradation of basement membrane
diapedesis
new leaky blood vessel formation

29
Q

What steps are involved in extravasation?

A

Attachment
degradation of basement membrane
diapedesis
new structural sound blood vessel formation

30
Q

Most cancer cells do not survive transport in the blood. Why is this?

A

shear stress of blood flow
immune detection
anoikis

31
Q

What is anoikis?

A

Form of programmed cell death which occurs in anchorage-dependent cells when they detach from the ECM

32
Q

Cancer cells in the blood start to slow down and marginalise then roll along the endothelium. What molecules mediate this?

A

Selectins

33
Q

The arrest of cancer cells on the endothelium during extravasation is mediated by which molecules?

A

Integrins

34
Q

Which molecules mediated diapedesis in extravasation of cancer cells?

A

Junctional adhesion molecules

35
Q

Spread and crawling of cancer cells. along the endothelium in extravasation is mediated by which molecule?

A

Cell adhesion molecules

36
Q

What are selectins?

A

Carbohydrate binding transmembrane molecules

37
Q

What is the main physiological function of selectins?

A

mediate leukocyte recruitment to sites of inflammation or to lymphoid tissues

38
Q

Enhances expression of selection ligands by cancer cells is correlated with metastasis and a poorer prognosis. T/F?

A

True

39
Q

Define angiogenesis

A

The formation of new vessels from existing vasculature

40
Q

When cancer cells become hypoxic, which transcription factor mediates VEGF production?

A

Hypoxia inducible factor (HIF)

41
Q

What molecules usually inhibit angiogenesis?

A

Thrombospondin
Endostatin
Tumstatin
Angiostatin

42
Q

Angiostatin is a fragment of….?

A

Plasminogen

43
Q

Endostatin is a fragment of….?

A

Collagen type XVIII

44
Q

Tumstatin is a fragment of….?

A

Collagen type IV

45
Q

What are the two models which determine where metastasis occur?

A

Seed and soil hypothesis

Mechanical model

46
Q

Describe the mechanical theory of metastasis?

A

Blood flow patterns determine which organ the cancer cells travel to first and the relative size of cancer cells and capillaries leads to the efficient arrest of most circulating cancer cells in the first capillary bed that they encounter

47
Q

The tumour microenvironment contains cancer associated fibroblasts. What do these secrete?

A

MMPs
Cytokines
IL-8
VEGF

48
Q

The tumour microenvironment contains cancer associated pericytes. What is the role of pericytes in cancer?

A

Low pericyte coverage results in leaky vessel structure which facilitates tumour cell invasion and extravasation

49
Q

How do M1 and M2 macrophages differ in their response to tumour?

A

M1 macrophages are tumorocidal

M2 macrophages promote tumour growth

50
Q

A large abundance of tumour associated macrophages is associated with poor clinical outcomes. T/F?

A

True

51
Q

The tumour microenvironment contains tumour associated macrophages. What do these secrete?

A

MMPS and growth factors

52
Q

Sustaining proliferative signalling is a hallmark of cancer. What type of drugs can be used to combat this?

A

EGFR inhibitors

53
Q

Evading growth suppressors is a hallmark of cancer. What type of drugs can be used to combat this?

A

Cyclin dependent kinase inhibitors

54
Q

Avoiding immune detection is a hallmark of cancer. What type of drugs can be used to combat this?

A

Immune activating anti-CTLA4 monoclonal antibodies

55
Q

Enabling replicative immortality is a hallmark of cancer. What type of drugs can be used to combat this?

A

Telomerase inhibitors

56
Q

Tumour promoting inflammation is a hallmark of cancer. What type of drugs can be used to combat this?

A

Selective anti-inflammatory drugs

57
Q

Activating invasion and metastasis is a hallmark of cancer. What type of drugs can be used to combat this?

A

inhibitors of HGF / c-met

58
Q

Inducing angiogenesis is a hallmark of cancer. What type of drugs can be used to combat this?

A

inhibitors of VEGF signalling

59
Q

Genome instability and mutation is a hallmark of cancer. What type of drugs can be used to combat this?

A

PARP inhibitors

60
Q

Resisting cell death is a hallmark of cancer. What type of drugs can be used to combat this?

A

Proapoptopic BH3 mimetics

61
Q

Dysregulating cell energetics is a hallmark of cancer. What type of drugs can be used to combat this?

A

Aerobic glycosides inhibitors

People and Illness (18 decks)

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