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Cancer Biology and Therapy > Invasion and metastasis > Flashcards

Invasion and metastasis Flashcards

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1
Q

what is metastasis

A

when tumour cells leave the primary tumour to travel to a distant site

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2
Q

what systems do tumour cells migrate through?

A

blood or lymth

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3
Q

TF cancer often involves drastic shape changes of cells

A

true- drastic

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4
Q

what is epithelial mesenchymal transition?

A

the conversion of a epithelial cell to non polarised motile spindle shaped cell resembling a fibroblast

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5
Q

what is epithelial mesenchymal transition influenced by?

A

tume me AT THE EDGE OF THE TUMOUR IN CONTACT WITH THE TUMOUR STROMA

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6
Q

5 STAGES OF METASTASIS?

A
  1. invasion
  2. intravasation
  3. transport
  4. extravasation
  5. angiogenesis
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7
Q

explain invasion?

A

stage at which the dissociated tumour cells infiltrate to the surrounding storm and invade through the membrane which has the blood and lymphs

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8
Q

explain intravasation

A

dissociated tumour cells get into the basculature

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9
Q

what must the tumour cells do before undergoing intravasiation?

A

successfully crossed the extracellular matriculates

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10
Q

2 ways cells move in the circulatory systems

A

actively by motility of be passively carried with fluid flow

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11
Q

what is anoikis

A

a form of apoptosis which is triggered by detachment of a solid substrate

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12
Q

what do some cells need to do in the circulatory system to avoid anoikis

A

anchorage to solid substrate

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13
Q

do metastatic cells tend to undergo anoikis?

A

they tend to be more resistant than non-metastatic cells

‘anchorage independent’

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14
Q

explain extravasation

A

the cells actively leaving the vasaclature

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15
Q

normal cells have a _____ level of E cadherin and a _____ level of N cadherin

A

high

low

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16
Q

cancer cells have a _____ level of E cadherin and a _____ level of N cadherin

A

low

high

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17
Q

2 features of mesenchymal cells compared to normal re polarity and adhesion

A

mesenchymal cells have no cell polarity and have a loss of cell adhesion

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18
Q

how are mesenchymal tumour cells able to become free from cell adhesions?

A

degradative enzymes are produced by them or immune cells to degrade the matrix and facilitate invasion

19
Q

4 enzymes implicated in tumour cell invasion?

A

serine proteinases plasmin
plasminogen activator
cathepsin b
metal dependent proteinases of the matrix metalloproteinase MMP fairy

20
Q

epithelial cell cell interactions are mediated primarily by?

A

cadherins

21
Q

what are cadherins

A

transmembrane glycoproteins

recognise and bind to molecules of the same kind in adjacent cells

22
Q

what is the rate limiting step in the metastatic process?

A

intravasation

23
Q

what is transendothelial migration?

A

tumour cells attach to the vasculature endothelial wall to create enough space to get into the vasculature

24
Q

what protects the cancer cells from shear stress in the circulatory system?

A

thrombus formation around the tumour cells

25
Q

what else does thrombus formation around the cancer cell do to help the tumour

A

secrete angiogenic growth factors to support secondary establishment of tumours

26
Q

role of P-selectin when the tumour cell is in the blood

A

helps them evade recognition by immune

released by leukocytes and platelets which bridge between endothelial cells and metastatic tumour cells

27
Q

explain extraversion process

A

cell is trapped physically in the capillary
with minutes a large number of platelets attach to the cell forming a micro thrombus
the cancer cell pushes endothelial cells aside and achieves direct contact with the underlying capillary basement membrane
proteases dissolve the microthrombus within a day
the cancer cell proliferates IN the lumen of the capillary
within a few days the cancer cells break through the capillary basement membrane and invade the surrounding tissue

28
Q

what happens to the micro thrombus which forms around a cancer cell which is undergoing extravasation

A

gets dissolved by proteases

29
Q

what are the most common sites of metastasis

A

lung and liver as most tumour cells enter the vasculature in small veins or capillaries

30
Q

does metastasis happen by chance?

A

no it only happens when the tumour cells have metastatic ability and the organs have growth advantage
they must both be compatible

31
Q

what is the seed and soil hypothesis

A

metastasis happens only when:
o The seed (the tumor cells with metastatic ability)
o The soil (the organs or tissues providing growth advantage to seeds) are compatible.

32
Q

role of matrix metalloproteases?

A

degrade components of the ECM facilitating angiogenesis, tumour invasion and metastasis

also activate signalling molecules ee.g. vascular GF

33
Q

how do MMPs modulate the interactions between tumour cells?

A

by cleaving E cadherin between tumour cells and the ECM

34
Q

why is MMP a good target for cancer therapies?

A

as they have multiple functions

35
Q

what does expression of N-cadherin do? what is the correlated with?

A

provokes E-cadherin down regulation which is correlated with increased invasion and metastatic progression

36
Q

how can we target N-cadherin in cancer?

A

antagonise

monoclonal antibody against

37
Q

what happens to platelets when they adhere to tumour cells in the blood?

A

they get activated which:
promotes platelet Shape change
intergrin activation
release of biologically active molecules (ATP,ADP,MMP, TFG-b, gf)

38
Q

What do the molecules released by activated intergrins when tumour cells bind to platelets promote?

A

ATP, ADP, MMP-2, TGF-b, GF
they cause platelets aggregation
epithelial mesenchymal transition
angiogenesis

39
Q

what causes intergrin activation when tumour cells and platelets interact?

A

activated upon Tallinn and kindling binding to the intracytoplasmic domain of the b3 chain

40
Q

what are selectins? where are they found

A

adhesion receptors on leukocytes, vascular endothelial cells and cancer cells
they’re bad as they facilitate the extravasation of cancer cells

41
Q

what can inhibitors of P-selectin do?

A

prevent interactions of platelets with cancer cells

= anti-metastatic activity

42
Q

how does CD44 promote metastasis

A

lymphocyte honing receptor
by forming a complex with MMP-9
concentrates the MMP-9 at the surface

43
Q

what can we do to CD44 in cancer therapy?

A

block it

Cancer Biology and Therapy (23 decks)

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