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MCB II Block 1 > Cancer II 4 > Flashcards

Cancer II 4 Flashcards

1
Q

drug that blocks VegF

A

Bevacizumab

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2
Q

as the tumor grows, the cells in center get

A

hypoxic

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3
Q

as cells get hypoxic they accumulate what TF

A

HIF

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4
Q

HIF does what

A

transcribes VEGF

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5
Q

VEGF goes to

A

VEGF receptors

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6
Q

what is function of VEGF

A

goes to endothelial cells to stimulate more growth

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7
Q

what drug would you use to block VEGF

A

Bevacizumab

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8
Q

mab is

A

monoclonial antibody

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9
Q

Sunitinib does what

A

inhibits tyrosine kinase activity

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10
Q

What does bevacizumab do

A

monoclonal antibody targets growth factor to block VEGF receptor

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11
Q

any cell migrating needs to secrete

A

MMPs - digest and get through tissue

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12
Q

besides blocking VEGF how can you stop angiogenesis

A

block MMP activity

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13
Q

thrombospondin

A

naturally occuring angiogenesis inhibitor

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14
Q

endostatin

A

naturally occuring angiogenesis inhibitor

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15
Q

if endothelial cells are exposed to VEGF signaling (proangiogenic) they start proliferating and VEGF will do what

A

activates ras/map kinase acitvity

stimualtes expression of FAS-R

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16
Q

what does FAS-R mean

A

fas receptor

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17
Q

besides activating ras/map kinase what does VEGF stimulate

A

expression of FAS-R

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18
Q

thrombospondin can stimulate cells to secrete

A

Fas ligand (Fas-L)

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19
Q

FasL stands for

A

Fas Ligand

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20
Q

stimualte expression of Fas-L what happens

A

endothelial cells express Fas-L, it will target only the newly divided endothelial cells so it will bind to FasR and lead to apoptosis

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21
Q

When FasL binds to FasR what happens

A

apoptosis

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22
Q

can FasL bind to mature endothelial cells

A

no

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23
Q

what does FasL target

A

newly devloping endothelial cells that express FasR

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24
Q

what is the purpose of new trials that are mimicking FasL

A

stopping angiogenesis - it will bidn Fas R and lead to apopt.

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25
Q

endostatin is a protein that helps

A

stabilize endothelial cell-cell interactions

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26
Q

newly formed blood vessels are very

A

leaky/permeable

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27
Q

endostatin could be therapeutic drug in US b/c

A

endostatin will anchor the endothelial cells and will stabilize the cells so they can’t sprout, it would inhibit the vessel sprouting

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28
Q

in chronic wounds there are not enough

A

angiogenesis promoters

there are too many angiogensis inhibitors

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29
Q

after ischaemic stroke the angiogenic response is direclty related to

A

prognosis for pt

the quickly we can supply bood to that area of the brain the better the outcome for that pt

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30
Q

metastasis is responsible for what percent of cancer death

A

90%

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31
Q

tumor cells are ___clonal & _____geneous

A

monocolonal

heterogeneous

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32
Q

main difference b/w benign and malignant tumor cells

A

malignant are invasive and capable of matastisizing

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33
Q

angiogenesis is very tightly correlated to

A

metastesis

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34
Q

direct extension of tumor

A

the cancer invading local tissue

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35
Q

lymphatic spread

A

spread into lymphatic circulation

36
Q

haematogenous cancer spread

A

spread of cancer into blood spread

37
Q

most common initial dissemination of carcinoma is into

A

lymphatic circulation

38
Q

most common type of cancer in humans

A

carcinoma

39
Q

carcinoma is

A

cancer of epithelial cells

40
Q

anatomical location from primary tumor can tell you where

A

cancer is likely to spread to first

41
Q

what organ is most commonly infiltrated by tumors

A

lung

42
Q

what is second most common organ to be infiltrated by tumors

A

liver

43
Q

what primary tumors are most likely to metastesize to liver

A

blood from digestive organs

44
Q

steps that need to occur for cancer to be successful at metastasis

A

break away from primary tumor, invade through connective tissue (MMP), attach to basal lamina surrounding endothelial cells, digest through, intravasate, get into blood stream, survive circulation, bind to endothelial cells of other organ, digest throgh endothelial cells, digest through new tissue, form secondary tumor through restimulatino of angiogenesis

45
Q

is it easy to complete the steps to become metasasis

A

no

46
Q

growth of secondary tumor is one of the major

A

rate limiting steps

47
Q

why is growth of second tumor rate limit step for tumor

A

the new enviornment might not be good for them to be able to grow. the types of stromal cells will be different, the whole enviornment different and the tumor cells might not be adapted to the new environment

48
Q

for tumor cells to invade they have to secrete

A

MMP

49
Q

to get through basal lamina tumor cells have to secrete

A

MMP

50
Q

what is first step of cell invasion

A

cell attachment

51
Q

what is second step of cell invasion

A

enzymatic degradation of ECM

52
Q

what is 3rd step of cell invasion

A

cell migration

53
Q

describe the first step of cell invasion

A

downregulation of cell-cell attachment, then it attaches to basal lamina, then it expresses MMP

54
Q

autocrine motility factor

A

stimualtes itself to migrate, a lot of cancer cells express this
when it binds to own AMF receptors it triggers rearrangement of cell to start migrating

55
Q

what is a common mutation found in the first step of metastesis (loss of cell-cell adhesion, loosening of intracellular junctions)

A

loss of e-cadherin

56
Q

what changes do cancer cells go through to have attachment to ECM

A

change in integrin expression profiles (ex: they might express integrins that are normally found in blood cells that migrate)
increased CD44 hyaluronan-binding proteins

57
Q

CD44 hyaluronan sequesters what to help with digestion

A

MMP

58
Q

very generally, what happens to cancer cells to allow them to attach to ECM

A

change the types of cell matrix receptors and start to express cell matrix receptors that are involved in invasion

59
Q

should epithelial cells normally express MMP

A

no

60
Q

in cancer cells what do they express to allow them to detach

A

MMP

61
Q

uPA and tPA are normally secreted by what

A

stromal cells

62
Q

uPA stands for

A

urokinase plasminogen activator

63
Q

tPA stands for

A

tissue-type plasminogen activator

64
Q

uPA and tPA do what

A

convert plasminogen into plasmin

65
Q

what does plasmin do

A

activate MMPs present in ECM
digests ECM
digests clots

66
Q

in cancer cells to degrade the ECM the cancer cells do what

A

serine proteases: uPA and tPA
matrix metalloproteinases
they can either make this themself, or stimulate the cells around them to make it

67
Q

uPA and tPA are both

A

serine proteases

68
Q

upregulation of MMP2 is commonly found in

A

metastasis cancer

69
Q

as the MMP degrades ECM and other cells what does it release

A

growth factor - this helps proliferation of cancer cells

70
Q

what is an example of a crytpic site

A

laminin

71
Q

laminin is a component of what

A

basal lamina

72
Q

when laminin is degraded by MMP what happens

A

its cleaved and cleavage product is a motility factor, when cell binds to the digested product it will stimualte the cell to migrating

73
Q

what are the two ways the cell can become mobile

A

binding to some of the digestive products from digestion of the matrix

tumor secreted motility factor - the cancer cell itself starts to express motility factor

74
Q

what is a major motility factor cancer releases

A

Autocrine Motility Factor (AMF)

75
Q

binding of cell receptors to the motility factor stimualtes what

A

Rho GTPases

76
Q

Rho GTPase stimualte what

A

changes in cytoskeleton resulting in movement

77
Q

besides AMF what are other tumor motility factors

A

HGF

EGF

78
Q

AMF is a what

A

chemokine

79
Q

increased expression of AMF cells in vitro become

A

motile

80
Q

AMF receptor activation activates what

A

Rho GTPases to stimualte cell migration
Ras Map kinase pathway
PI3 kinase pathwy
expression of VEGF

81
Q

EGFR signling can activate

A

Ras Map kinase pathway
Rho GTPases
expression of AMF

82
Q

VEGF signaling is goign to cause endocytosis of

A

the VE-cadherin receptors

83
Q

vascular endothelial cadherin receptors are responsible for

A

keeping endothelial cells together

84
Q

with VEGF signaling it activates proliferation of endothelial cell and downregulates

A

cell-cell adhesions (increases permeability so it’s easier for cancer cells to get inside the newly formed vessels)

85
Q

when cancer cell wants to transport what does it need to express

A

receptors to clump together and be able to bind to platelets to form emboli to better their chance of survival

86
Q

what do cancer cells in order to better their chances of survival when they are being transported down vasculature

A

emboli

87
Q

cancer cells can influence other cells, how do they hide from the immune system

A

downregulate the MHC complex

MCB II Block 1 (12 decks)

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