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BIMM 134 - Cancer > Final content - week 9 > Flashcards

Final content - week 9 Flashcards

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1
Q

What is VEGF? is it considered a tumor suppressor? or pro-oncogenic?

A

a major pro-angiogenic factor

a pro-oncogene

oncogene, if mutated, promoting the formation of cancer cells

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2
Q

what is TAM? TAMR?

define TAM + what kind or receptor

A

(a) tumor-Associated Macrophage - a type of white blood cell involved in the immune system’s response to inflammation and tissue repair

(b) tyrosine kinases receptor

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3
Q

what is CAF?

3 points

A
  • Cancer-Associated Fibroblast - a type of connective tissue cell involved in wound healing and tissue structure
  • Activated CAFs create an environment that prmotes growth of pre-exsisting tumors
  • CAF activation is up-regulated in cancer

regardless of how they’re activated

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4
Q

Steps of angiogenesis

A

step 1: Activation of the angiogenic switch via oncogene activation/tumor suppressor mutations/hypoxia

step 2: VEGF production via cancer cells, TAM, and CAF

step 3: VEGF binds to VEGFR triggering downstream signaling pathways in endothelial cells

step 4: Endothelial cell responses

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5
Q

how is the angiogenic switch turned on? what happens once its turned on?

A

via oncogene activation/tumor suppressor mutations/hypoxia

Decreased anti-angiogenic factors (thrombospondin & statins)

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6
Q

How do Endothelial cell responses to form new blood vessel formation?

A

Via Proliferation, matrix degradation, survival, motility

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7
Q

what is thrombospondin?

A

a natural inhibitor of angiogenesis

downregulated in cancer
–> reduced levels or activity can contribute to uncontrolled blood vessel growth

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8
Q

what is statins?

A
  • Inhibit the production of pro-angiogenic factors like VEGF
  • inhibit the growth of new blood vessels
  • downregulated in cancer
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9
Q

what do endostatins - a type of statins - bind?

what does binding lead to?

A

bind integrins found on endothelial cells

leads to the inhibition of migration, proliferation, and survival

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10
Q

what do angiostatins - a type of statins - bind?

A

bind integrins found on endothelial cells

inhibits endothelial cells

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11
Q

VEGF and VEGFR: what does VEGFA binding VEGFR-2 promote? how?

A
  • vascular permeability, cell proliferation, survival, motility, protease production
  • via increase in NOS
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12
Q

what is NOS?

A

Nitric Oxide Synthase

enzymes responsible for producing nitric oxide

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13
Q

is VEFG increased or decreased in cancer cells?

A

increased

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14
Q

VEGF and VEGFR: VEGF receptors are

(a) what kind of receptors?

(b) what does it increase?

A

(a) tyrosine kinase receptors

(b) RAS/MAPK/PI3K pathway which are downstream of VEGFR

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15
Q

VEGF has how many isoforms? VEGF-A

A

VEGF has 6 isoforms A -E

VEGF-A has 4 isoforms

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16
Q

VEGFR have how many isoforms?

A

three isoforms (1-3)

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17
Q

what does VEGFA-VEGFR2 binding do?

A

stimulates angiogenesis

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18
Q

what does VEGFA-VEGFR1 binding do?

A

modulates VEGFR2 such that it prevents excessive angiogenesis

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19
Q

what does VEGFA-NRP binding do?

A

stimulates angiogeneses indirectly

enhance VEGFR-2 signaling

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20
Q

what does VEGFA-VEGFR3 binding do?

A

lymph angiogenesis - growth of lymph system

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21
Q

what are EPHRINS?

A

ligands - signaling molecules

bind to tyrosine kinase receptors on cell surface

Control blood vessel formation

Altered levels in cancer angiogenesis

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22
Q

what are some examples of EPHRINS?

A

B4 and B2

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23
Q

What EPHRINS does VEGF increase in cancer? which does it decrease? why do levels have to change?

A

increase B2

decrease B4

they change for the max amount of vascular growth

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24
Q

VEGF binding to epithelial cells promotes…

A

angiogenesis

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25
if B4 is on the surface of the cell, what will happen?
it will decrease cell sprouting which DECREASES angiogenesis
26
if B2 is on the surface of the cell, what will happen?
it will INCREASE cell sprouting
27
what surface will B4 bind to? what about B2?
surface of veins surface of arterioles
28
what happens when B4 binds to its receptor ? | what decreases?
decrease VEGF
29
what happens when B2 binds to its receptor ?
veins + arterials will grow inconjunction to one another | such that they are developing together in a way that complements each ot
30
what is ANGIOPOIETINS 1?
a protein that promotes structural integrity of existing blood vessels
31
what is ANGIOPOIETINS 2?
a protein that promotes the formation of NEW blood vessels
32
what happens when ANGIOPOIETINS 1 binds to its receptor? what receptor does it bind?
it promotes survival + pericyte attachment it binds to TIE-2, a TKR receptor located on the surface of endothelial cells in the blood vessel
33
what happens when ANGIOPOIETINS 2 binds to its receptor? what receptor does it bind?
it promotes pericyte Detachment + proliferation it binds to TIE-2, a TKR receptor located on the surface of endothelial cells in the blood vessel
34
ANGIOPOIETINS 2: are they tumor suppressors or pro-oncogenes?
pro-oncogene
35
endothelial vs epithelial cells
endo: Endothelial cells line the inner surface of blood vessels (arteries, veins, and lymphatics) epa: Epithelial cells form the lining of various surfaces throughout the body, both internal and external
36
how are ANGIOPOIETINS secreted
by pericyetes
37
what are pericytes?
supporting cells recruited upon vessel formation
38
what is meant by angiogenic effect observed after the binding of ANGIOPOIETINS2 - TIE2 | aka. what is needed to form angiogenic vaasculature? 2 things
to form angiogenic vasculature... permeability has to increase and tear down existing vasculature in order to form NEW vessels
39
ANGIOGENIC PROMOTERS: purpose?
drives angiogenesis
40
example of ANGIOGENIC PROMOTERS
PDGFB
41
PDGFB function? what to they bind? | what and when are they released
released by endothelial cells once blood vessels are formed they will bind to receptor on surface of pericytes indirect function
42
what happens once PDGFB binds to PDGFR?
it tells the pericyte to begin association to existing epithelial cells
43
matrix degradation: what is MMP?
Matrix metalloproteinases - zinc dependent protease degrade ECM (extra cellular matrix)
44
MMP: what is it and what is its purpose?
enzyme that degrades the extracellular matrix (ECM)
45
Matrix degradation steps
step 1: MMPs degrade the ECM during angiogenesis step 2: endothelial cells migrate and sprout through the newly created gaps in the matrix. --> These endothelial cells then proliferate and form new blood vessels. step 3: Growth factors + VEGF are released to bind receptors on endothelial cells step 4: Degradation of the ECM reveals matrix components
46
what are INTEGRINS? | type of receptor AND location
dimeric transmembrane receptor proteins located on surface of blood vessels interact with cell-matrix
47
which INTEGRINS does cancer upregulate?
AVB3 + AVB5
48
how do INTEGRINS interact with the cell matrix? | bind what and promote what?
bind to matrix components promoting survival, growth, and motility
49
what will increased interactions with cell matrix components lead to?
leads to the release of more VEGF and more MMP
50
What is VEGFR-2? | what type of receptor
A pro-angiogenic receptor
51
what is TSP (thrombospondin) | what type of proteins?
glycoproteins found in the extracellular matrix anti-angiogenic - inhibit the growth of new blood vessels
52
what is one of the things TSP does? e.g. what does it bind? | 2 points
bind endothelial cells via CD36R binding leads to inhibition of angiogenesis binding leads to apoptosis
53
what is one of the things TSP does? e.g. what does it release? | 2 points
FASL released upon TSP-CD36 binding FASL-FASR interaction triggers endothelial cell apoptosis
54
Where is FASR present?
Only in endothelial cells
55
what is one of the things TSP does? e.g. what does it inhibit?
TSP-CD47R binding on endothelial surface inhibits VEGFR2 activity
56
what is one of the things TSP does? e.g. what does it sequester?
Sequesters growth factors making them unavailable for endothelial cells
57
what is one of the things TSP does? e.g. what does it inhibit?
inhibits MMP when released by cancer and endothelial cells - prevents them from aiding blood vessel growth
58
is TSP considered a tumor suppressor? or pro-oncogenic?
a tumor suppressor and if mutated, it will promote formation of cancer cells
59
Therapeutics - VEGF inhibitors: Aflibercept
soluble VEGF receptor
60
Therapeutics - VEGF inhibitors: Avastin
monoclonal antibody (mAb) against VEGF
61
Therapeutics - VEGF inhibitors: Ramucirumab
mAb against VEGFR-2
62
Therapeutics - VEGF inhibitors: Small molecule inhibitors
TK inhibitors
63
Therapeutics - Pericytes: SU688
PDGFB receptor inhibitor Combining pericyte and EC therapy -> removing pericyte protection before targeting endothelial cells
64
Angiogenic vasculature can result in poor chemotherapeutic delivery Incentive used to normalize cancer vasculature. Why? how can this be treated?
its easy for therapeutics to leak out or get wedged into cancer vasculature can deliver drugs that improve their vasculature surrounding cancer cells
65
Hallmarks of resistance: Redundancy of growth factors explain
endothelial cells release several growth factors so if there is 1 GF that docent work , its okay bc others are present
66
Hallmarks of resistance: cancer cells engage in bone marrow cell recruitment explain | what is recruited?
once endothelial cells release several growth factors... Myeloid-derived suppressor cells which suppress the immune system Endothelial progenitor cells which contribute to the formation of new blood vessels are recruited
67
Hallmarks of resistance: Increasing metastatic properties explain
cancer cells leave if environment isn't suitable via increasing MMP and GF create a hypoxic state which leads to HIF-alpha expression leads to the following: 1) increased metastatic potential 2) Increased Tregs 3) Increased MDSC 4) Increased cancer stem cells 5) Increased tumor-associated cell activation 6) release of VEGF
68
Hallmarks of resistance: Activation of stroma cells explain
Stromal cells such as CAF and pericytes are the connective tissue components surrounding tumors CAF releases SDF-1 and MMP Pericytes release PDGFB
69
Hallmarks of resistance: Alternative vascularization explain
vessel co-option: cancer cells grow in the direction of blood vessels to use it for their own blood supply Vascular mimicry: cancer cells differentiate to a cell of their choice to build their own blood vessels
70
explain what the Metastatic Cascade is. What are the steps? 5 total
series of steps allows cancer cells to spread from the primary tumor to distant organs Step 1: epithelial state - cancer cells are stationary step 2: stroma is activated step 3: cells undergo transition to mesenchymal state - cancer cells are motile, allowing for metastasis step 4: metastasis - from a secondary tumor step 5: secondary tumor transitions into the epithelial state

BIMM 134 - Cancer (4 decks)

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