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Cellulaire Oncologie > HC9- Invasion & metastasis > Flashcards

HC9- Invasion & metastasis Flashcards

1
Q

primary tumors are noticed when they

A

influence the function of organs or tissues

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2
Q

percentage of deaths caused by primary tumors

A

10%

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3
Q

tumors in certain tissues have

A

high metastatic potential

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4
Q

example high metastatic potential

A

primary melanomas

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5
Q

examples low metastatic potential (2)

A
  • basal cell carcinomas skin
  • astrocytomas
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6
Q

invasion-metastasis cascade

A

primary tumor formation - local invasion - intravasation - transport through circulation - arrest in microvessels of various organs - extravasation - colonization = formation of micrometastasis

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7
Q

carcinomas location

A

thin sheets of epithelial cells sit on top of deep, complex layers of stroma

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8
Q

malignant cells that breach the basement membrane gain exces to

A

growth factors and blood supply

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8
Q

carcinomas charachteristic

A

breaching basement membrane of epithelium with proteases that cleave the ECM

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9
Q

intravasation

A

cancer cells enter blood vessels from stroma

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10
Q

for the invasion of the lumen of capillaries > cooperation between

A

carcinoma cells, macrophages and endothelial cells

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11
Q

intravasation stimulated by signaling

A

EGF from macrophages

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12
Q

blood

A

hostile environment for carcinoma cells

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13
Q

hostile environment because of (4)

A
  • no contact with other cells
  • hydrodynamic stress
  • no stromal support
  • diameter of carcinoma cells is larger > 3-8 um
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14
Q

circulating cancer cells are a

A

readout value for therapy efficacy

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15
Q

readout value therapy efficacy (2)

A
  • comparison between cancers and patients is complicated
  • measuring tumor DNA in blood > accumulated mutations and translocations
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16
Q

circulating cancer cells spend very little time in circulation because they

A

are immobilized in the lungs > can escape to other organs

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17
Q

primary mechanism metastasis

A

trapping in small vessels

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18
Q

extravasation

A

invasion into surrounding tissue

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19
Q

for extravasation help is needed from

A

macrophages for certain factors

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20
Q

forms of extravasation (2)

A
  • through the vessel wall
  • growth within the vessel
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21
Q

colonization

A

most complex step

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22
Q

first step colonization

A

formation of micrometastases

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23
Q

probability for the formation of a macroscopic metastase

A

low

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24
micrometastases breastcancer
30% of patients have hundred-thousand micrometastases in the bone marrow
25
presence of micrometastases
indactive for a bad prognosis
26
initial micrometastases
genetically distinct > cells that were able to disseminate but not colonize > strong selective pressure
27
second wave of metastases
genetically similar > well adapted cells > faster growth in hostile environments
28
metastatic showers
responsible for most deaths > metastases of metastases
29
micrometastases can
remain dormant for a long time
30
epithelial-mesenchymal transition (EMT)
shedding of epithelial phenotype and detaching
31
EMT is necessary for
motility and invasiveness
32
EMT is essential in
embryogenesis and wound healing
33
EMT can occur through fundemental changes in gene expression
- downregulation of E-cadherin and cytokeratins - upregulation of vimitin
34
vimitin
intermediate filament mesenchymal tissue
35
EMT is seen at
edges of carcinomas that invade
36
E-cadherin
tethered to the actin filaments via a complex of alpha and beta catenins
37
E-cadherin cancer
- internalized - expression suppressed
38
suppressed expression of E-cadherin in carcinoma
breast, colon, prostate, stomach, liver, esophagus, skin, kidney and lung
39
EMT induction
stromal signals can be conveyed by many factors that act in paracrine/autocrine fashion
40
tumor-associated macrophages express
TNF-alpha, EGF
41
factors expressed in embryogenesis and wound healing
snail, slug, twist
42
EMT transcription factors can
induce a stem cell state > critical for metastasis
43
mesenchymal-epithelial transition (MET) occurs
after extravasation and invasion of other tissues > helps to colonize
44
extracellular proteases
excavate a passage through ECM
45
ECM contains
fibronectin, tenascin, laminin, collagens and proteoglycans
46
matrix metalloproteinases (MMPs) are secreted by
macrophages, mast cells and fibroblasts
47
activities of MMPs occur with
normal cell proliferation and tissue maintenance
48
controling MMPs
excreted as inactive pro-enzymes > must be cleaved by other proteases
49
proteolysis in cancer
continous process
50
ectotopic expression of MMPs
carcinogenesis
51
network of lymphatic vessels in tissue
drain interstitial fluid
52
lymhatic vessels in cancer and stimulated cells
generation is promoted
53
collapse of lymphatic vessels in cancer
insufficient pressure
54
cancer cell positive lymph nodes
surrogate marker of metastasis
55
tropism
diffent cancers display distinct tropism towarda colonizing various organs or tissues
56
explanation tropism
certain cancer cells are uniquely equipped
57
seed and soil hypothesis
metastatizing cancer cells (seeds) find a compatible home in certain hospitable tissues (soil)
58
sites of metastasis (5)
- seed and soil hypothesis - determined by layout vessels - sites of chronic inflammation - tumor self-seeding - vascular ZIP-code
59
sites of chronic inflammation
can attract certain cells
60
tumor self-seeding
tropism towards site of primary tumor
61
vascular ZIP-code
receptors on the walls of capillaries attract circulating tumor cells
62
dormant micrometastases can
reduce long-term survival > non-cycling > therapy resistant
63
immune system may suppress growth of
micrometastases
64
genetic determinants of metastases
only a subpopulation of the genetic diversity of the primary tumor found

Cellulaire Oncologie (14 decks)

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