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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
Q

micrometastases breastcancer

A

30% of patients have hundred-thousand micrometastases in the bone marrow

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25
Q

presence of micrometastases

A

indactive for a bad prognosis

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26
Q

initial micrometastases

A

genetically distinct > cells that were able to disseminate but not colonize > strong selective pressure

27
Q

second wave of metastases

A

genetically similar > well adapted cells > faster growth in hostile environments

28
Q

metastatic showers

A

responsible for most deaths > metastases of metastases

29
Q

micrometastases can

A

remain dormant for a long time

30
Q

epithelial-mesenchymal transition (EMT)

A

shedding of epithelial phenotype and detaching

31
Q

EMT is necessary for

A

motility and invasiveness

32
Q

EMT is essential in

A

embryogenesis and wound healing

33
Q

EMT can occur through fundemental changes in gene expression

A
  • downregulation of E-cadherin and cytokeratins
  • upregulation of vimitin
34
Q

vimitin

A

intermediate filament mesenchymal tissue

35
Q

EMT is seen at

A

edges of carcinomas that invade

36
Q

E-cadherin

A

tethered to the actin filaments via a complex of alpha and beta catenins

37
Q

E-cadherin cancer

A
  • internalized
  • expression suppressed
38
Q

suppressed expression of E-cadherin in carcinoma

A

breast, colon, prostate, stomach, liver, esophagus, skin, kidney and lung

39
Q

EMT induction

A

stromal signals can be conveyed by many factors that act in paracrine/autocrine fashion

40
Q

tumor-associated macrophages express

A

TNF-alpha, EGF

41
Q

factors expressed in embryogenesis and wound healing

A

snail, slug, twist

42
Q

EMT transcription factors can

A

induce a stem cell state > critical for metastasis

43
Q

mesenchymal-epithelial transition (MET) occurs

A

after extravasation and invasion of other tissues > helps to colonize

44
Q

extracellular proteases

A

excavate a passage through ECM

45
Q

ECM contains

A

fibronectin, tenascin, laminin, collagens and proteoglycans

46
Q

matrix metalloproteinases (MMPs) are secreted by

A

macrophages, mast cells and fibroblasts

47
Q

activities of MMPs occur with

A

normal cell proliferation and tissue maintenance

48
Q

controling MMPs

A

excreted as inactive pro-enzymes > must be cleaved by other proteases

49
Q

proteolysis in cancer

A

continous process

50
Q

ectotopic expression of MMPs

A

carcinogenesis

51
Q

network of lymphatic vessels in tissue

A

drain interstitial fluid

52
Q

lymhatic vessels in cancer and stimulated cells

A

generation is promoted

53
Q

collapse of lymphatic vessels in cancer

A

insufficient pressure

54
Q

cancer cell positive lymph nodes

A

surrogate marker of metastasis

55
Q

tropism

A

diffent cancers display distinct tropism towarda colonizing various organs or tissues

56
Q

explanation tropism

A

certain cancer cells are uniquely equipped

57
Q

seed and soil hypothesis

A

metastatizing cancer cells (seeds) find a compatible home in certain hospitable tissues (soil)

58
Q

sites of metastasis (5)

A
  • seed and soil hypothesis
  • determined by layout vessels
  • sites of chronic inflammation
  • tumor self-seeding
  • vascular ZIP-code
59
Q

sites of chronic inflammation

A

can attract certain cells

60
Q

tumor self-seeding

A

tropism towards site of primary tumor

61
Q

vascular ZIP-code

A

receptors on the walls of capillaries attract circulating tumor cells

62
Q

dormant micrometastases can

A

reduce long-term survival > non-cycling > therapy resistant

63
Q

immune system may suppress growth of

A

micrometastases

64
Q

genetic determinants of metastases

A

only a subpopulation of the genetic diversity of the primary tumor found

Cellulaire Oncologie (14 decks)

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