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FS YEAR 2 > CANCER TRAITS 2 > Flashcards

CANCER TRAITS 2 Flashcards

1
Q

What is angiogenesis?

A

Formation of new vessels from pre-existing blood vessels (sprouting)

Normal angiogenesis:
Embryonic development
Wound healing
Female reproductive cycle

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2
Q

How are blood vessels essential

A

Supply nutrients & O2
Remove metabolic waste & O2
Enable immune surveillance

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3
Q

What is abnormal angiogenesis?

A

Abnormal angiogenesis contributes to disease:
Insufficient vessel growth–> stroke, myocardial infarction, neurodegeneration
Excessive vessel growth–> cancer, inflammatory disorders

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4
Q

What is tumour hypoxia

A

upregulation of angiogenic inducers (e.g. VEGF)
*Hypoxia: not enough oxygen

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5
Q

What are angiogenic inhibitors

A

Anti-angiogenic factors
Endogenous angiogenesis inhibitors (e.g. thrombospondin-1) regulate angiogenesis during tissue remodelling & wound healing
Act as barriers to induction of angiogenesis in tumours

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6
Q

What are angiogenic inducers

A

Pro-angiogenic factors
Tumour cells produce angiogenic factors (e.g. VEGF)–> directional growth of endothelial cells
Matrix metalloproteinases (MMPs) help secrete some of these factors

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7
Q

What is angiogenic switch

A

During tumour development, “angiogenic switch” allows cells to induce & sustain angiogenesis from vascular quiescence
Counterbalancing positive & negative signals, encourages or blocks angiogenesis

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8
Q

What are the names of growth of the tumour

A

small tumour -> sprouting capillary -> growing tumour

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9
Q

What is tumour angiogenesis

A

a.Tumours can’t grow beyond 1-2mm^3, due to lack of O2 & nutrients–> cells become hypoxic
b.Hypoxia stabilises hypoxia inducible factors in tumour cells–> increased gene expression of angiogeneic inducers
c.New network of blood vessels grows in & around tumour
- Oxygen & nutrients delivery increases
- Tumour can grow
- Provides a route for cells to shed off & metastasise

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10
Q

How does tumour cells evade apoptosis

A

Loss of p53 tumour suppressors–> removes p53 damage control form apoptosis-inducing system
Increased expression of anti-apoptotic proteins (Bcl-2) or downregulate proapoptotic factors (Bax) or interfere with extrinsic death receptor pathway

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11
Q

What results in dysregulated apoptosis and cancer

A
  • disrupted dance of bcl-2 family of proteins
  • increased expression of IAP’s
  • reduced expression of caspases
  • defects/mutations in p53
  • impaired receptor signalling pathway
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11
Q

How is apoptosis triggered

A

in response to physiologic stress during carcinogenesis or due to anticancer therapy

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12
Q

why does invasion and metastasis occur

A

Cancer cells escape primary tumour mass & colonise new areas in the body with more nutrients & space
Metastases are mixture of cancer & normal cells from host tissue

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12
Q

What is autophagy

A

mediates both tumour cell survival and death
- metabolites generated during autophagy support survival of stressed, nutrient-limited cancer cell enviroments

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13
Q

What are factors to consider in necrosis and cancer

A

Seems beneficial–> removes hyperproliferating cancer cells
Can be pro-inflammatory & tumour promoting
Releases pro-inflammatory signals in tissue microenvironment–> recruitment of inflammatory cells
These check for tissue damage & remove necrotic debris

But tumours gain an advantage by tolerating necrosis:
Allows recruitment of inflammatory cells
These bring growth-stimulating factors to surviving cells within tumours–> stimulate angiogenesis, cell proliferation & invasiveness

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14
Q

What is invasion + EMT

A

Initiation of metatasis requires invasion–> enabled by epithelial-mesenchymal transition (EMT)

14
Q

What is the invasion and metastasis cascade

A

Local invasion of basement membrane & cell migration (2)
Intravasation of cancer cells into nearby blood & lymphatic vessels (3)
Transit & survival of cancer cells in circulation (4)
Escape of cancer cells from vessel lumina into parenchyma of distant tissues (extravasation) (6)
Formation of small cancer cells nodules at secondary site (micrometastases) (7)
Growth of micrometastases into macroscopic tumours (colonisation)

15
Q

what is MET

A

Mesenchymal-epithelial transition (MET): reverse process of EMT, important for establishing metastasis

15
Q

What is EMT

A

transdifferentiation program of epithelial to mesenchymal cells–> offers cell plasticity

16
Q

what occurs in epithelial cells in EMT

A

Epithelial cells:
Lose polarity & cell-cell adhesion (loss of E-cadherin)
Gain migratory & invasive properties
Become mesenchymal stem cells (multipotent cells that can differentiate into various types)

17
Q

How is replicative immortality enabled in normal cells

A

limited cell division = lead to stop of growth due to 2 barriers t proliferation: senescence & crisis

18
Q

what is senescence

A

irreversible non-proliferative viable state
Cells that overcome this barrier enter crisis

19
Q

What is crisis?

A

Crisis involves cell death & genomic instability
If cells emerge from crisis, they acquire unlimited replicative potential (immortalisation)

20
Q

What are telomeres

A

protective end caps of chromosomes (thousands of TTAGGG repeats)

21
Q

What do cancer cells do to telomerase

A

overexposes telomerase to overcome telomere shortening, senescence and cell death this is as telomeric DNA from chromosomes ends shorten during each cell cycle 50-100 bp

22
Q

How is telomeres maintained in cancer cells

A

Upregulation telomerase expression
Activation of ALT
Telomeres maintained above critical length threshold allow unlimited cell multiplication

22
Q

What can telomeres not do?

A

protect ends of chromosomes from end-to-end fusions
Results in genetic instability–> crisis–> cell death
Telomerase absent in non-immortal cells but overexpressed in immortalised cells (e.g. cancer cells)

23
Q

why are up mechanisms of telomere up regulation surpressed

A

These mechanisms are suppressed in normal cells to avoid unlimited replication

24
Q

What is ALT

A

alternative lengthening of telomeres; a telomerase-independent mechanism by which cancer cells avoid the degradation of telomeres

25
Q

What is the invasion metastasis cascade involve?

A

invasion
intravasion
survival in circulation
extravasin
micrometastases
colonisation

26
Q

What do tumours need

A

new vessels to survive, achieved by up regulation of angiogenesis usually in response to hypoxia

FS YEAR 2 (10 decks)

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