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PATH3309 > 16 - Hallmarks of Cancer > Flashcards

16 - Hallmarks of Cancer Flashcards

1
Q

Hallmark 1

A

Sustaining proliferative signalling

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2
Q

Sustaining proliferative signalling

A
  • Normal tissues control the production and release of growth-promoting signals that govern cell growth and division
  • Cancer cells deregulate these signals
  • Enabling signals are conveyed by growth factors
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3
Q

Ways of sustaining proliferative signalling

A
  • Autocrine proliferative signalling
  • Elevated levels of receptor proteins
  • Signalling to normal cells within associated stroma
  • Growth factor independence by constitutive activation of downstream signalling pathways
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4
Q

Disruptions of negative-feedback mechanisms that
attenuate proliferative signalling

A

RAS mutations

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5
Q

Hallmark 2

A

Evading growth suppressors

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6
Q

Evading growth suppressors

A

Evasion of RB and TP53

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7
Q

Evasion of RB effects

A
  • Metastasis
  • Angiogenesis
  • Senescence
  • Genome stability
  • Cell death
  • Differentiation
  • g1-s Cell cycle
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8
Q

Hallmark 3

A

Resisting cell death

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9
Q

How do tumour cells avoid cell death

A
  • Loss of TP53 tumor suppressor function
  • Increasing expression of antiapoptotic regulators (Bcl-2, Bcl-xl)
  • Short-circuiting the extrinsic ligand-induced death pathway
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10
Q

How do Bcl-2 family regulator proteins (Bcl-2, Bcl-x) inhibit apoptosis

A

Bind to and suppress Bax and Bak

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11
Q

Necrotic pathway

A
  • Cell enlargement
  • Loss of membrane integrity
  • Leakage of cell contents
  • Inflammation (recruitment of immune cells)
  • Nuclear degeneration
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12
Q

Hallmark 4

A

Enabling replicative immortality

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13
Q

Enabling replicative immortality

A

Through telomerase

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14
Q

Additional functions of telomerase (TERT) in
tumorigenesis

A
  • Amplify signalling by the Wnt pathway
  • Enhancement of cell proliferation and/or
  • Resistance to apoptosis
  • Involvement in DNA-damage repair
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15
Q

Hallmark 5

A

Inducing angiogenesis

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16
Q

Angiogenic regulator

A

Signalling proteins that bind to stimulatory or inhibitory cell-surface receptors

17
Q

Examples of angiogenic regulators

A
  • Vascular endothelial growth factor (VEGF-A)
  • Thromboplastin-1 (TSP-1) (inhibitory)
18
Q

Hallmark 6

A

Activating invasion and metastasis

19
Q

Multistep process of metastasis

A
  • Local invasion
  • Intravasation
  • Extravasation
  • Micro-metastases
  • Colonisation
20
Q

E cadherin

A
  • Mediates Contact Inhibition of Proliferation
  • Normal cells stop proliferating once they reach confluence upon homophilic E-cadherin binding
  • When cells either lose E-cadherin, they continue proliferating, grow on top of each other and lose CIP
21
Q

Loss of E cadherin

A

Key characteristic of EMT

22
Q

Hallmark 7

A

Evading immune destruction

23
Q

Reprogramming energy metabolism

A
  • Upregulation of glucose transporters (eg GLUT1) to
    increase glucose transport into the cytoplasm
  • Associated with activation of oncogenes
  • Hypoxia can also upregulate glucose transporters
24
Q

Aerobic glycolysis / warburg effect

A

Cancer cells have increased rates of glucose uptake and lactate production, even in the presence of sufficient oxygen and low rate of oxidative phosphorylation

25
Q

Hallmark 8

A

Reprogramming energy metabolism

26
Q

TGFβ

A

Significant role in inhibiting T helper cell differentiation and promoting antitumor immunity

27
Q

Enabling characteristics

A
  • Genome instability and mutation
  • Tumour-promoting inflammation
28
Q

Genomic instability and mutation

A
  • Characteristic of almost all human cancers
  • The most common is chromosomal instability (CIN)
29
Q

Hereditary cancer genomic instability

A

The presence of both CIN and non-CIN forms of genomic instability have been linked to mutations in DNA repair genes

30
Q

Sporadic cancer genomic instability

A

not due to mutations in DNA repair genes or mitotic checkpoint gene

31
Q

Tumour promoting inflammation

A
  • Linked to transformation, proliferation, angiogenesis, and metastasis
  • Supplying bioactive molecules such as growth factors and survival factors
  • Immune cells, through the production of inflammatory mediators (e.g. cytokines) contribute to the survival of the tumor in its microenvironment
  • The aberrant expression and secretion of proinflammatory by the tumor cells result in the recruitment of immune cells, thus creating a mutual
    crosstalk

PATH3309 (26 decks)

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