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Biology 465 > Lecture 3 & 4 > Flashcards

Lecture 3 & 4 Flashcards

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1
Q

Which genes can mutations occur in?

A
  1. Oncogenes - eg., protooncogenes
  2. Tumour suppressors - eg., p53
  3. DNA repair
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2
Q

What were the original “Hallmarks of cancer” by Hanahan and Weinberg?

A
  • self-sufficiency in growth signals
  • insensitivity to antigrowth signals
  • evades apoptosis
  • limitless reproductive potential
  • sustained angiogenesis
  • tissue invasion and metastases
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3
Q

What were the revised Hallmarks of Cancer?

A
  • avoiding immune destruction
  • tumour promoting inflammation (lack of resolution)
  • genome instability and mutation
  • deregulation of cellular energetics
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4
Q

What induces growth signals in a cell?

A

Various growth factors, a change in the metabolism that allows the cell to perform DNA synthesis or an increase in glucose/mitochondrial activity

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5
Q

What are the four mechanisms in DNA synthesis?

A
  1. Signalling molecules: cytokines and growth factors (IL-3 or EGF)
  2. Signal receptors and intracellular receptors: cytokine receptor/ tyrosine kinases/ intracellular receptors
  3. Intracellular transducers
  4. Transcription factors and cell cycle regulators
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6
Q

What are the five different components in a cell that tells it to enter cell cycle or enter a quiescent state?

A
  • growth factor receptors
  • monitors of genome integrity
  • TGF-beta receptors
  • integrins
  • monitors of cell metabolism
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7
Q

What are the three stages a cell can enter when planning to divide?

A
  • G0 (G not) or quiescent state
  • active cell cycle which leads to G1 -> S -> G2 -> M
  • programming of cell cycle phases then into any of the four phases
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8
Q

What is one example of monitoring genome integrity?

A

The length of telomeres is important. A short telomere indicates the age of the cell and is not stable genomically.

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9
Q

How do integrins play a role in the cell cycle?

A

They will recognize if there are cells beside it (contact inhibition) and prevent the cell from entering G1.

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10
Q

What is the quiescent stage?

A

G0 (G zero) stage where a cell is neither dividing nor preparing to divide.

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11
Q

What is the G1 entry controlled by?

A

Cyclin D1

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12
Q

How can the control of cyclin D1 be partially explained by the effects of mitogens?

A

They modulate the transcription of the cyclin D1 gene. Different mitogens diverge at D1.

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13
Q

What is a mitogen?

A

A chemical substance that encourages a cell to commence cell division, triggering mitosis, usually a protein.

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14
Q

How do cytokines effect D1 levels?

A

A cytokine binds to a cytokine receptor which activates Jak, which activates STAT, thus resulting in the activation of cyclin D1.

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15
Q

How do growth factors effect D1 levels?

A

A growth factor binds to a tyrosine kinase receptor (RTKs) -> Grb2 -> Sos -> Ras -> Raf -> Erk -> p90Rsk -> Elk-1/SRF -> Fos -> AP-1 -> D1

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16
Q

What are the sources of extracellular signal that induce cyclin D1 and D2 expression?

A

Estrogen receptor - AP-1 TF -> D1
HER2/Neu receptor - E2F and Sp1 TFs -> D1
Bcr/Abl -> D2

17
Q

How do cancer cells produce growth factors?

A

They acquire the ability to synthesize growth factors, through mutations, to which they respond (autocrine stimulation)

18
Q

What are two examples of growth factors produced by cancer?

A

eg 1. Platelet-derived growth factor (PDGF) production by glioblastomas
eg 2. TGFalpha production by sarcomas (dimerization of the receptor)

19
Q

What are four mechanisms that can deregulate the receptor tyrosine kinases on the cancer cell surface?

A
  1. Point mutation
  2. Deletions
  3. Chromosomal rearrangements
  4. Overexpression
20
Q

How would a point mutation effect the deregulation of a receptor tyrosine kinase?

A

It results in continuous phosphorylation

21
Q

How would a deletion effect the deregulation of a receptor tyrosine kinase?

A

If, for example, the cytosolic, ligand binding portion of the receptor is deleted then the receptor is constantly dimerized and continuously on.

22
Q

In breast cancer, which growth factors are continuously overexpressed?

A

ErbB1 and ErbB2 (EGF and Her2)

23
Q

How is Ras activated?

A

Ras is in an inactive state when bound to GDP. Sos, an adapter protein, binds to Ras and Ras undergoes a conformational change. The conformational change allows it bind GTP and become active. Allowing it to bind and activate Raf.

24
Q

Why is Ras so significant in tumours?

A

Ras is an oncogene in 25-30% of human tumours. Undergoes intracellular transducers activating mutations.

25
Q

How is Mapkinase activated?

A
  1. Ras is activated by the exchange of GDP for GTP
  2. Active Ras recruits, binds and activates Raf
  3. GTP hydrolysis leads to dissociation of Ras from Raf
  4. Raf activates MEK
  5. MEK activates MAPK
  6. Dimeric form of active MAP kinase translocates to nucleus; activates many transcription factors
26
Q

What occurs when Raf becomes active?

A

Raf is inactive in cytosolic space, but when bound to Ras it becomes active and releases 14-3-3 proteins, which plays an important role in apoptosis.

27
Q

What does the activation of Map kinase lead to?

A

The activation of transcription factors TCF and SRF and the production of Fos.

28
Q

What is the role of Fos/Jun?

A

They control the expression of genes important for G1 progression and G1/S transition.

29
Q

What does Ras control?

A
  • growth
  • survival
  • cell division
  • migration
  • motility
  • the proteins involved with the inhibition of apoptosis (PI3K, PIP3, Akt/PKB and Bad)
  • the proteins Raf, MEK and Erk1 or 2
30
Q

What occurs to Src activity in cancer?

A

The activity is frequently deregulated which can lead to changes in adhesion and increase proliferation.

31
Q

What is Src?

A

A proto-oncogene encoding a tyrosine kinase

32
Q

How can transcription factors act as oncoproteins?

A

Eg., Fos/jun overepression which leads to myc overexpression. Myc leads to the overexpression of cyclin D and entry into G1.

33
Q

How would cyclin D be inhibited if overepressed?

A

At a DNA damage checkpoint, p53 amount increases which produces p21CIP which inhibits cyclin D. If there’s a mutation in this area, then there’s a problem.

34
Q

What is E2F?

A

An important transcription factor for production of proteins that controls G1 to S transition.

35
Q

What is the role of Rb?

A

It sequesters E2F and prevents cell cycle progression. When phosphorylated, it is inhibited and cannot bind to E2F.

Biology 465 (15 decks)

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