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Core 2 > PET imaging > Flashcards

PET imaging Flashcards

1
Q

What is catabolic metabolism?

A

Extraction of energy and reducing power from the environment

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2
Q

What is anabolic metabolism?

A

Macromolecule synthesis from simple biological building blocks

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3
Q

Which hallmark of cancer is caused by anabolic changes in a cancer cell

A

Enabling replicative immortality

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4
Q

What hallmark of cancer is caused by catabolic changes in a cell

A

Deregulating cellular energetics.

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5
Q

Which metabolic pathways are upregulated in cancer cells?

A

Oxidative phosphorylation and glycolysis

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6
Q

What advantage is gained by upregulation of glycolysis

A

glucose metabolism provides intermediates that feed into subsidary pathways. These include nucleic acid (PPP) and non essential amino acid production and TCA (krebs) pathways. All sustain proliferative signalling and resist death.

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7
Q

How does FDG get stuck in cells following uptake.

A

Uptake via Glut-1. It is then phosphorylated where it becomes stuck in the cell. This is because of the fluorine replacing the OH group, which is normally required for glucose to be transported for further glycolysis.

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8
Q

What gland shows FDG uptake?

A

Salivary

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9
Q

What effect does inflammation have on FDG uptake?

A

Inflammatory response to infection, chemo, surgery leads to high glucose metabolism

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10
Q

Why does inflammation cause a high uptake of FDG?

A

Inflammatory cells (T cells etc) begin to replicate very quickly at the site of inflammation. This requires high metabolism which increases FDG uptake.

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11
Q

What two reasons mean that FDG is not tumour specific?

A

1) Glut-1 may not be expressed on the tumour cells

2) Inflammatory cells and other metabolic organs exhibit FDG signalling.

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12
Q

What tumour types show low avidity for FDG?

A

Prostate tumours have very low Glut-1 expression.

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13
Q

What is the result of high glucose backgroun in FDG imaging?

A

Hard to delineate the tumour due to a lack of contrast in the image

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14
Q

What is the role of pyruvate kinase M2?

A

Catalyses the conversion of phosphoenolpyruvate to pyruvate by transfering the high energy phosphate group onto ADP to form ATP

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15
Q

Which spliceoform of PK is upregulated in all known cancers to date?

A

PKM2

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16
Q

What happens after the conversion of PEP into pyruvate?

A

It is a commitment step for the cell which will now undergo either glycolysis or oxidative phosphorylation of pyruvate.

17
Q

In what structure does PK exist?

A

Tetramer

18
Q

What effect does a PKM2 tetramer have on the choice of metabolic pathway?

A

Tetramer has high affinity for PEP which induces its conversion into pyruvate and the formation of ATP

19
Q

What effect does a PKM2 homodimer have on the choice of metabolic pathway?

A

Homodimer of PKM2 has a lower affinity for PEP. This reduces glycolytic flux through pyruvate leading to the accumulation of precursors for biosynthesis of nucleic acids, phospholipids and amino acids.

20
Q

What is the important role that PKM2 plays in normal cells with regard to anaboilc and catabolic pathways?

A

By switching between dimeric and tetrameric structures, the cell can decide if it is to undergo anabolic or metabolic pathways. Anabolic = dimer
catabolic = tetramer.

21
Q

How does PKM2 expression change in cancer cells?

A

It is upregulated which causes anabolic pathways to produce macromolecules required for cellular proliferation

22
Q

What is the problem with using PKM2 targeted PET-radiotracers?

A

whilst it does have good tumour uptake. There are combined excretion pathways in the kidney and bladder; but also in the liver and spleen. Therefore it cannot be used for body tumours

23
Q

What tumour could PKM2 directed PET-radiotracers be used for imaging? (compared to FDG)

A

Brain tumours as it can pass through the BBB. This coupled with the fact that there is lower background noise in the brain compared to FDG makes it more suitable in this scenario.

24
Q

What are the limitations of PKM2 tracers?

A

Tumour-to-muscle and blood background ratios are below those observed in FDG, this limits PKM2 to the brain.
Although PKM2 is tumour specific, PKM2 has the same low avidity in low GLUT-1 expressing tumours as FDG (prostate).

25
Q

What is the main use for radiolabelling amino acid uptake?

A

Used for diagnosis and for monitoring treatment response in tumours where the expression of certain genes and therefore uptake of amino acids is increased.

26
Q

What are two examples of amino acid uptake radiolabels.

A

18F-FET, artificial amino acid of methionine for brain tumour imaging.
18F-FDOPA a phenyl-alanine which is used for brain tumour imaging

27
Q

What is the Xc amino acid transporter system and how does it change in cancer?

A

It’s a cystine/glutamate antiporter (1 molecule of cysteine in for one glutamat out).
Cystine is reduced to cysteine for glutathione synthesis which protects the cell from oxidative stress. Cancer cells stabilise this system so they can increase their capacity to withstand oxidative stress which gives chemoresistance.

28
Q

What effect does stabilization of the Xc amino acid transporter have on chemotherapy treatment and why?

A

Increases their capacity to withstand oxidative stress so gives an element of chemotherapy resistance.

29
Q

Why does the glutamate derivative (18F-FSPG) have low levels of retention in cells that also exhibit low intracellular cysteine?

A

Depletion of intracellular cysteine acts to increase the influx of cytsine which corresponds with an efflux of glutamate.
Reduced uptake may therefore be a consequence of elevated 18F-FSPG efflux.
Increased cystine competes for higher occupancy of the transporter and will also lower 18F-FSPG uptake into the cell.

30
Q

Why do cancer cells see an uptake of lipid droplet formation?

A

Seen as a result of apoptosis. Whilst there is cellular proliferation, some cells will still undergo apoptosis within a rapidly dividing tumour. This produces lipid droplets.

31
Q

What fatty acid signatures are seen in tumours?

A

Lipid droplet formation
Fatty acid oxidation
Increased fatty acid synthesis

32
Q

What radiotracer accumulates in cells via entry on the fatty acid transport protein. Where does this tracer become trapped.

A

18F-FTO - gets trapped inside mitochondria

Core 2 (20 decks)

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