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MIMS > Easter Term > Flashcards

Easter Term Flashcards

1
Q

What are nonspecific probes for?

A

Physiology eg) blood volume

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2
Q

What are target probes for?

A

Protein location and structure

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3
Q

What are smart sensor probes for?

A

Enzyme location and function

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4
Q

What are anapleurotic fluxes and which is common in cancer?

A

Other ways into the Krebs cycle - eg alphaKG (glutamine to glutamate) in cancer

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5
Q

What is HIF-1?

A

Hypoxia inducible factor

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6
Q

How does HIF1 affect glycolysis and oxy phos?

A

Upregulates glycolysis, suppresses oxy phos

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7
Q

What stabilises HIF1?

A

VHL/p53/PTEN

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8
Q

What stimulates HIF1?

A

PI3K, ERBB2, EGFR

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9
Q

What can upregulated glycolysis cause in surrounding tissues?

A

Upregulated H+ transport out of cells so may kill surrounding tissues

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10
Q

Why is glycolysis upregulated in tumours?

A

Increases flux to pentose phosphate pathway for NAPDH synthesis for lipid synthesis, provide carbon for amino acid and nucleotide synthesis

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11
Q

What is used to look at hexokinase in cancer metabolism?

A

[18F] FDG-PET

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12
Q

What is used to look at LDH in cancer metabolism?

A

hyperpolarised MRI of [1-13C] pyruvate

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13
Q

What is used to look at fatty acid synthase in cancer metabolism?

A

[11C] acetate-PET

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14
Q

How does PET work?

A

Biomolecule tracer with positron emitter, annihilation with electron, gamma rays detected and traced back

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15
Q

What are the three types of coincidence in PET detection?

A

True, scatter, random

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16
Q

Which length half life is ideal in imaging?

A

A long one for longer measurements

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17
Q

How does SPECT work?

A

NUclei admit gamma rays only in one direction, 3D images, slits for detection

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18
Q

What do smaller or larger slits in SPECT do to the image?

A

Smaller = clearer/accurate, wider = more sensitive

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19
Q

What are some common isotopes for SPECT?

A

99mTc, 111In

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20
Q

What is a Larmor frequency?

A

The frequency the nuclei “precess” at - when they return to normal spin after the field is turned off. Different in different tissues.

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21
Q

What is MRI?

A

Static magnetic field (can be in gradient across body), fire radio waves and detect response

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22
Q

How are relaxation rates used in MRI?

A

Tissue specific so MRI pulses can be adapted to give contrast between tissues

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23
Q

Which kind of metal shortens relaxation rates so can be used as a contrast medium?

A

Transition metals

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24
Q

What is T1 relaxation?

A

Spin-lattice, slower, return to resting energy levels

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25
Q

What is T2 relaxation?

A

Spin-spin, faster, spins create own magnetic fields and start to move at different times

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26
Q

What is the NIR window?

A

The wavelengths where light has its maximum penetrance in tissues

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27
Q

How can luciferin test gene expression?

A

Fluoresces under luciferase so will fluoresce where a gene has been expresses

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28
Q

What is photoacoustic tomography?

A

Laser excites tissue and creates a temperature and pressure gradient, tissue expansion creates an ultrasound picture

29
Q

What does fMRI look at?

A

Blood flow in brain

30
Q

Why does oxygen affect relaxation parameters?

A

Paramagnetic

31
Q

What is BOLD?

A

Blood oxygen level-dependent MRI

32
Q

What recyles glutamate and what is this linked to?

A

Astrocytes, glucose metabolism

33
Q

If a water molecule moves, what happens to the coherence of the signal?

A

Decreases

34
Q

How can you look at possible increased fatty acid synthesis in a tumour?

A

Look at lipid synthesis using [11C]-acetate PET

35
Q

How can the tracer FLT be used?

A

Replace thymidine with 18F, gets phosphorylated and trapped in tumour cell by thymidine kinase I (lots of this in tumour cells)

36
Q

What does labelled annexin bind to?

A

Phosphatidylserine which is expressed by cells undergoing apoptosis

37
Q

What can be put in nanoparticles to change relaxation times?

A

Iron oxide

38
Q

How can you change the NMR T term?

A

Lower temp using another superconducting magnet with 13C in liquid helium

39
Q

Which tumours are the most difficult to diagnose and treat?

A

Epithelial

40
Q

Which areas is radiotherapy less effective on?

A

Hypoxic areas of tumour

41
Q

What do copy number alterations in tumours cause?

A

Alterations in gene products

42
Q

What affects tumour behaviour?

A

Interaction between cancer and mesenchymal cells

43
Q

An ideal curative cancer therapy must:

A

Act on mechanisms vital for viability or growth of cancer cells, permeate tumours at effective concentrations, spare normal cells, eliminate sufficiently to prevent recurrence

44
Q

WHy can’t antibodies be used for cancer therapy?

A

Intracellular targets are inaccessible

45
Q

What does Gleevec bind to?

A

Inhibits Abl kinase activity

46
Q

What does Vemurafenib inhibit?

A

Activated BRAF kinase

47
Q

What does ipilimumab do?

A

Prevents T cell inactivation

48
Q

What do homozygous BRCA2 inactivation do?

A

Sensitizes cells to agents that stall DNA replciation

49
Q

Which inhibitors can be used to treat BRCA-deficient tumours?

A

PARP-1

50
Q

What does SH2 bind to?

A

Phosphorylated tyrosine

51
Q

What does SH3 bind to?

A

Polyproline

52
Q

What do kinases phosphorylate?

A

OH groups (Tyr, Thr or Ser)

53
Q

Why is Philadelphia chromosome oncogenic?

A

SH3 domain can’t inhibit kinase and there’s two kinase domains now

54
Q

What inhibits kinase activity in ABL?

A

SH3 domain

55
Q

What changes Bid to tBid and what does it do?

A

Caspase, activates Bak/Bax

56
Q

Why use Warburg metabolism?

A

G6P can make purines or pyrimidines and DHAP can make lipids

57
Q

What does myc use to always be switched on?

A

Antibody promoter

58
Q

What do MHC and TCR do?

A

MHC presents the antigen, TCR recognises it

59
Q

What do CD80/86 and CDT8 do?

A

CD80/86 on APC recognised by CDT8 on cell

60
Q

How can you prevent CTLA4 binding?

A

Use anti-CTLA4 antibody

61
Q

How is T cell apoptosis signalled?

A

CD80/86 and CDT8 signal CTLA4 production on T cell which binds CD80/86 better which signals T cell apoptosis

62
Q

What does PARP1 do?

A

Repairs single strand breaks

63
Q

What does BRCA2 do?

A

HR

64
Q

What is the tumour suppressor for G1/S phase?

A

Rb

65
Q

Which cyclins are for S phase?

A

E and A

66
Q

What do Rb and E2F do?

A

Use E2F to transcribe S phase genes, Rb prevents this

67
Q

What do CDK 4 and 6 do?

A

Phosphorylate Rb to prevent S phase inhibition

68
Q

What does e-Cadherin do?

A

Makes cells stick together, tumour cells don’t do this and spread

69
Q

What are HGF and CMET?

A

Growth factor and RTK

MIMS (8 decks)

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