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RadBio > RBE, LET & OER > Flashcards

RBE, LET & OER Flashcards

1
Q

What is the OER ratio?

A
  • The ratio of hypoxic to aerated doses needed to achieve the same effect.
  • It always takes more dose to achieve cell killing under hypoxia. Thus, OER is never < 1.
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2
Q

Which radiation energy has the highest OER?

A

The one with the highest energy

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3
Q

What is the usual range of OER?

A

2.5-3.0

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4
Q

What’s the usual range of the dose reduction factor (DRF) for a radioprotector?

A

2.5-3.0

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5
Q

How do neutrons deposit their dose?

A

They are indirectly ionizing, leading to the production of:

  • recoil protons (main mechanism)
  • heavier nuclei fragments
  • α particles
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6
Q

What is the OER for high LET radiation?

A
  • It is the lowest for α particles (OER = 1)
  • It is intermediate for neutrons (OER ~ 1.5)
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7
Q

Does OER require O2 to be present during radiation?

A

No. It requires O2 be present for 4 ms right after

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8
Q

What is the OER for radiation predisposed to killing cells by a single-hit mechanism?

A

It is usually lower.

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9
Q

What is the OER for rapidly growing cells?

A

It is generally lower (~2)

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10
Q

Does OER vary with dose?

A

Yes!

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11
Q

Why is high LET radiation not affected by oxygen/hypoxia?

A

It causes DNA damage via direct action.
There is no free radical intermediary.

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12
Q

At what oxygen concentration do tumor cells reach full radiosensitization?

A

20-40 mmHg; 2%

This is the concentration of O2 in venous blood (2-5%)

O2 concentration in arterial blood is much higher (8-13%)

O2 in room air (20%)

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13
Q

At what partial pressure of O2 do radiated cells exhibit radiosensitivity halfway between their fully aerobic and fully hypoxic responses?

A
  • 4 mmHg
  • 0.5% O2

Mnemonic: half-way → 0.5%

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14
Q

What is the conversion between mmHg and Torr?

A

1 mmHg = 1 Torr

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15
Q

What is the graphical relationship b/w O2 tension and radiosensitivity?

A

Graph:

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16
Q

Where do hypoxic cells in a tumor reside?

A

They lie between necrotic cells and aerobic tumor cells (actively dividing).

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17
Q

What are tumor cords?

A

Tumor forming cylindrical structures around blood vessels

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18
Q

At what tumor radius does a tumor not have a necrotic core?

A

≤ 160 microns

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19
Q

At what tumor radius does a tumor start to develop a necrotic core?

A

≥ 200 microns

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20
Q

Do tumors with 160 microns ≤ radius ≤ 200 microns have a necrotic core?

A

They may or may not.

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21
Q

Why is hypoxia relevant to tumor treatment?

A
  • Hypoxia selects cells with decreased apoptotic potential (harder to kill)
  • increased metastatic potential
  • more mutations compared to oxic cells
  • pH is decreased (6.2)
  • Tumor-associated macrophages localize to hypoxic regions
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22
Q

How far can O2 diffuse at the arterial end of the capillary network?

A

150 microns (radius)

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23
Q

What is chronic hypoxia?

A

Hypoxia due to diffusion limit of O2 within the tumor

Causes necrosis and formation of a necrotic core

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24
Q

What is acute hypoxia?

A

Intermittent hypoxia that results from temporary blood vessel closure

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25
Q

What is a biphasic survival curve?

A

A survival curve that has two portions with different D0’s.

The steeper, proximal portion of the curve represents oxic cell killing.

The shallower, distal portion of the curve represents hypoxic cell killing.

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26
Q

What happens to oxic vs. hypoxic cells after radiation?

A

Oxic cells are selectively killed off. The remaining hypoxic (radioresistant) cells redistribute in terms of oxygenation areas.

eg: We begin w/ 15% hypoxic cells within the tumor and kill off all oxic cells with the first RT dose. The remaining hypoxic cells redistribute such that 85% now become oxic and the remaining 15% remain hypoxic (Note that the % remains the same but the absolute cell number reduces). The second RT dose then kills off the now-oxic cells and the cycle repeats. This is called reoxygenation.

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27
Q

How long does it take a tumor to reoxygenate following a dose of 10 Gy?

A

6 hours.

Hence, you wait at least 6 hours between your RT fractions.

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28
Q

What is the evidence of hypoxia in tumors in vivo?

A
  • In vivo and in vitro survival curves are similar to those in curves where hypoxia is known
  • Tumor histology demonstrates hypoxia
  • O2 probe binds to hypoxic areas
  • Pre-treatment Hb levels are prognostic indicators in SqCC of H&N, cervix, bronchus, and bladder
29
Q

What percentage of carbogen is O2?

A
  • O2: 95%
  • CO2: 5%
30
Q

How does hypoxia regulate tumor progression?

31
Q

How does reoxygenation affect radiotherapy?

A
  • Hypoxia confers resistance to radiation.
  • Human tumors that do not respond to radiotherapy may not re-oxygenate.
  • Optimal fractionation depends on reoxygenation.

NB: Hypoxia also makes tumors resistant to chemotherapeutic drugs since the agents cannot diffuse to the hypoxic/necrotic areas.

32
Q

How do tumors that do not reoxygenate respond to RT?

A

They are usually very resistant to RT.

33
Q

Which growth factors are associated with angiogenesis?

A
  • VEGF
  • PDGF-BB
34
Q

What are FGF2 and FGF7?

A

FGF2 is a proangiogenic agent that synergizes with VEGF and may reduce endothelial cell apoptosis.

FGF7 aids in angiogenesis by stimulating epithelial cell growth. Its receptor is a therapeutic target.

35
Q

What is endostatin?

A
  • Inhibitor of angiogenesis
  • Induces endothelial cell apoptosis and migration
36
Q

What is IL8?

A

It increases angiogenesis and metastasis

Mnemonic: 8 → ∞ (infinitizes tumor proliferation and metastasis)

37
Q

How does heparin affect angiogenesis?

A

It inhibits angiogenesis.

Mnemonic: Heparin causes bleeding, hence it definitely ain’t keeping blood within the vessels!

38
Q

What role does Hypoxia Inducible Factor (HIF)-1alpha play in angiogenesis?

A

It is a major transcription factor of VEGF.

39
Q

How does the body sense O2 and know to turn on angiogenesis?

A
  • Prolyl hydroxylase domain (PHD) proteins play a major role in this
    – Mnemonic: Cells have a PhD in sensing hypoxia!
  • In the presence of O2, they hydroxylate the P groups on HIF-α, which causes its degradation by proteasomes.
  • In the absence of O2, this hydroxylation does not occur. HIF-α goes on to activate VEGF, which promotes angiogenesis.
40
Q

What’re the units of LET?

41
Q

What’re the units of RBE?

A
  • It’s unitless
  • Since its a ratio of two doses, the units cancel out.
42
Q

Which LET gives the most RBE?

A

100 keV/μm

43
Q

How are the energy of a particular radiation and LET related?

A

↑ energy leads to ↓ LET

44
Q

What is RBE?

A

R250 / RX

it is the dose of X radiation required to produce the same effect as that produced by 250 KeV X-rays

45
Q

How is OER related to LET?

A

OER decreases with increasing LET

46
Q

How is RBE related to LET?

A

It increased, reaching a maximum at 100 keV, after which it start to decrease sharply.

47
Q

What is the LET of clinically relevant energy of protons?

A

They are low LET except for at the end of tracks, when they become high LET (Bragg peak)

48
Q

1 Gy (1J/kg) produces how many ionizations?

A
  • 2x107 ionizations/kg
  • 106 ionizations per mammalian cell
49
Q

Why does RBE decrease after LET of 100 keV/μm?

A

Wasted energy or overkill effect.

Many more ionizations are produced per cell than are required to kill it. This wastes the energy of the beam.

50
Q

Between what LET values does RBE change the most?

A

20 and 100

51
Q

After what value of LET does OER start to fall rapidly?

52
Q

How does the RBE of neutrons compare to protons?

A

Clinically relevant, high-energy protons have low LET/RBE for most of their track. Neutrons, on the other hand, have high LET/RBE.

The RBE of charged particles, generally, is low at the beginning of the track than at the end (Bragg peak).

53
Q

How much energy (eV) does generating an ion cluster require?

A

1 ion cluster requires 110 eVs.

54
Q

Modifying which parameter of high LET radiation would have the greatest change in LET?

A

Total dose

55
Q

How does OER of clinically relevant protons compare to X rays?

A

They are very similar.

56
Q

How do Nitroimidazoles affect radiosensitivity?

A

Enhance cell killing under hypoxic conditions.

They include nimorazole, misonidazole, etanidazole, pimonidazole.

Use is limited by sig neutotox at required doses.

57
Q

How does Tirapazamine affect cell killing?

A
  • Hypoxic cytotoxin (toxic by itself under hypoxic conditions)
  • Sensitizes hypoxic cells to RT
58
Q

How does amifostine affect radiosensitivity?

A
  • Radioprotectant
  • Given PRIOR to RT (no effect if given after)
  • a/w severe nausea & vomiting
59
Q

What were the results of nimorazole addition to convention H&N treatment in the DAHANCA trial?

A
  • Improved LRC and DSF
  • No improvement in OS
  • High osteopontin increases response to nimorazole
60
Q

What is the OER for X rays?

61
Q

What is the OER for clinical energy protons?

62
Q

What is the OER for neutrons?

63
Q

What is the OER for carbon ions?

64
Q

For patients with which syndrome can high LET radiation be especially recommended?

A

Keap1 syndrome:

  • Keap1 inhibits NRF2.
  • NRF2 promotes resistance to oxidative stress caused by low LET radiation.
  • People w/ Keap1 syndrome have an inactive or deleted Keap1 gene, making them resistant to low LET radiation and sensitive to high LET radiation.
65
Q

How does the variation in radiosensitivity during the cell cycle compare between low LET and high LET radiation?

A
  • Radiosensitivity profiles are similar (max sensitivity in G2/M, lowest sensitivity in late S phase).
  • Variations in this sensitivity are much less pronounced for high LET radiation.
66
Q

What’s the OER for the different phases of the cell cycle?

A
  • G1: 2.3-2.4
  • S: 2.9-2.9 (highest OER)
    – Highest capacity for sublethal damage repair, so oxygen-fixation that impairs repair has the largest effect
  • G2: 2.6-2.7
  • M: lowest OER
66
Q

What’s the OER for the different phases of the cell cycle?

A
  • G1: 2.3-2.4
  • S: 2.9-2.9 (highest OER)
    – Highest capacity for sublethal damage repair, so oxygen-fixation that impairs repair has the largest effect
  • G2: 2.6-2.7
  • M: lowest OER
67
Q

What’s the OER for the different phases of the cell cycle?

A
  • G1: 2.3-2.4
  • S: 2.9-2.9 (highest OER)
    – Highest capacity for sublethal damage repair, so oxygen-fixation that impairs repair has the largest effect
  • G2: 2.6-2.7
  • M: lowest OER
    – Cells are already maximally sensitive to radaition

RadBio (10 decks)

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