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Radiotherapy Year 3 > Radiobiology > Flashcards

Radiobiology Flashcards

1
Q

What is the criteria for a radiation induced secondary tumour

A

Second tumour occurs in location irradiated by primary or secondary therapeutic beam
Histology of second tumour is different to first so cannot be a met
Latency period, typically of several years
Second tumour not present at time of radiation treatment
Patient does not have a cancer prone syndrome

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2
Q

Where is evidence for cancer induction from?

A

A Bomb survivors
Biological studies
Patients exposed to radiation
Occupationally exposed workers

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3
Q

What models should you assume for cancer induction risk for low and high doses

A

Low: linear no threshold model
High: non-linear model with parameters fitted from epidemiological evidence

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4
Q

What is ICRP 103 conclusion on cancer induction

A

Combined detriment to excess cancer and heritable effects is 5% per Sv

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5
Q

What is EAR?

A

Excess absolute risk
Fraction RT patients contracting Ca - Fraction non RT patients contracting cancer

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6
Q

What is RR?

A

Relative risk
Fraction RT patients contracting Ca/Fraction non-RT patients contracting Ca
Breast cancer RT patients have a RR of about 1.3 for secondary breast cancer

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7
Q

What is ERR?

A

Excess relative risk
ERR = RR - 1
Fraction or % per Gy

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8
Q

What has evidence from atomic bomb survivors shown?

A

ERR of secondary cancer induction depends on the age at exposure
Decreases with age up to 20
Increases slightly up to older age (60)
Decreases after 60

Due to initiation and promotion processes

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9
Q

How would you calculate risk with linear no threshold hypothesis?

A

Sum dose distributions from different sources of radiation dose
Apply organ specific coefficients
Age and sex dependent
Apply generalised risk coefficient (5% per Sv)

Does not account for individual factors such as smoking or diet

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10
Q

How does higher doses affect cancer induction

A

Cell sterilisation is thought to reduce response gradient and reduce the chance of cancer induction, as cell sterilisation rates overtake cell cancer induction
Linear exponential dose response curve

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11
Q

Where are we mostly likely to see secondary cancers according to the shape of linear exponential curves?

A

Near margins of RT TVs or in low dose bath volumes (not necessarily the case, it is likely that there is a plateau or slower fall off with large dose according to dose date from RT patients, may be caused by repopulation)

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12
Q

How does cancer induction in atomic bomb survivors differ to RT patients?

A

A bomb survivors suffer carcinoma ((in rapidly dividing epithelial cells) and little sarcoma
RT patients have significant induced sarcomas (MSK tissue)
Implies different response from fractionated treatment

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13
Q

What is OED and how is it calculated

A

Organ equivalent dose
For an inhomogeneous dose distribution, OED is the uniform dose with the same risk of radiation induced cancer as DVH
Uses linear exponential dose risk model
Break DVH into equal volume dose bins, lookup alpha beta values and sum over all dose bins to calculate

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14
Q

What is downside of IMRT in terms of radiobiology and why?

A

Risk of second malignant neoplasms can increase by almost twice as much, caused by:
IMRT requires more fields so larger volume is exposed to radiation
Exposure of out of field tissues form leakage x rays ig reater because IMRT requires more MUs

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15
Q

What is integral dose

A

Total energy deposited in total irradiated volume of patient in kg x Gy
ID = m.D
For inhomogeneous dose distribution, summed across dose bins

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16
Q

What are concomitant exposures

A

Exposures other than treatment exposures: imaging exposures alongside RT

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17
Q

What are the 5 Rs of radiotherapy

A

Repair (of sublethal damage)
Repopulation (following irradiation)
Redistribution (of cells within cell cycle)
Reoxygenation (of surviving cells)
Radiosensitivity (intrinsic)

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18
Q

What are the issues to consider with fraction timing?

A

Incomplete repair between fractions (repairable DNA strand breaks are not repairs, problem for normal tissue tolerance)
Treatment gaps (repopulation issue with unintentional prolongation of treatment)

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19
Q

When might incomplete repair occur

A

Accelerated radiotherapy (intervals < 24 hours, most repairable damage is repaired after 6 hours, debated evidence shows slow repair components in which case may be some unrepaired damage)
Pulsed brachytherapy (time between fractions 1 hour)
Continuous LDR BT (ongoing repair during irradiation - different BED formula)

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20
Q

What is an example of accelerated RT and was it effective?

A

CHART Trial
1.5Gy/fr 3fr/day every day instead of conventional 5fr/week

Local control/OS not improved in H&N
Significant benefit to lung patients (although more difficult for hospital to deliver)

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21
Q

What is expected impact of accelerated RT?

A

Late normal tissue reaction expected to decrease, but this happened less than expected
Acute normal tissue reaction increases with accelreated RT, more severe, peaks earlier

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22
Q

How is incomplete repair accounted for in equations?

A

Adjustment is derived from the fact that the beta d^2 term is modified such that the relative effectiveness per unit dose is greater due to incomplete repair

Fractionated radiotherapy, h term which is described by a number of functions depending on how repair is modelled
LDR, R and mu

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23
Q

Why are equivalent regimes used?

A

To compare regimes, may want to know how an existing OAR tolerance varies when # is moderated

24
Q

What is Withers formula

A

Formula for calculating EQDX

EQDX = D (a/B + d) / (a/B + X)

25
Why are reirradiations more common?
Technical advances mean improved outcomes and increased survival Higher probability that patients will experience recurrence or new primary tumour or need palliative care
26
How are OARs considered in reirradiation?
Often based on OAR BEDs, recovery taken into account where possible, in form of increased constraint for BED typically
27
What are the four types of reirradiation?
1 - overlap of irradiated volumes with or without concern for toxicity 2 - no overlap of irradiated volumes with concern for toxicity from cumulative doses Repeat organ irradiation - no overlap of irradiated volumes or concern for toxicity but TVs in same organ Repeat irradiation - no overlap of irradiated volumes, no concern for toxicity, TVs in different organs
28
What is often issue with reirradiation data?
Poor quality, heterogeneous evidence, lack of QoL data, lack of clinical data, or lots of clinical data but no doses, no a/b values Usually small cohorts, poorly reported, not correlated with clinical follow up Recovery poorly modelled and poor assumptions made Ambiguous dose stats (lung, right +left? lungs - targets? lungs - old vs new target?)
29
What does amount of recovery depend on?
Amount of recovery depends on OAR, time between treatments, initial dose (consider distribution, max, mean?)
30
What are the primary sources of evidence about radiobiology?
Emami data Data from clinical trials QUANTEC PENTEC
31
What is one approach for re irradiations of complex dose distributions
Deformable registration and dose propagation Summing EQD2 maps
32
How can you deal with a treatment gap?
Treat on weekends Treat twice a day Accelerated treatment
33
What are time factor considerations of missing treatments?
Repopulation of tumours and normal tissues can take part in treatments, although this is less an issue for normal tissues Extending course of RT means cells repopulate and increase the number of cells to kill
34
How do we account for repopulation and proliferation
Use proliferation correction to account for BED loss due to tumour proliferation No PC for normal tissue - won't respond in timescale of treatment
35
When does repopulation begin and how do we compensate for it?
Repopulation in rapidly growing human cancer accelerates at about 28 days after initiation of RT Higher doses must be delivered to compensate
36
Where is guidance on gaps?
RCR has published guidance on gaps Timely delivery of radical radiotherapy: guidelines for the management of unscheduled treatment interuptions
37
What do we consider for lungs in reirradiation
Want Dmean below 20Gy EQD2 If higher, check areas of overlap and whether new course of RT adds to Dmean by previously unirradiated tissue or not (if same area, risk of pneumonotis lower than new are; area of 25-30Gy can help judge loss of total lung function) Keep volume comparable to one remaining lung below 25-30 Gy
38
What do we consider for parallel organs for re irradiation?
Clinical judgement along with risk patient is willing to accept No real answers, large uncertainties without good evidence DIR and register previous plans to current CT, if uncertainty in match then use caution in critical areas of OARs and use PRVs
39
Why would we want to use TCP NTCP models?
Generate hypotheses for new clinical trials To understand effects in uncertainty in dose For relative plan evaluation For plan optimisation
40
What is worse, cold or hot spots on a DVH?
Cold spots quickly drive TCP to zero Overdose does not compensate for similarly sized underdose
41
How does tumour size impact DVH?
Greater probability of controlling smaller tumours, TCP higher in same DVH with smaller TV
42
What are added complexities for TCP?
Spread of alpha across patients (including radiosensitivity) TCP across a cohort is shallower than TCP with a unique alpha value Proliferation and repopulation requires longer TT
43
What are grading systems?
Systems grading toxicity, generally 1 - 5, mild to lethal. Different ones, some grade patient reported, physician reported, subjectivity Often grouped (1-2) due to low numbers
44
What are serial and parallel organs sensitive to?
Serial - hot spots Parallel - mean dose although often more complicateed, rectum bleeding, fistula based on high dose to small volume Intermediate dose also important for late effects
45
What are the properties of acute effects?
Usually within 90 days Tend to be in cells with low sensitivity to fractionation Shorter overall treatment time increases acute effects Transient, usually resolve Can be serious if they will cause treatment gap Eg dermatitis, mucositis
46
What are the properties of late effects?
Occur after months or years Occur in cells with high sensitivity to fractionation Greater damage may lead to shorter latent period Little variation with treatment time Irreversible
47
What are some patient factors of normal tissue effects
Age Smoking Diet Genetic factors Co morbidities
48
What are some sources of NTCP data
QUANTEC, HyTEC
49
What is method most often used for NTCP - DVH reduction
Lyman Kutcher Burman (LKB) model Transform DVH into equivalent uniform dose and work out Veff (effective volume of uniform radiation) - uniform partial organ irradiation which is radiobiologically equivalent to true inhomogeneous dose distribution Use empirical formula to determine NTCP, with TD50, m, n relevant to tissue
50
What are precautions to consider of TCP NTCP models
They are only models Model patient cohort should match dataset Volume definition should be checked Consider dose grid, algorithm
51
What are some examples of TCP NTCP applications
Covid reduced fractionation Cyber attack, natural disaster Clinical trials: isotoxic lung escalation CT: oesophagus dose escalation for improved TC Investigating dose algorithm effects
52
What is BED equation taking into account proliferation?
BED = D(1+d/(a/B)) - K(T-T_delay) K is daily BED equivalent of repopulation T_delay is time from onset ot treatment to beginning of repopulation
53
What factors would impact how you decided to compensate for missed fractions?
How many fractions are left Magnitude of tumour proliferation Delay time before onset of proliferation
54
What datasets have replaced EMAMI?
QUANTEC - Quantitative Analysis of Normal Tissue Effects in the Clinic and Emami Update 2013
55
What cohorts are initiation and promotion associated with?
Initiation: younger patients Promotion: increases with age
56
Which tissues are spared more by fractionation?
Lower a/B tissues

Radiotherapy Year 3 (12 decks)

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