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Y3 Exam Revision > Radiobiology > Flashcards

Radiobiology Flashcards

1
Q

What are the two types of TCP/NTCP models?

A

Theoretical: gives insights into tissue response but are very sensitive to radiobiological parameters.
Empirical: patient data is used to construct mathematical models therefore they generally are in agreement when averaged over large cohorts of patients.

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2
Q

Why should TCP/NTCP models be used with caution?

A

1) Individual patients vary in radiobiological response
2) Some parameters have large uncertainties
3) models are complex and require expertise to run and interpret

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3
Q

What do NTCP models generally do?

A

They model what an Equivalent Uniform Dose (EUD) to an OAR would be for a particular complex/inhomogeneous dose distribution.

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4
Q

Name two NTCP models

A

1) Niemeirko NTCP model

2) Lynman Kutcher Burman (LKB) model

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5
Q

What is the Survival Fraction (SF)?

A

SF=plating efficiency (control cells)/Plating efficiency (irradiated cells)

plating efficiency=# of colonies/# cells (pre-irradiation)

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6
Q

What is alpha?

A

The mean number of fatal (double strand) DNA breaks per cell, per Gy, due to a single ionisation(Gy-1).

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7
Q

What is beta?

A

The mean number of fatal (double strand) DNA breaks per cell, per Gy2, due to 2 independent ionisation events (Gy-2).

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8
Q

What does the alpha/beta ratio signify?

A

Dose at which the double-strand break damage caused by single events equals that caused by two independent single strand breaks.

It also is a measure of the fractional sensitivity and repair capacity of the tissue.

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9
Q

What is the SF equation?

A

SF=e-D(alpha+beta*d)

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10
Q

What is the Tumour Control Probability (TCP)?

A

TPC is the fraction of tumour with no active clonogenic cells after all treatment.

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11
Q

What is the TCP sigmoid equation?

A

Double exponential:
TCP = e-[k0e-(alphaBED)]
where k0 is the number of active clonogentic cells at time=0

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12
Q

Generally, how is the TCP determined from the DVH?

A

By determining the products of the individual TCP from each dose bin.

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13
Q

What is the equation for k0?

A

k0=clonogenic cell density*volume recieving dose Di

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14
Q

What is the equation for calculating TCP from a DVH?

A

TCP = PRODUCT[e-k0e-(Di{alpha+beta*Di/n})]

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15
Q

Hot spots vs cold spots, which one is more detrimental to TCP and why? Assume equivalent dose difference.

A

Cold spots as they rapidly force the TCP to zero.

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16
Q

Basic TCP (LKV, Linear-Quadratic) can be enhanced by adding terms for what?

A

1) Tumour proliferation
2) Variation in tumour cell density - higher in centre, lower at extremities
3) variation in radiobiological parameters

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17
Q

Clinically, is there one value of alpha per patient/patient cohort? What is the difference between TCP curves with a single alpha or a range of alphas?

A

No, clinically there is a range (Gaussian spread) of alphas which result in a shallower slope of the TCP graph.

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18
Q

Why do parameters vary?​

A

Due to differences within patient tissue and between tissues from different patients; i.e. individual radiobiological responses.

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19
Q

How might clonogenic cell density typically vary?

A

Higher clonogenic cell density at the centre of the tumour, density dropping towards the tumour exterior.

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20
Q

Generally which has a more homogeneous dose distribution, tumour tissue or OAR and why?

A

Tumour tissue has a more uniform dose distribution as similar cell structure (i.e. one tissue). OARs cell structures differ, e.g. the kidney, as they have different tissues within them, therefore different cell types and cell distributions so dose is deposited heterogeneously.

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21
Q

What part of the cell cycle is most radiosensitive and why?

A

G2 possibly as this is just prior to mitosis and therefore shorter time to repair before dividing compared to other parts of the cycle.

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22
Q

Do cells fatally damaged by radiation die immediately?

A

Generally no, depends on where in the cell cycle they are. However, Lymphcytes do die at mitosis.

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23
Q

What is the Oxygen Enhancement Ratio (OER)?

A

It is the ratio of dose between hypoxic and oxic cells to deliver the same biological effect. OER is approx 3 for most cells.

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24
Q

Does oxygen content of cells affect radiosensitivity?

A

Yes, the lower the oxygen concentration (the more hypoxic a cell is) the more radioresistant the cell is. This is why patients having treatment are advised not to smoke as this lowers oxygen concentration in cells reducing treatment effectiveness.

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25
Q

What is the hypoxic fraction?

A

The proportion of clonogenic cells that have radiosensitivity typical of hypoxic cells.

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26
Q

Is the linear-quadratic model applicable at low doses?

A

No, below 1Gy, the LQ model breaks down.

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27
Q

How much is the local tumour control affected by a 1 day gap?

A

Local tumour control is reduced by approx 1.4% per day gap.

28
Q

What are the categories when managing treatment gaps?

A

Category 1 - rapid growing tumours, should not have gaps more than 2 days
Category 2 - slower growing tumours, recommend gaps less than 2 days but up to 5 days is acceptable (no safe minimum established).
Category 3: palliative, interruptions are common due to illness, possibly requiring compensation; recommend <7days but this limit is more flexible depending on the situtation.

29
Q

What affect on patient outcome does increasing total treatment time have?

A

Tumour control decreases with increased treatment time as neoplastic stem cells have time to repopulate.

30
Q

What effect on patient outcome does increasing total treatment time have?

A

Tumour control decreases with increased treatment time as neoplatic stem cels have time to repopulate.

31
Q

What are typical alpha/beta ratios for:

a) Tumours (early reacting)
b) normal tissue (late reacting)
c) for CNS
d) for lung

A

a) 10Gy
b) 3Gy
c) 2Gy
d) 4.5Gy

32
Q

Why do we fractionate treatments?

A

Fractionation ‘pushes apart’ tumour and normal tissue survival curves causing less damage to normal tissue. Each fraction repeats the fractional loss of cells from previous fraction. When given enough time for repair between fractions, healthy cells have a survival advantage over tumour cells, so fractional losses are comparatively less.

33
Q

On the SF curve, changing what parameter will affect the curve gradient at low doses?

A

Alpha is dominant at low doses.

34
Q

What are the five categories for classifying secondary cancers?

A

1) second tumour located in areas irradiated by primary or secondary therapeutic beams
2) histology of the second tumour is different from that of the original disease, therefore excluding metastasis
3) existence of latency period (e.g. several years)
4) the second tumour was not present at the time of treatment
5) patient does not have a cancer-prone syndrome

35
Q

Where does cancer induction evidence come from?

A

1) Animal studies
2) Atomic bomb survivors
3) patients exposed to diagnostic/therapeutic radiation doses
4) occupationally exposed workers

36
Q

Generally, for atomic bomb survivors, how does Excess Relative Risk of secondary cancer change with age?

A

15% for <10 years old and decreases to 1% for people aged >60

37
Q

Low dose exposure: what document assesses risk and what value does it put on is the detriment due to excess cancer and heritable effects?

A

ICRP103 - 5% per Sv

Assumes a linear response at low doses.

38
Q

What is Excess Absolute Risk (EAR)?

A

EAR is the fraction of RT patients who develop cancer minus the fraction of non-RT patients that develop cancer. It is expressed per 10^4 person-years (PY) per Gy or Sv.

EAR = (Cp-Co)/(PY/D)

39
Q

What is Relative Risk (RR)?

A

RR is the ratio of the fraction of RT patients that develop cancer to the fraction of non-RT patients that develop cancer.

RR = Cp/C0

E.g. RR are:
Breast: 1.3 for inducing secondary cancer within 5 years of RT
Oesophagus: 2.2 or inducing secondary cancer within 5 years of RT.

40
Q

What is Excess Relative Risk (ERR)?

A

ERR = 1 - RR

expressed as a fraction or %, per Gy or Sv.

41
Q

How do ERR, EAR and RR appear on a number line?

A

0—————1——————-2———————3+

42
Q

What differences in cancer types exist between atomic bomb survivors and RT patients with induced cancers? Why could this be the case?

A

Around 50% A-bomb survivors went on to develop Carcinomas while RT patients have significant levels of Sarcomas induced. This implies that the fractionation nature of RT treatment (small doses) elicits a different response to a single large dose from atomic bomb radiation exposure.

43
Q

For the Linear-no-Threshold (LNT) hypothesis, what is the approach to cancer risk calculation?

A

Sum of Dabsorbed * Wradiation * Wtissue, in Sv; then a rough calculation of risk as 5% per Sv.

AAPM report 75 gives info regarding imaging dose management during treatment.
ICRU Report 103 gives tissue weighting factors.

44
Q

What is Organ Equivalent Dose (OED)?

A

The uniform dose of an OAR which gives the same risk of secondary induce cancer as the patients actual DVH. i.e. it takes account of different dose response for different organs. It is an assumed linear-exponential relationship, starting linear at small doses then exponential at higher doses (increasing then reaching a max risk before decreasing).

45
Q

How would you go about calculating OED and the radiation-induced cancer incidence (I¬org)?

A

1) import DVH to excel
2) break into equal dose bins
3) look up parameters AlphaOrg (an organ-specific cell sterilisation parameter) and I0Org (radiation induced cancer incidence at low (<2Gy) dose.
4) Calculate OEDorg = (1/N)sum[Die-(alphaOrg * Di)]
N = number of dose calc points#Di = dose in bin
5) Calculate I¬org = IOrg0*OEDorg

46
Q

What is a radiation risk consequence of moving from 3D-CRT to IMRT?

A

Now have a dose bath (more healthy tissue receiving low dose), therefore presentation of secondary malignant neoplasms (SMNs) can increase (can double). Additionally, tissues that are out of field are exposed to leakage x-rays as IMRT requires up to three times as many MUs to deliver treatment compared to 3D-CRT.

Note: for proton treatments, also get neutron leakage that irradiates a larger volume of patient in some circumstances.

Also, approx 80% of children and young adults survive cancer for >5 years; however, around 73% develop treatment related conditions (SMNs are particularly common) developing years or more after treatment.

47
Q

Is dose a good indicator of SMN risk?

A

No. SMNs risk depends on other factors:

1) organ tissue (different organs have different risks)
2) age of the patient
3) sex of the patient
4) patient genetic profile

e.g. given was of 9-year old pediatric cranio-spinal patient where risk was highest in the bowls and upper abdomen, well away from the spine.

48
Q

Define Integral Dose (ID) and state what it is used for.

A

ID is the total energy deposited in the total irradiated volume of a patient.

ID (kg Gy)= m*D

ID is used to compare different radiotherapy modalities.

ID = rho * V(D)
Integrating dose over the DVH is the same as integrating the mean dose by total DVH volume where rho=1 (water).

49
Q

What are Concomitant doses?

A

These are exposures other than those for treatment, e.g CTsim or CBCT portal imaging. Defined in Medical and Dental guidance notes document from IPEM.

These contribute dose to healthy tissue, to the potential detriment of the patient. These issues are covered in AAPM report TG179.

50
Q

From TG179, what are typical doses for:

1) kv-CBCT?
2) Fan beam CBCT?
3) MV CBCT?

A

1) 0.2-2cGy for kv-CBCT
2) 0.7-4cGy for fan beam cbct
3) 0.7-10.8cGy for MV-CBT

51
Q

Does imaging dose need to be accounted for in RT planning?

A

From AAPM Report 180, if imaging dose >5% therapeutic dose, the imaging dose needs to be accounted for in RT planning. The value of 5% was determined from the CHART pilot study.

52
Q

What are the two main issues to consider when deciding timing for fractions?

A

1) Incomplete normal tissue repair between treatments, e.g.s accelerated RT, pulsed brachy (1 hour between treatments) and continuous LDR brachy (more historical issue with, for e.g., Ir192 wire).
2) treatment gaps

53
Q

What can cause treatment gaps?

A

Patient illness
Patient non-compliance (DNA) - quite common near end of treatment
Machine breakdown and insufficient backup capacity
Staffing shortages/issues/illness
Admin/booking failures

54
Q

What is the approximate normal tissue sub-lethal repair half time?

A

1.5 hours, therefore most damage will be repaired within 6 hours.
6hr = 94%
8hrs=97.5%
24hrs=99.998%

55
Q

What is the normal tissue repair equation?

A

%repair = 1-e-{Ln2*t/T1/2}

with T1/2 = 1.5 hours half life, t = time passed since treatment (hours).

56
Q

What is the incomplete repair BED equation for fractionated RT?

A

BED = nd[1+d(1+h))/alpha/beta]

57
Q

In relation to mitigating treatment gaps, what must you try and maintain?

A

1) original number of fractions
2) original dose per fraction
3) original total treatment time (this includes time for surgery and chemo)
4) original OAR repair time between fractions

I.e. aim to retain intended TCP and NTCP

58
Q

What are the options to deal with treatment gaps?

A

1) treat on weekends
2) treat more than once per day but maintain at least 6 hours between treatments, preferably 8 hours
3) If total time needs extending, change d and retain n to maintain intended tumour BEDbut at expense of OAR BED.

59
Q

What is the cell loss factor?

A

1 - Tpot/Tvol

where Tpot is the potential doubling time of clonogenic cells, Tvol is the volume doubling time (which is usually greater than Tpot due to cell loss).

Carcinomas have high (>70%) cell loss factors whilst sarcomas have low (<30%) cell loss factors. This may be explained due to carcinomas originating from epithelial tissue which continuously replenishes and, therefore, has a cell loss of 100%. This would also explain differing responses to RT.

60
Q

List and describe the RCR categories regarding gap management for RT.

A

Cat 1
Radical intent, patients with fast growing tumours as there is strong evidence that prolonging treatment has significant adverse effects on patient outcome, treatment extension should not be longer than 2 days.

Cat 2
Radical intent, patients with slower-growing tumours, recommend <5days extension to treatment but try and retain <2 days.

Cat 3
Palliative, treatment extension <7 days where possible but this may be exceeded due to patient illness.

61
Q

What does Relative Biological Dose (RBD) depend on?

A

1) Type of radiation
2) energy of radiation
3) dose (energy/unit mass)
4) biological end point

62
Q

What is Effective Dose (both the equation and conceptually)?

A

Deff = sum of (Da * Wr * Wt)

It is an indication of stochastic risk from an exposure; i.e. the risk/probability of random complications (such as secondary cancers).

63
Q

Names sources of dose limit data for OAR.

A

1) Emami data
2) clinical trials (e.g. CHIPP)
3) QUANTEC data
4) upcoming data (text books collated data, etc)

64
Q

What information does QUANTEC organ specific papers contain?

A

1) Clinical significance
2) Endpoints
3) Challenges in defining volumes
4) Review of dose/volume data
5) Factors affecting risk
6) Mathematical/biological models
7) Special situations
8) REcommended dose/volume limits
9) Future toxicity studies
10) Toxicity scoring

65
Q

From literature, which organs do not have any long term recovery after treatment?

A

1) Heart
2) Bladder
3) Kidney

Nieder et al 2000

66
Q

From literature, which organs have very good recovery after treatment?

A

1) Skin
2) intestines

reirradiation to almost full tolerance in 1-3 months. Nieder et al 2000

67
Q

What is EQD2?

A

Equivalent Dose for 2Gy fractions.

EQD2 = D[abratio+d]/[abratio+2]

D is the total dose in the local regime with d = dose per fraction in the local regime

Note, replacing 2 with a quantity X allows other EQD regimes to be calculated.

Y3 Exam Revision (6 decks)

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