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000 Radiobiology > ***Secondary cancer induction and fraction timing issues > Flashcards

***Secondary cancer induction and fraction timing issues Flashcards

1
Q

What 5 criteria must a cancer meet to be classified as a secondary cancer?

A

Occurs in locations irradiated by primary or secondary beams
Histology of second cancer is different from first - not a met
Latency period - typically a few years
Second tumour not present at RT
Patient does not have cancer prone syndrome

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2
Q

What is the radiation based cancer induction evidence?

A

Biolgical studies
A-bomb survivors
Patients expossed to diagnostic and therapeutic radiation
Occupationally exposed workers

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3
Q

What is the evidence for cancer induction by low doses of radiation?

A

ICRP 103 - assumes 5%/Sv
Biological effects of ionising radiation report VII - concludes linear no threshold model
UNSCEAR 2000 and 2006 reports

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4
Q

How is cancer induction risk expressed? What are the equations?

A
  • Excess absolute risk per 10^4 person-years per Gy
    EAR = Fraction of RT patients contracting cancer - Fraction of non-RT patients contracting cancer
  • Relative risk
    RR = Fraction of RT patients contracting cancer / Fraction of non-RT patients contracting cancer
  • Excess relative risk
    ERR = RR - 1
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5
Q

How should the linear no threshold approach be applied?

A

Sum dose distribution from different sources of radiation - apply organ specific coefficients - it is age and sex dependent
Apply a generalised risk coefficient of 5%/Sv

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6
Q

What does the linear exponential dose curve suggest?

A

Cell sterilisation can overtake cell cancer induction, reducing the response curve

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7
Q

Why might the linear exponential dose curve not be accurate?

A

Suggests the most likely location of secondary cancer is at the margins of treated areas and in IMRT low dose bath but this doesn’t correlate with RT patient data which suggests there is a plateau, potentially caused by cell repopulation

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8
Q

Why might A-bomb survivor data not be applicable for RT patients?

A

A-bomb data suggests only getting carcinoma whereas RT data suggests patients also get sarcomas

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9
Q

What is the organ equivalent dose?

A

For an inhomogeneous dose distribution the OED is the uniform dose with the same risk of radiation-induced cancer as the patient’s DVH

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10
Q

Why is OED good?

A

Accounts for dose response relationship for radiation-induced cancer in different organs - uses linear exponential dose risk model

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11
Q

What is the equation for OED?

A

OED = 1/N . sum(Di.e^(-alpha.Di))

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12
Q

How is the radiation induced cancer incidence rate at a uniform dose defined?

A

Iorg = Iorg,0 . OED

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13
Q

What 2 reasons contribute to IMRT treatments increasing the risk of second malignant neoplasms?

A

IMRT requires more fields so a larger volume is exposed to radiation
Out of field tissue is more exposed to leakage x-rays as IMRT requires 2 or 3 times as many MU

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14
Q

How is the integral dose for the IMRT dose bath?

A

Total energy deposited in the total irradiated volume of the patient: ID = m.D
For inhomogeneous dose distributions the total ID is the summed ID across all dose beams: ID = sum(Di.Vi)

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15
Q

What are concomitant doses?

A

All exposures within the course of RT other than treatment exposures. Include simulation, CT localisation, portal localisation, and verification images
They irradiate normal tissue outside the target volume or the intended path of the primary beam and therefore contribute to the potential detriment of the patient

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16
Q

What is the problem if there is incomplete repair between fractions?

A

A significant proportion of single strand breaks are not repaired so normal tissue tolerances are lower

17
Q

What situations lead to incomplete repair?

A

Accelerated RT - reduce proliferation
Pulsed Brachytherapy - time between fractions = 1 hour
Continuous low dose Brachytherapy - ongoing repair during treatment

18
Q

How long does it take for repairable damage to be repaired?

A

~6 hours

19
Q

What is the correction that is made to the BED equation for fractionated RT?

A

beta.d^2 term in the survival fraction is modified as the relative effectiveness per unit dose is greater due to incomplete repair:
BED = nd(1 + (d(1+h)/(alpha/beta)))

20
Q

What is the correction that is made to the BED equation for low doserate brachy?

A 
BED = RT(1 + 2R/(mu(alpha/beta)))
R = dose rate
T = time
21
Q

What are the possible causes of treatment gaps?

A

Patient non-attendance - too ill to attend, adverse weather, non-cooperation
Machine breakdown

22
Q

How can both TCP and NCTP be kept constant after a treatment break?

A

Original number of #s and dose/#
Original treatment time - may need to treat on a weekend
Original repair between fractions

23
Q

What are some issues with repair?

A

Have different repair half times between tissues - 1.5hrs for normal tissue, 0.5hrs for tumour tissue
Can have multiphasic repair - get quick initial repair followed by prolonged subsequent repair past 6 hours

24
Q

What is the equation for BED considering tumour repopulation?

A

BED = D(1 + d/(alpha/beta)) - (ln2/alpha).((T - Tdelay)/Tp)

25
Q

How should treatment gaps with time longer than T be handled?

A

Try to treat in time T by doubling up treatment days

If not then increase d and n to give same BED

26
Q

What is the equation for the tumour potential doubling time?

A

Tpot = Tc/GF
Where Tc = cell cycle time
GF = Growth fraction - actively proliferating cells /all tumour cells

27
Q

What is the equation for the maximum tumour growth rate with no cell loss?

A

1/Tpot

28
Q

What is the equation for the actual tumour growth rate?

A

1/Tvol

29
Q

What is the equation for the cell loss factor?

A

phi = 1-(Tpot/Tvol)

30
Q

What are the cell loss factors for carcinomas and sarcomas? Why?

A

Carcinomas - high, >70%, due to origin as rapidly renewing epithelial cells -cell loss factor = 100%
Sarcomas - slow, <30%

31
Q

What happens to the GF value of tumours before and during RT? Why?

A

Before GF slows down as the tumour is large

GF speeds up to maximum during RT as remaining cells get better nutrition as there are fewer of them

32
Q

What factor should be used for radiobiology calculations during RT with proliferation?

A

Tpot

33
Q

What are the 3 categories of patients? What do they mean?

A

1 - should not have their radical treatment prolonged
2 - every effort should be made to keep any prolongation of treatment to a minimum
3 - palliative care

34
Q

How should unscheduled interuptions be prevented?

A

Transfer patient

Ensure schedule is properly managed

35
Q

What compensation is recommended by the RCR for unavoidable and unscheduled gaps?

A

Acceleration (>6hr gap)
Weekend/bank holiday treatments
Adjust d,n to maintain T - sacrifice the therapeutic ratio a little
Add fractions if maintaining T is impossible - sacrifices therapeutic ratio more

36
Q

What is the RCR equation for BED?

A

BED = nd(1 + (d/(alpha/beta))) - K(T-Tdelay)
K = ERD loss/day
= ln2/(alpha.Tpot)

000 Radiobiology (52 decks)

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