basics radiobiology for radiotherapy

02/05/2023 Dr. Nik Noor Ashikin Bt Nik Ab Razak 1

TOPIC 2

BASICS RADIOBIOLOGY FOR RADIOTHERAPY

(2 hours)


2.1 Introduction2.2 Radiation Chemistry2.3 Volume Definition

2.3.1 Gross Tumour Volume (GTV)2.3.2 Clinical Target Volume (CTV)2.3.3 Planning Target Volume (PTV)2.3.4 Treated Volume (TV)2.3.5 Irradiated Volume (Iv)2.3.6 Organs At Risk (Oar)

Dr. Nik Noor Ashikin Bt Nik Ab Razak 3

2.4 5 Rs2.4.1 Repair2.4.2 Repopulation2.4.3 Reoxygenation2.4.4 Redistribution2.4.5 Radiosensitivity

2.5 Biological Effect of Ionizing Radiation2.5.1 Dose Response Curve2.5.2 Cell Survival Curve2.5.3 Systemic Effects2.5.4 Oxygen Effect2.5.5 LET2.5.6 Relative Biological Effectiveness (RBE)

02/05/2023


2.1 Introduction

02/05/2023 5

INTERACTIONS between

Ionizing radiation and living systems

radiation

physics +

biology

Radiation

oncology

2.1 IntroductionACTION Of

ionizing radiatio

n on biologic

al tissues

radiation

physics +

biology

Radiobiology

02/05/2023 Dr. Nik Noor Ashikin Bt Nik Ab Razak

2.1 Introduction

6


2.2 Radiation Chemistry



Radiation may impact the DNA directly,

causing ionization of the atoms in the DNA

molecule (“direct hit”). It is a fairly uncommon occurrence due to the small size of the target; the diameter of the DNA

helix =2 nm.

Dominant process in the interaction of high LET

particles such as neutrons or alpha

particles with biological material.

1) DIRECT ACTION


2) INDIRECT ACTION


The radiation interacts with non-critical target

atoms or molecules, usually water.

This results in the production of free

radicals, which are atoms or molecules that have an unpaired electron and

thus are highly reactive

These free radicals can then attack critical targets such as the DNA. Damage from

indirect action is much more common than damage from

direct action

•Indirect action: Electrons produce free radicals which break chemical bonds and produce chemical changes

•Direct Action: Photon ejects an electron which produce a biological damage on the DNA



2.3 Volume Definition2.3.1 Gross Tumour Volume (GTV)2.3.2 Clinical Target Volume (CTV)2.3.3 Planning Target Volume (PTV)2.3.4 Treated Volume (TV)2.3.5 Irradiated Volume (Iv)2.3.6 Organs At Risk (Oar)

•Volume definition is a prerequisite for meaningful 3-D treatment planning and for accurate dose reporting.

• ICRU reports No. 50 and 62 define and describe several target and critical structure volumes that aid in the treatment planning process and that provide a basis for comparison of treatment outcomes.

• The following volumes have been defined as principal volumes related to 3-D treatment planning: gross tumour volume (GTV), clinical target volume (CTV), internal target volume (ITV) and planning target volume (PTV)

2.3 Volume Definition

GTV – Gross Tumour Volume

CTV – Clinical Target Volume

PTV – Planning Target Volume

OAR – Organ at Risk

TV – Treated Volume

IV – Irradiated Volume

2.3 Volume Definition

The gross palpable, visible and

demonstrable extent and location of the malignant growth

(ICRU Report No. 50)

2.3.1 Gross Tumour Volume (GTV)

• This is determined by physical examination by the oncologist and the results of radiological investigations relevant to the site of the tumour.

• As the term suggests, tumours have a length, breadth and depth, and the GTV must therefore be identified using orthogonal 2D or 3D imaging (computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, etc.), diagnostic modalities (pathology and histological reports, etc.) and clinical examination.

2.3.1 Gross Tumour Volume (GTV)

Part VIII.3.7 Operational Considerations – Planning of physical treatment

Slide 19

Gross Tumour Volume (GTV)– Gross palpable or visible/demonstrable

extent and location of tumourGTV

•“The clinical target volume (CTV) is the tissue volume that contains a demonstrable GTV and/or sub-clinical microscopic malignant disease, which has to be eliminated. This volume thus has to be treated adequately in order to achieve the aim of therapy, cure or palliation” (ICRU Report No. 50)

2.3.2 Clinical Target Volume (CTV)

•Usually determined by the radiation oncologist, often after other relevant specialists such as pathologists or radiologists have been consulted.

•This volume may not be defined separately but considered when defining the planning target volume (PTV) (e.g. CTV = GTV + 1 cm margin)

2.3.2 Clinical Target Volume (CTV)


Slide 22

Clinical Tumour Volume (CTV)

CTV Contains a GTV and/or sub-clinical microscopic malignant disease, which has to be eliminated CTV

•“The planning target volume (PTV) is a geometrical concept, and it is defined to select appropriate beam arrangements, taking into consideration the net effect of all possible geometrical variations, in order to ensure that the prescribed dose is actually absorbed in the CTV” (ICRU Report No. 50)

2.3.3 Planning Target Volume (PTV)


• The PTV includes the internal target margin (ICRU Report No. 62) and an additional margin for the set-up uncertainties, machine tolerances and intratreatment variations

• It fully encompasses the GTV and CTV (e.g : PTV = CTV + 1 cm).



• In practice, it is often the result of a compromise between two contradictory issues: making sure that the CTV will receive the prescribed dose while at the same time ensuring that OARs will not receive an excessive dose.



Slide 26

Planning Target Volume (PTV)• Contains a CTV and a margin to account for

variation is size, shape and position relative to treatment beams

PTV

•The volume of tissue enclosed by an isodose surface selected and specified by the clinician as being appropriate to achieve the aim of treatment.

•For example, this may be the volume encompassed within the 95% isodose surface (with 100% in the centre of the PTV) for a curative treatment plan.

2.3.4 Treated Volume (TV)

•The TV should not be significantly larger than the PTV. The use of 3D treatment planning and shaping the radiation fields to the shape of the PTV using conformal radiation delivery techniques ensures that the TV encloses the PTV with as narrow a margin as possible. This ensures minimal irradiation of surrounding OARs while coverage of the PTV is assured.

2.3.4 Treated Volume (TV)


Slide 29

Treated volumeTreated volume – Volume enclosed by an isodose

surface selected as appropriate to achieve purpose of treatment

Treated Volume

•The tissue volume receiving a radiation absorbed dose that is considered significant in relation to normal tissue tolerance.

•This concept is not often considered in practice but may be useful when comparing one or more competing treatment plans.

•Clearly, it would be preferable to accept the plan with the smallest IV, all else being equal.

2.3.5 Irradiated Volume (Iv)


Slide 31

Irradiated volumeIrradiated volume – The volume that receives a

dose that is significant in relation to normal tissue tolerance

Irradiated Volume

•Organs adjacent to the PTV which are non-target; do not contain malignant cells

• The aim should therefore be to minimise irradiation of OARs as they are often relatively sensitive to the effects of ionising radiation and, if damaged, may lead to substantial morbidity.

• The OARs to be considered will vary greatly according to the anatomical region being treated, the size of the PTV and the location of the PTV in these regions.

2.3.6 Organs At Risk (Oar)

• The following are examples of the most common OARs that must be considered:

1.Brain: lens of eye, optic chiasm, brain stem2.Head & neck: lens of eye, parotid glands3.Thorax: spinal cord, lungs4.Abdomen: spinal cord, large bowel, small bowel,

kidneys5.Pelvis: bladder, rectum, femoral heads, large

bowel, small bowel

2.3.6 Organs At Risk (Oar)


Slide 34

Organs at Risk (OAR)• Normal tissues whose radiation

sensitivity could significantly influence treatment planning and/or the dose prescription

OARs• Lung

• Spinal cord


2.4 Biological Factors (5 Rs)2.4.1 Repair2.4.2 Repopulation2.4.3 Reoxygenation2.4.4 Redistribution2.4.5 Radiosensitivity

Repair

Repopulation

Reoxygenation

Redistribution

Radiosensitivity

•The biological factors that influence the response of normal and

neoplastic tissues to fractionated radiotherapy

2.4 Biological Factor (5 Rs)


2.4.1 Repair

•All cells repair radiation damage•Repair is very effective because DNA is damaged significantly more due to ‘normal’ other influences (e.g. temperature, chemicals) than due to radiation

•The half time for repair, tr, is of the order of minutes to hours

2.4.1 Repair

• It is essential to allow normal tissues to repair all repairable radiation damage prior to giving another fraction of radiation.

•This leads to a minimum interval between fractions of 6 hours

•Spinal cord seems to have a particularly slow repair - therefore, breaks between fractions should be at least 8 hours if spinal cord is irradiated.

2.5.1 Repair


2.4.2 Repopulation


• In both tumours and normal tissues, proliferation of surviving cells may occur during the course of fractionated treatment.

• Furthermore, as cellular damage and cell death occur during the course of the treatment, the tissue may respond with an increased rate of cell proliferation.

• The effect of this cell proliferation during treatment, known as repopulation or regeneration (increase the number of cells during the course of the treatment and reduce the overall response to irradiation)

2.4.2 Repopulation


• This effect is most important in early-responding normal tissues (e.g., skin, gastrointestinal tract) or in tumours whose stem cells are capable of rapid proliferation; it will be of little consequence in late-responding, slowly proliferating tissues (e.g., kidney), which do not suffer much early cell death and hence do not produce an early proliferative response to the radiation treatment.

• Repopulation is likely to be more important toward the end of a course of treatment, when sufficient damage has accumulated (and cell death occurred) to induce a regenerative response.

2.4.2 Repopulation

• The repopulation time of tumour cells appears to vary during radiotherapy - at the commencement it may be slow (e.g. due to hypoxia), however a certain time after the first fraction of radiotherapy (often termed the “kick-off time”, Tk) repopulation accelerates.

• Repopulation must be taken into account when protracting/prolong radiation e.g. due to scheduled (or unscheduled) breaks such as holidays.

2.4.2 Repopulation


2.4.3 Reoxygenation

•Oxygen is an important enhancement for radiation effects (“Oxygen Enhancement Ratio” (OER)

• The tumor may be hypoxic (in particular in the center which may not be well supplied with blood)

• One must allow the tumor to re-oxygenate, which typically happens a couple of days after the first irradiation

2.4.3 Reoxygenation


• The response of tumours to large single doses of radiation is dominated by the presence of hypoxic cells within them, even if only a very small fraction of the tumour stem cells are hypoxic.

• Immediately after a dose of radiation, the proportion of the surviving cells that is hypoxic will be elevated. However, with time, some of the surviving hypoxic cells may gain access to oxygen and hence become reoxygenated and more sensitive to a subsequent radiation treatment.

• Reoxygenation can result in a substantial increase in the sensitivity of tumours during fractionated treatment.

2.4.3 Reoxygenation


2.4.4 Redistribution

• Cells have different radiation sensitivities in different parts of the cell cycle

• Highest radiation sensitivity is in early S and late G2/M phase of the cell cycle

G1

G1

S (synthesis)

M (mitosis)G2



• Variation in the radiosensitivity of cells in different phases of the cell cycle results in the cells in the more resistant phases being more likely to survive a dose of radiation.

• Two effects can make the cell population more sensitive to a subsequent dose of radiation.

1. Some of the cells will be blocked in the G2 phase of the cycle, which is usually a sensitive phase.

2. Some of the surviving cells will redistribute into more sensitive parts of the cell cycle.

• Both effects will tend to make the whole population more sensitive to fractionated treatment as compared with a single dose.

• .

•The distribution of cells in different phases of the cycle is normally not something which can be influenced - however, radiation itself introduces a block of cells in G2 phase which leads to a synchronization

•One must consider this when irradiating cells with breaks of few hours.



2.4.5 Radiosensitivity

•For a given fractionation course (or for single-dose irradiation), the haemopoietic system shows a greater response than the kidney, even allowing for the different timing of response.

•Similarly, some tumours are more radioresponsive than others to a particular fractionation schedule, and this is largely due to differences in radiosensitivity.


MuscleBonesNervous system

SkinLiverHeart Lungs

Bone MarrowSpleenThymusLymphatic nodesGonadsEye lensLymphocytes (exception to the RS laws)

Low RSMedium RSHigh RS


Dr. Nik Noor Ashikin Bt Nik Ab Razak 62

2.5 Biological Effect of Ionizing Radiation2.5.1 Dose Response Curve

2.5.1.1 Deterministic 2.5.1.2 Stochastic Effect2.5.1.3 Sigmoid Curve2.5.1.4 Cell Survival Curve

2.5.2 LET2.5.3 OER2.5.4 RBE


2.5 Biological Effect of Ionizing Radiation

Module Medical IX. 70

Biological effects of radiation in time perspective

Time scale

Fractions of seconds

Seconds

Minutes

HoursDays

WeeksMonths

Years

Decades

Generations

Effects

Energy absorption

Changes in biomolecules(DNA, membranes)

Biological repair

Change of information in cell

Cell death

Organ Clinicaldeath changes

Mutations in a

Germ cell Somatic cell

Leukaemia

or Cancer

Hereditary effects


71

Dose to the tumor determines probability

of cure Dose to normal structures determines

probability of side effects and

complicationsDose to patient, staff and visitors determines

risk of radiation detriment to these

groups

What matters in the end is the

biological effect!




2.5 Biological Effect

Biological Effect

Stochastic Effects(carcinogenic and genetic effects)

Deterministic Effects(tissue reactions)


2.5.1 Dose Response Curve


2.5.1.3 Sigmoid Curve (non-threshold)

DOSE

RESPONSE

CURVE

Line 3: Non linear dose

response

Line 1: No level of radiation can be

considered safe.

Diagnostic Imaging

Line 2:

Threshold is assumed, response

expected at lower doses.(Radiotherap

y)

Stochastic Effect

Dete

rmin

istic

Effec

t


2.5.1.1 Deterministic Effect


DETERMINISTIC EFFECTS/ (High Dose)

erythemaskin

breakdown cataracts

death

Have a dose

threshold

Due to cell killing

(high dose given over

short period)

Severity of harm is dose dependent

Specific to

particular tissues

Acute effect/ short term effect/

early effect

Acute radiation syndrome(ARS)

ARS is the most notable deterministic effect of ionizing radiation Signs and symptoms are not specific for radiation injury but

collectively highly characteristic of ARS Combination of symptoms appears in phases during hours to

weeks after exposure - prodromal phase - latent phase - manifest illness - recovery (or death)


2.5.1.2 Stochastic Effect

2.5.1.2 Stochastic Effect

STOCHASTIC EFFECT

(low dose)

Eg:-cancer

induction (Somatic effect)

-hereditary effects

Severity (example cancer)

independent of the dose

Due to cell changes and proliferation towards a malignant disease

No dose threshold -

applicable also to very small

doses

Probability of effect

increases with dose

Late effect / Chronic effect)

2.5 Biological Effect2.5.1.2 Stochastic Effect

Phases of cancer induction and manifestation

In itia tio n Mu ta te d C e lls

Elim ia tio n Re p a ra tio n

Pro g re ssio n

Pre -c a n c e r

No rm a l C e lls

Pro m o tio n

Min im a l C a n c e r

C lin ic a l C a n c e r

Sp re a d in g

% E

ffect

Dose

Repairing cell structures is still possible No repairing: a low

dose means a great damage

Practically all the cells are dead

dose




LD 50/60amount of radiation that will cause 50%

of exposed individuals to die within 60 days


2.5.1.4 Cell Survival Curve

Biological Effects At Cellular Level

Possible mechanisms of cell death:

•Physical death•Functional death

• Death during interphase

• Mitotic delay• Reproductive failure

Cellular effects of ionizing radiation are studied by cell survival curves

% su

rviv

al c

ells

(sem

i log

arith

mic

)

Dose

n = targets

Dq

D0

(threshold)

(radiosensitivity)


• Do = 37% dose slope- Dose required to reduce the number of clonogenic cells to 37% of their former value

• Dq = Quasi threshold dose- Dose at which straight portion extrapolated backward cuts the dose axis

• n = extrapolation number- Extrapolating the straight portion of the survival curve until it cuts the “surviving fraction” axis

Radiosensitive cells are characterized by curves with steep slope D0 and/or small shoulder (low n)

Loge n = Dq / D0

% su

rviv

al c

ells

(sem

i log

arith

mic

)

Dose

n = targets

Dq

D0

(threshold)

(radiosensitivity)


2.5.2 LET


2.5.2 LET


LETthe linear rate of

energy absorption by

absorbing medium as

charged particle traverses the

medium(dE/dl,

KeV/mm)

defining the quality of

an ionizing radiation

beam

Photon

Proton

Helium

Carbon

Oxygen

Neon

gamma rays

deep therapyX-rays

soft X-rays

alpha-particle

HIGH LETRadiation

LOW LETRadiation

Separation of ion clusters in relation tosize of biological target

4 nm

The Spatial Distribution of Ionizing Events Varies with the Type of Radiation and can be defined by LET

http://dmco.ucla.edu/McBride_Lab

WMcB2008

• A dose of 1 Gy will give 2x103 ionization events in 10-10 g (the size of a cell nucleus). This can be achieved by:– 1MeV electrons

•700 electrons which give 6 ionization events per m.

– 30 keV electrons •140 electrons which give 30 ionization events per m.

– 4 MeV protons •14 protons which give 300 ionization events per m.

• The biological effectiveness of these different radiations vary!

-ray

’-ray

excitation

ionization

particle

excitation and ionization


WMcB2008

Repairable Sublethal Damage

X- or -radiation is sparsely ionizing; most damage can be repaired

4 nm

2 nm


WMcB2008

Single lethal hitAlso known as - type killing

4 nm

2 nm

Unrepairable Multiply Damaged Site

It is hypothesized that the lethal lesions are large double strand breaks with Multiply Damaged Sites (MDS) that can not be repaired. They are more likely to occur at the end of a track


WMcB2008

At high dose, intertrack repairable Sublethal Damage may Accumulate forming unrepairable, lethal MDS

Also known as - type killing


2.5.2 LET


2.5.3 Oxygen Enhancement Ratio



1

• Oxygen is a powerful oxidizing agent and therefore acts as a radiosensitizer if it is present at the time of irradiation (within msecs).

• Its effects are measured as the oxygen enhancement ratio (O.E.R.)

2

• The presence or absence of molecular oxygen within a cell influences the biological effect of ionizing radiation: the larger the cell oxygenation above anoxia, the larger is the biological effect until saturation of the effect of oxygen occurs, especially for low LET radiations



3• The effect is quite dramatic for low LET

(sparsely ionizing) radiations, while for high LET (densely ionizing) radiations it is much less pronounced

4• The ratio of doses without and with

oxygen (hypoxic vs. well-oxygenated cells) to produce the same biological effect is called the oxygen enhancement ratio (OER).

• O.E.R. = D(anox)/D(ox)

02/05/2023 108




5

• For densely ionizing radiation, such as low-energy α-particles, the survival curve does not have an initial shoulder

6

• In this case, survival estimates made in the presence and absence of oxygen fall along a common line; the OER is unity – in other words, there is no oxygen effect


WMcB2008

Oxygen Enhancement Ratio (OER)

Dose required to produce a specific biological effect in the absence of oxygenDose required for the same effect in its presence=

OER varies with level of effect but can be 2.5 - 3 fold1) Culture Cells

(

3) Count cells in hemocytometer

4) irradiate under oxic or hypoxic conditions

0 Gy 2Gy 4Gy 6Gy

5) Plate cells and grow for about 12 days

. . ..

... .

6) Count colonies

Dose (Gy)

S.F.

0 2 4 6 8 10

1.0

0.1

0.01

oxichypoxic

Physical Dose = Biological Dose

2) Suspend Cellstrysinization)


WMcB2008

• Hypoxic areas occur almost solely in tumors and are more radioresistant than oxic areas.

• Hypoxia contributes to treatment failure• Reoxygenation occurs between radiation dose fractions giving a

rationale for dose fractionation• The oxygen effect is greater for low LET than high LET radiation

Giacca and Brown

Pimonizadole (oxygen mimetic) staining colorectal carcinoma

The effects of hypoxia were first discovered in 1909 by Schwarz who showed that strapping a radium source on the arm gave less of a skin reaction than just placing it there. This was used to give higher doses to deep seated tumors.

Clinical Relevance of Hypoxia


2.5.4 Relative Biological Effectiveness (RBE)

113

2.5.4 RBE

1• Equal doses of different LET radiation DO

NOT produce equal biological effects

2•A term relating the ability of radiations with different LETs to produce a specific biologic response is relative biological effectiveness (RBE)

114

2.5.4 RBE

3• RBE is defined as the comparison of a dose of

some test radiation to the dose of 250 kV x-rays that produces the same biologic response

4•250 kV x-rays or 1.17/1.33 MeV 60Co as the standard radiation

RBE is end-point dependent

Fractionated doses of dense vs. sparse ionizing beam:The RBE of high LET beam becomes larger when the fraction number is increasing.

2.5.4 RBE

The ICRP 1991 standard values for relative effectiveness

Radiation EnergyWR (also RBE or

Q)x-rays, gamma rays, electrons,

positrons, muons 1neutrons < 10 keV 5

10 keV - 100 keV 10 100 keV - 2 MeV 20 2 MeV - 20 MeV 10 > 20 MeV 5

protons > 2 MeV 2alpha particles, nuclear fission

products, heavy nuclei 20

Weighting factors WR (also termed RBE or Q factor, to avoid confusion with tissue weighting factors Wf) used to calculate equivalent dose according to ICRP report 92

2.5.4 RBE


WMcB2008

ACUTE RESPONDING TISSUES(responses seen during standard therapy)GutSkinBone MarrowMucosaLATE RESPONDING TISSUES(responses seen after end of therapy) BrainSpinal CordKidneyLungBladder

Tissue Type Matters

Dose (Gy)

SurvivingFraction

2016128400.01

.1

1

Late RespondingTissues

Acute RespondingTissues and Many Tumors

Physical Dose = Biological Dose

Example• To achieve 50% survival fraction, 250 kV x-ray needs 2

Gy, but the tested particle needs 0.66 Gy only

RBE = D250/Dt 2 = 2 / 0.66 = 3RBE at survival fraction of 0.5 for the tested particle is 3.

2.5.4 RBE

2.5.4 RBE


WMcB2008

Questions on Interaction of Radiation with Biological Matter:

what is biological dose?

Bill McBrideDept. Radiation Oncology

David Geffen School MedicineUCLA, Los Angeles, Ca.

[email protected]


WMcB2008

1.The lifetime of radicals in target molecules is about– 10-3 secs– 10-6 secs – 10-9 secs– 10-12 secs

#2 – free radicals are highly unstable and reactive


WMcB2008

2.Electromagnetic radiation is considered ionizing if it has a photon energy greater than– 1.24 eV– 12.4 eV– 124 eV– 1.24 keV

#3 – this is sufficient to break bonds in biological molecules


WMcB2008

3.The S.I. unit of absorbed dose is– Becquerel– Sievert– Gray– Roentgen

#3 The International System (IS) unit is the Gray, named after the radiobiologist Louis “Hal” Gray who was based in London


WMcB2008

4.Which of the following are not charged particles?– Electrons– Neutrons– Protons– Heavy ions– Alpha particles

#2 – which is why they are called NEUTRons


WMcB2008

5. Which of the following is NOT a characteristic of the indirect action of ionizing radiation– Production of diffusible free radicals– Production of reactive oxygen species– Involvement of anti-oxidant defenses– Causes a change in redox within a cell favoring

reduction of constituents

#4 the free radicals produced makes ionizing radiation an oxidative stress overall


WMcB2008

6. Which of the following is true about the oxygen enhancement ratio – Is the same at all levels of cell survival– Can be measured by the dog-leg in a cell survival

curve after single high dose irradiation of tumors– Is the ratio of doses needed for an isoeffect in the

absence to the presence of oxygen– Is low for cells in S cell cycle phase compared to

cells in G2/M phase

#3 responses should be compared by the doses needed for a particular isoeffect. The OER varies with the level of effect eg survival


WMcB2008

7. Which of the following is true about Linear Energy Transfer– It is a measure of the biological effectiveness of

ionizing radiation– Shows an inverse correlation with the oxygen

enhancement ratio– Is maximal at a relative biological effectiveness of

150 keV/micrometer– Is measured in keV/micrometer

#4 LET is an average value imparted per unit path length. Because the radiations vary in energy, the LET is not biologically very useful


WMcB2008

8.The Relative Biological Effectiveness of a radiation is– Assessed by the dose required for to

produce the same effect as 250kVp X-rays– Is the ratio of the dose required of 250 kVp

X-rays to that of the test radiation for a given isoeffect

– Is directly related to Linear Energy Transfer– Is about 3 for alpha particle radiation

#2 - again, measured by isoeffective doses – classically relative to 250kVp x-rays, but often more recently 60Co has been used


WMcB2008

9. Which of the following radiobiological phenomena occurring between dose fractions has little or no effect on normal tissue radiation responses?

– Repair– Redistribution of cells in the cell cycle – Repopulation– Reoxygenation

#4 – Normal tissues are generally considered to be well oxygenated

basics radiobiology for radiotherapy

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