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FRCR Clinical Oncology Part 1 COPY > Radiobiology > Flashcards

Radiobiology Flashcards

1
Q

Roughly how many SSBs and DSBs occur per Gy of radiation?

A

SSB 1000

DSBs 40

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2
Q

What are hierarchical tissues?

A

Have populations of stem cells, transit (maturing partially differentiated) and functionally fully differentiated cells.
Acute toxicity after radiation

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3
Q

What are flexible tissues?

A

Cells rarely divide but may be induced to by damage. Cells are functional but retain ability to re-enter cell cycle.
Respond more slowly to radiation

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4
Q

Name some F-type tissues (flexible)?

A

Liver
Thyroid
Dermis of skin

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5
Q

What is serial behaviour of an organ? Name some serial organs.

A

Small critical functioning volume
Susceptible to high point doses
Spinal cord, brainstem, optic nerve, bowel

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6
Q

What is parallel behaviour of an organ? Name some parallel organs

A

Large critical functioning volume
Each functional subunit is able to function independently
More susceptible to volume effects
Lung (can be both), kidney, liver

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7
Q

What is the equivalent uniform dose?

A

EUD is the absorbed radiation dose which when given homogeneously to a tumour results in the same degree of clonogen cell kill as a non-homogenous dose.
Reflects the overall cell kill produced by a nonuniform dose distribution and so potentially a better indicator of biological outcome than simple average physical dose.

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8
Q

The normal tissue complication probability is a function of…

A

1, FSU inactivation probability

  1. Number of FSUs
  2. Doses received by the FSUs
  3. Assumed hierarchial structure (serial, parallel)
  4. Minimum numbers of FSUs to remain intact to ensure functionality
  5. Consequential functional links between groups of FSUs
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9
Q

How is the generalised EUD calculated?

A

Equation which uses a biological parameter “a” which is derived from clinical observation and chosen to reflect the desired radiobiological property.
a <1 = lower doses are given higher weight so that the cold spots influence EUD to a larger extent. Useful if cold spots on target
a =1 : cold and hot spots given equal value - good for parallel organs.
a >1 : larger doses are given higher weight so that hot spots influence the EUD to a larger extent- good for serial organs.

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10
Q

What is a clonogenic tumour cell?

A

Has the capacity to generate a new tumour
Requires viability AND capacity for sustained cell division
Cells that form colonies exceeding 50 cells (5-6 generations) - this excludes cells with limited growth potential.

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11
Q

When do cells lose their reproductive ability after radiation?

A

Cells do not die immediately after dose of radiation. Some undergo division before dying but the loss of reproductive integrity that is thought to be the critical response to radiotherapy occurs within a few hours
Some clonogenic normal tissue cells can regenerate.

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12
Q

What is a clonogenic assay?

A

Used to assess the response of cells to ionising radiation. They may be used to assess cell survival following radiation by measuring colony formation after a particular dose. Several types of assay exist. A control assay, where no radiation is given, must be used to determine the efficacy of the test and adjust the observed outcome. This is known (for in vitro colony assays) as plating effectiveness.

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13
Q

Name some types of clonogenic assay?

A

In vitro - plates

Spleen colony assays
- If bone marrow cells are injected into a synergistic mouse recipient, colonies in the spleen will form from the surviving stem cells. The number of colonies can be counted to assess cell survival of bone marrow cells following irradiation. This technique is also used for some types of mouse lymphoma cells.

Lung colony assays
This is similar to a spleen colony assay. Transplanted mouse tumours will often grow more readily in the lung and the number of colonies that form on the lung surface is related to the number of surviving tumour cells.

Limiting dilution assays
Different sizes of tumour colonies may be inoculated into the subcutaneous tissue of a creature (usually a mouse). The number and size of colonies which grow is then observed. By taking into account the size of the inoculated tumour colony, highly accurate readings of cell survival can be obtained (down to 1 x 10-6 surviving cells)

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14
Q

If you have a single suspension of tumour cells and split them into 2 parts, one was irradiated and one was not.
They are then plated out.
Plate 1: 100 control cells -> 20 control colonies
Plate 2: 400 irradiated cells -> 8 irradiated colonies

What is the plating efficiency and surviving fraction?

A

Plate 1: efficiency = 20/100 = 0.2
Plate 2 efficiency = 8/400 = 0.02

Surviving fraction = plating efficiency treated/plating efficiency of control = 0.02/0.2 = 0.1 = 10%

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15
Q

After treatment a linear survival curve would have what shape?

A

Sigmoig shape

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16
Q

A logirithmic survival curve would have what kind of shape?

A

Has a shoulder at top then exponential decrease

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17
Q

What is the LD50?

A

Lethal dose that kills 50%

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18
Q

What is the TGTv5?

A

Time it takes for tumour to get to 5 x treatment volume

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19
Q

How do you calculate the tumour growth delay?

A

Tumour growth treated minus tumour growth of control

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20
Q

What is linear energy transfer?

A

The density of ionisation in particle tracks.

LET is the average energy (in KeV) given up by a charged particle traversing a distance of 1 micrometre.

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21
Q

What type of radiation has a high LET?

A

Alpha particles

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22
Q

What types of radiation has a low LET?

A

XR, gamma rays, protons (most of the time)

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23
Q

How does low LET Radiation cause damage?

A

1/3 direct DNA damage

2/3 indirect damage - ROS

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24
Q

Is low or high LET radiaiton more likely to cause cancer?

A

Low LET
Causes more mutations in surviving cells due to indirect damage and these can go on to form cancer.
High LET radiation more likely to kill cell then cause mutation in a surviving cell

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25
Q

As LET increases how does the survival curve change

A

Steeper without a shoulder

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26
Q

As LET increases what happens to the RBE?

A

RBE rises with increasing LET up to a certain point.
At very high values of LET you get overkill.
Very high LET radiation is inefficient as it deposits more energy per cell and so produces more DSBs per cell than is needed to kill it, so has less energy to kill other cells.

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27
Q

What is the optimum LET for cell kill?

A

Around 100kev/micrometre

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28
Q

As LET increases what happens to the OER?

A

Decreases as less depedend on oxygen.

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29
Q

What is the RBE?

A

Ratio of effectiveness of one type of ionising radiation relative to antoher given the same amount of energy is absorbed.

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30
Q

What is RBE measured in?

A

Sieverts

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31
Q

How do you calculate relative biological effectiveness?

A

Dx/Dr

Dx = reference absorbed dose of radiation of standard type X
Dr = absorbed dose of radiation of type R that causes the same biological effect
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32
Q

What is the equivalent dose?

A

Measured in Sieverts
Takes into account the radiation weighting factor
Radiation weighting factor = 1 for xrs, gamma rays, beta
= 20 for alpha particles.

1Gy of XRs = 1 Sv
1Gy of alpha particles = 20 Sv

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33
Q

What is the effective dose?

A

Measured in Sieverts

Takes into account the radiation weighting factor + tissue weighting factor

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34
Q

What does alpha tell us on linear quadratic model?

A

Indicates sensitivity to low doses of radiation

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35
Q

What does beta on LQ model tell us?

A

Indicates sensitivity to high doses of radiation

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36
Q

What does the alpha/beta ratio tell us? Is it a marker of radiosensitivity?

A

does NOT relate to radiosensitivity
Indicates the sensitivity to changes in dose per fraction
Determines the bendiness of the survival cruve

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37
Q

Would a radiosensitiser affect the alpha/beta ratio?

A

No not the ratio but it would affect the alpha and beta seperately

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38
Q

If a cell has a low alpha/beta ratio, is it sensitve to dose per fraction?

A

Very sensitive to dose per fraction
Some tumours, notably prostate cancer and melanoma, have low α/β values. This makes them more sensitive to large fraction sizes and resistant to small fraction sizes

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39
Q

If a cell has a high alpha/beta ratio is it sensitive to dose per fraction?

A

No

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40
Q

What is the alpha/beta ratio of H+N, breast and prostate cancer?

A

H+N = 10
Breast = 4.5
Prostate =1.5

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41
Q

What is the alpha/beta ratio of spinal cord/brain/lens, skin, and other late organs?

A

Spinal cord/brain and lens = 2
Skin = 10 acute, 3 late
Other late organs = 3

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42
Q

According to the LQ model what is the effect of radiation proportional to ?

A

αD + βD^2

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43
Q

What is the mean inactivation dose?

A

An estimate of the average radiation dose to inactive a cell. Calculated as the area under the survival curve (survival probability).

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44
Q

If you reduce the overall treatment time then what happens to acute tox, late tox and tumour control?

A

Acute tox: worse
Late tox: same
Tumour control: better

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45
Q

If you give more fractions with same dose and treatment time then what happens to acute tox, late tox and tumour control??

A

Acute tox: same
Late tox: better
Tumour control: same

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46
Q

If you increase the total dose then what happens to acute tox, late tox and tumour control?

A

Acute tox: worse
Late tox: worse
Tumour control: better

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47
Q

If you treat 2 x a day then what happens to acute tox, late tox and tumour control?

A

Acute tox: same/worse (needs 6hrs between)
Late tox: worse - due to repair
Tumour control: same /better

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48
Q

What happens to cells during acute toxicity after radiotherapy?

A

Differentiated cells - cell depletion, hypoplasia, desquamation
Vascular endothelium- increase permeability, oedema, erythema
Mediated by cytokines - paracrine signalling.
- IL1, IL6,
- TNF-alpha- promotes apoptosis

Healing of depleted mature cells via migration of stem cells from outside the area and division of surviving stem cells.

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49
Q

How long does repair take in late responding tissues?

A

Longer than acute responding

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50
Q

Does total dose have more effect on early or late responding tissues?

A

Early but effects both

51
Q

The latent time for chronic radiation effects is proportional to what…

A

Inversely proportional to dose

Higher dose the quicker the onset and progression

52
Q

Describe the early and late radiation effects on skin?

A

Early:
Dry skin -> erythema -> dry desquamation -> hyperpigmentation -> wet desquamation -> re- epitheliasation -> hair growth (over 1-10 weeks)

Late: subcutaneous fibrosis, telangiectasia, atrophy, dyskeratosis.

53
Q

What are the risks of irradiating the teeth?

A

Radiation caries common - due to direct radiation effects at the dentine-enamel border zone and also effects on salivary glands
Risk of osteoradionecrosis of jaw

54
Q

How does radiotherapy affect the salivary glands?

A

Dose of 40Gy saliva production stops

Dose of > 60Gy no recovery

55
Q

Describe the acute and chronic effects of radiation on the intestine?

A

Acute

  • increase in motility followed by atonic phase
  • loss of epithelium and villi owing to proliferative impairment in the crypts causing water, electrolyte and protein loss -> diarrhoea
  • Risk of sepsis

Late

  • chronic ulcers + fibrosis -> stenosis, ileus
  • telangiectasia - bleeding
56
Q

How does radiation affect the liver?

A

Liver is radiosensitive but only dose limiting when the whole liver is irradiated.
Acute radiation hepatitis- 2-6 weeks after, usually presents as veno-occlusive disease
Chronic hepatopathy- 6m -years, progressive fibrosis

57
Q

How are the kidneys affected by radiation?

A

Radiation nephropathy- takes years
- manifests as proteinuria, hypertension, impairment in urine concentration. Usually with anaemia
Glomerular endothelial injury starts a cascade leading to glomerular sclerosis and later tubo-insterstitial fibrosis- upregulation of plasminogen activator inhibitor 1 and enhanced fibrin deposition.

LOSS OF TOLERANCE OVER TIME- dose tolerated by kidney reduces with increasing time from radiotherapy due to continuous progression of damage.

58
Q

What happens to bladder when irradiated?

A

Early: hyperaemia and mucosal oedema

Chronic- progressive mucosal breakdown from superficial ulceration to fistulae. Fibrosis and telangiectasia

59
Q

How is the brain affected by radiation?

A

Transient demyelination - somnolence syndrome or leukoencephalopathy- occurs within 6 months
Radiation necrosis - 6m -2yrs
Changes that occur in the first 6-12 months are in white matter only, after that grey matter also shows changes with pronounced vascular lesions (telangiectasia and focal haemorrhages)

60
Q

How is spinal cord affected by radiotherapy?

A

Lhermittes sign: usually due to reversible demyelination- severeal months after treatment and lasts months- years. Does not predict later development of myelopathy

Later myelopathy:

  • 6-18 months- demyelination and necrosis of white matter
  • 1yr-4yrs- vasculopathy
61
Q

Does the spinal cord recover its tolerance?

A

Yes - around 50% after 1 year

62
Q

How are peripheral nerves effected by radiation?

A

Dose of 60Gy in 2Gy # assoc with < 5% risk but increases steeply after this.
Plexopathy characterised by mixed sensory and motor deficits
Develops from 6m - years
PathogenesisL vascular degeneration, fibrosis and demyelination

63
Q

How is the heart affected by radiation?

A

Low doses: reversible functional ECG changes
High doses: pericarditis + effusion, 50% occur in 1st 6 months and rest within 2 years. Usually asymp and clears within a year.

Cardiomyopathy -10-20yrs later, conduction blocks or reduced EF
Cardiovascular disease

Pathogenesis: diffuse interstitial and perivascular fibrosis, loss of cardiomyocytes

64
Q

How is the eye effected by radiotherapy?

A

Keratoconjuncitvitis: resolves after radiotherapy
Lens: epithelial degeneration in the equator zone where proliferation occurs, damaged fibres develop vacuolation and partly retain nuclei -> posterior subcapsular radiation cataract. 6m -> years.

65
Q

What is lethal damage?

A

Hits to critical targets are sufficient to cause death at next mitosis.
Irreversible, irreparable damage- direct effect of radiation

66
Q

What is sublethal damage?

A

Hits to critical targets not sufficient to cause death.
Repairable if given time, nutrients etc, unless additional radiation dose given
Corresponds to initial slow of survival curve
Effect of indirect damage - low LET radiation

Found when single dose of radiation split into two doses. Found less cell death in split dose due to repair inbetween.

67
Q

What is potentially lethal damage?

A

Hits are sufficient to cause cell death but may be repairable under certain conditions or with period of cell cycle arrest.
May become lethal if misrepair occurs.

68
Q

What is the law of bergonie and tribondeau?

A

From 1906

States rapidly diving cells are more sensitive to radiation

69
Q

What is hyperfractionation?

A

Reducing dose per fraction <1.8Gy

70
Q

What is hypofractionation?

A

Increases dose per fraction >2Gy

71
Q

What is accelerated fractionation?

A

Rate of dose accumulation exceeds 10Gy/week

72
Q

Why is the time between fractions important for late toxicities?

A

Take longer to repair

Need sufficient time to repair or worse late toxicity

73
Q

What is SF2?

A

Clinically useful assessment of radiosensitvity
Surviving fraction after 2 Gy
Does NOT predict SF at other doses

74
Q

Is SF2 related to alpha beta ratio?

A

No

Same ratio can be assoc with a high or low SF2

75
Q

What is D0?

A

Another measure of radiosensitivity

the radiation dose that reduces survival to e^-1 of its previous value on the exponential portion of the survival curve.

76
Q

What is radiation tolerance of normal tissues determined by?

A

Number of tissue stem cells

Their intrinsic radiosensitivity

77
Q

What mechanisms allow repopulation?

A

Asymmetry loss

  • seen during lag period
  • once repopulation is started this effect is counteracted.
  • usually a stem cell divides into one stem cell and one differentiated cell -> called asymmetrical
  • for repopulation- stem cell divides into two stem cells- symmetrical division

Acceleration of stem cell proliferation - shorten stem cell cycle time

Abortive divisions- cells that have had high doses of radiation undergo a few more cell cycles before dying.

78
Q

What is the most common form of cell death after radiotherapy?

A

Mitotic castastrophe

79
Q

When does apoptosis occur after cell death and what happens?

A

Occurs in very radiosensitive tissues eg lymphoma/testicular.
Mainly intrinsic pathway -> activation caspase 9
- p53 activation and induction of pro-apoptotic proteins BAX and PUMA
- some cells almost never undergo apoptosis as despite activation it is not enough to activate cytochrome c
- other cells readily undergo apoptosis

Apoptotic sensitvity may be altered by mutation in p53

80
Q

What is autophagy?

A

Can protect cells and can lead to senescence or death (through PTEN, mTOR)
Formation of double membrane bound structure that grows and engulfs cytoplasmic components forming a cytoplasmic filled vacuoles - autophagosomes.

81
Q

What is necrosis?

A

Uncontrollable, irreversible chaotic form of cell death
Can be induced by radiation
Activated by extreme change in conditions eg pH, ion imbalance, energy loss

82
Q

What is senescence and how is it controlled?

A

Usually p53 dependent

  • via p21- temporary
  • via p16 permanent

Cells usually experience initial period of exponential growth followed by permanent arrest termed replicative senescence - Hayflick limit.
Premature senescence can happen as response to radiation - characterised by flattened cytoplasm and increased granularity.

83
Q

What is mitotic castastrophe?

A

Most cells try to undergo mitosis with DNA damage
Chromosomes can’t properly separate
Eventually after at least one mitosis the damage will b e so severe it will cause cell death
Formation of micro-nuclei
Multi-nucleated giant cells containing uncondensed chromosomes with aberrations and micronuclei.

84
Q

What is a chromosome aberration?

A

Single chromosome is broken before duplication in S phase, may cause:

  • broken ends may rejoin in original position
  • fragment of chromosome may be lost
  • broken ends may attache to incorrect broken ends -> lethal/stable

Reciprocal translocations

85
Q

What is a dicentric chromosome?

A

Lethal chromosome damage

  • short arm of two separate chromosomes are deleted
  • 2 chromosomes (long arm with centromere each) attach to each other rather than their separated short arms
  • new chromosomes have two centromeres then get duplicated.

May manage to complete mitosis however, loss of genetic material in the acentric fragment (micronuclei) in subsequent mitosis might lead to cell death.

86
Q

What is a ring chromosome?

A

Lethal chromosome damage
Both ends are lost from same chromosome
- chromosome attaches its two ends together and forms a ring

87
Q

What is an anaphase bridge?

A

Happens after chromosome is duplicated
Both chromatids suffer DSBs and sticky ends join together
At anaphase unable to separate the fused arms after centromere breaks.

88
Q

What is an acentric fragment?

A

A segment of chromosome that lacks a centromere

89
Q

What is bystander effect?

A

Cells respond to their neighbours being irradiated. Most relevant at low doses which cause damage to only a small number of cells
- via gap junctions
- via soluble factors, cytokines, ROS, NO
Responses can include DNA damage, mutations and cell death

90
Q

List the radiosenstivity of each stage of cell cycle from most sensitive to least sensitive.

A

G2/M - most radiosensitive

  • G1
  • Early S
  • Late S
91
Q

What is the major transducer of DSBs? How does it do this?

A

ATM
Acts as inactive homodimers
DNA damage causes autophosphorylation which promotes dissociation of 2 components of dimer
Monomers then go on the phosphorylate proteins targets eg p53, Chk2, Chk1, BRCA1, Nbs1

92
Q

What is the difference between ATM and ATR?

A

ATM activated by DSBs
ATR activated by single stranded DNA breaks at collapsed replication forms or distorted DNA.
ATR is slower onset and more sustained than ATM

93
Q

What is p53s role in repair after radiotherapy?

A

Continiously synthesised and degraded by MDM2
Detects high levels of damage and activates apoptotic mechanisms
If moderate damage -> activated G1/S checkpoint for repair.
Commonly mutated in cancer
p53 mutant cells lack, G1-S checkpoint, also impaired apoptosis

94
Q

What is Chk2?

A

Key target of ATM
Amplifies G1-S and G2-M checkpoint signals
Mutation in Chk assoc with familial breast cancer

95
Q

What is Chk1?

A

Key target of ATR and ATM

Amplifies S phase and G2-M checkpoint signals.

96
Q

What is the oxygen enhancement ratio?

A

Radiation dose in hypoxia / radiation dose in air

97
Q

How does oxygen increase radiosensitvity?

A

Radiation induced free radicals are fixed (damage made permanent) by oxygen
Most indirect damage caused by water
Molecule splits to OH• and causes damage
DNA produces R• which is unstable and reacts with oxygen to produce RO2• then ROOH - damage fixed

In hypoxia:
R• reacts with H+ chemically restoring original form

98
Q

What does a tumour make in response to oxygen?

A

HIF- 1a - a transcription factor

Promotes angiogenesis, invasion and motility, less apoptosis and increased genomic instability

99
Q

How can you make a tumour less hypoxic?

A

Blood transfusion - cervical >110
Carbogen gas (oxygen - chronic hypoxia) + nicotinomide (vit B3 - acute hypoxia, vasodilator) - in laryngeal + bladder
Nimorazole - mimics free radicals, specifically taken up by hypoxic cells, H+N

100
Q

What causes cells to be chronically or acutely hypoxic?

A

Chronic hypoxic cells have a short half life and are continually replaced as displaced away from blood vessel
Acutely hypoxic cells occur when blood vessels transiently occluded

101
Q

What is an abscopal effect in radiotherapy

A

Regression of distant mets after localised radiation enhanced by immune checkpoint blockade

102
Q

What are the immune stimulating and suppressing factors with radiotherapy?

A

Lymphocyte depletion, increased Treg - at standard fractionation
Pro inflammatory factor release: DAMP
Tumour antigen presentation

Does depend on dose/fractionation

103
Q

Why do gaps in radiotherapy matter?

A

Repopulation

104
Q

Which cancers are priority 1?

A 
Squamous cell tumours
Adeno oesophagus
SCLC
NSCLC
Medulloblastoma
Treatment duration must not be prolonged by >2 days
105
Q

What are priority 2 cancers?

A

Breast cancer
TCC bladder
Prostate cancer
Advised no prolonged interruption >2 days

106
Q

What are category 3 patients

A

Palliative patients

107
Q

What is accelerated repopulation?

A

Dog leg curve
Phenomonent that net clonogen doubling time during or shortly after irradiation exceeds clonogen doubling time in untreated tumour
? due to reoxygenation or due to nutrient supply improving
EGFR signalling has also been implicated

108
Q

What are the options for making up for gaps in radiotherapy and which are used?

A

Give 1 extra fraction - maintain tumour BED
- worse so not done

Give 2 fractions per day

  • same tumour control
  • worse for late responding tissue due to repair time
  • 2nd best way to compensate

Treat at weekends

  • same tumour control
  • same early and late responding tissues
  • best way
109
Q

What is EQD2 equation?

A

Equivalent dose in 2Gy fractions

EGD2 = D (d + α/β / 2 + α/β)

110
Q

What equation can you use to compare different fraction sizes and calculate total dose required?

A

D1 = D2 x (α/β + d2 / α/β +d1)

111
Q

Define biologically effective dose (equation)

A

BED = nd ( 1 + d/α/β)

112
Q

Can you add BEDs together for different stages of treatment?

A

Yes eg external beam then brachy

you CANT add BEDs with different α/β ratios

113
Q

How is BED effected by α/β ratio and dose per fraction?

A

α/β ratio - inversely related to fractionation sensitivity- smaller ratio provides larger fractionation sensitivity and higher BEDs

As you increase dose per fraction the BED goes up

114
Q

How do you use BED to work out how to compensate for delays?

A

BED = nd ( 1 + d/α/β) - k x (T- Tdelay)

k = dose per day to compensate for repopulation
k = 0.9 for H+N cancer
k = 0.1 for prostate cancer
T = overall treatment time
Tdelay = time to onset for repopulation 21-28 days
115
Q

What is the dose rate for EBRT?

A

Usually around 1-5Gy/min

So exposure usually 1-3 mins and during this time no repair occurs

116
Q

Which mechanism of cells recovering is the fastest?

A

Intracellular repair- starts at around 1 hr

Repopulation takes days to weeks

117
Q

With a low dose rate what does the survival curve look like?

A

Radiosensitivity of cells decreases and so shouldered cell survival curve becomes straigher and flatter

118
Q

What are the advantages of LDR brachy?

A

Allows max tissue recovery over shortest overall time.
However tolerance of early tissues reduced as the rely on repopulation more than repair.
Spare late responding tissues due to repair

Disadvantage - inadequate time for reoxygenation

119
Q

At what dose rate would repopulation occur during brachy?

A

<1cGy/min

120
Q

What is LDR, MDR and HDR brachy?

A 
LDR = 0.4 - 2 Gy/hr
MDR = 2-12 Gy/hr
HDR = >12 Gy /hr
121
Q

What is pulsed brachy and what are its advantages/disadvantages?

A

High dose rate, multiple times
Worse for late responding tissues
More accurate with todays planning systems

122
Q

What is the disease modifying factor

A

Ratio of isoeffective radiation doses in the absence and presence of radiosensitisers
Also called sensitiser enhancement ratio

123
Q

How do you convert BED to EQD2?

A

EQD2 = BED / (1 + 2 /α/β)

124
Q

Name some radiosensitising chemotherapy agents?

A

Inhibit repair of radiation damage

  • nucleoside analogues
  • cisplatin
  • bleomycin
  • doxorubicin

Directly damage DNA - radiation SSBs may be converted to DSBs
- platinium adducts

Block cells in most radiosensitive phase - G2/M - taxanes

Apoptosis enhanced- taxanes and most drugs

FRCR Clinical Oncology Part 1 COPY (5 decks)

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