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Time, Dose and Fractionation in Radiotherapy

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Time, Dose and Fractionation in Radiotherapy 2/25/2013 The introduction of Fractionation 2-13/13 Radiobiology lecture Time, Dose and Fractionation in Radiotherapy The Four Rs of Radiobiology Repair of Sublethal Damage • Cells exposed to sparse radiation experience • Efficacy of fractionation based on the 4 Rs: sublethal injury that can be repaired – Repair of sublethal damage • Cell killing requires a greater total dose when given –Repopulation in several fractions – Reassortment of cells within the cell cycle • Most tissue repair occurs in about 3 hours and up –Reoxygenation to 24 hours post radiation • Allows for repair of injured normal tissue and gives a potential therapeutic advantage over tumor cells Reoxygenation Redistribution • Oxygen stabilizes free radicals • Position in cell cycle at time of radiation • Hypoxic cells require more radiation to kill determines sensitivity •Hypoxic tumors • S phase is radioresistant – Temporary vessel constriction •G2 phase delay results in increased radiation – Outgrowth of blood supply and capillary collapse resistance • Tumor shrinkage reduces hypoxic areas • Fractionated RT redistributes cells • Reinforces fractionated dosing • Rapidly cycling cells like mucosa, skin are more sensitive • Slower cyclers like connective tissue, brain are spared 1 2/25/2013 Repopulation • Increased regeneration of surviving fraction Basics of Fractionation • Rapidly proliferating tumors regenerate faster • Determines the length and timing of therapy course • Dividing a dose into several fractions spares normal tissues • Accelerated Repopulation – Repair of sublethal damage between dose fractions – Repopulation of cells • Dividing a dose into several fractions increases damage to the tumor – Reoxygenation of tumor environment – Reassortment of cells into radiosensitive phases of the cell cycle between dose fraction • Prolongation of treatment reduces early reactions • However, excessive prolongation allows surviving tumor cells to proliferate Impact of the 4Rs The Time Scale of the 4 Rs • Inherent radiosensitivity/repair capacity will make a •Repair = fast tumor either sensitive or resistant to therapy, or a • Reoxygenation and normal cell more or less prone to radiation-induced redistribution = moderate damage • Repopulation = slow • Reoxygenation of tumor during radiotherapy will have anet sensitiz ing effec t • Redistribution in the cell cycle is used to advantage in fractionated radiotherapy •Repopulation – Has the net effect of making the tumor seem more resistant – Is a way for normal cells to recover from acute radiation reactions Early vs. Late Responding Tissues Dose Response for Early and Late Responsive • In normal tissue, there is Tissues a clear difference between tissues that are • If fewer and larger dose fractions are early responding and those given, late reactions are more severe that are late responding • Dose-response for late-responding tissues is more curved • Early-responding tissues • For early effects, α/β is large are triggered to – α dominates at low doses proliferate within a few – Linear and quadratic components of cell weeks of the start of killing are not equal until about 10 Gy fractionated radiation • For late effects, α/β is small – β term has an influence at low doses • Prolongation of – Linear and quadratic components are radiotherapy has little equal at about 2 Gy sparing effect on late responding tissues 2 2/25/2013 Early vs. Late Responding Tissues and Radiosensitivity M Early vs. Late Responding Tissues and Radiosensitivity G2 G1 • Fraction size is the dominant factor in • Cells are most resistant in late S phase S determining late effects; overall treatment – Rapidly proliferating cells may have a major portion of cells in S time has little influence. phase – These cells are resitistan tbecause new cellsoffse t those kille d by dose fractions • Slowly growing cells with a long cell cycle may have a second • Fraction size and overall treatment time both resistant phase in early G1 determine the response of acutely responding – A slowly proliferating population may have many cells in early G1 or tissue not proliferating at all (resting cells) – Many late-responding normal tissues are resistant because of the presence of many resting cells – Applies to small doses per fraction and disappears at higher doses per fraction Radiation therapy fractionation schedule Treatment: 60 Gy/3 fractions Conventional Fractionation Hyperfractionation To further reduce late effects, same or slightly increased early effects Achieve the same or better tumor control Accelerated Treatment Continuous Hyperfractionated Accelerated Radiation Therapy (CHART) Hypofractionation Review of Cell Survival Curves Following Characteristic radiographic findings Radiation •S= e-α D-βD2 – Where S is the fraction of cells surviving a dose D – α is the number of logs of cell kill per Gy from the linear po rtio n of the curve – β is the number of logs of cell kill per Gy2 from the quadratic portion of baseline the curve • Linear and quadratic 4 mos, CR 8 mos, components of cell kill subtle fibrosis 12 mos, are equal at D=α/β mature fibrosis 18 mos, NED 3 2/25/2013 Fractionated Radiation Survival Curves Biologically Effective Dose (BED) • Shoulder of curve is repeated • Effective dose- survival curve for multi-fractionation d –an exponentia l BED = (nd)( 1+ ) function of dose – i.e. a straight line from the origin through a point on the single dose survival curve Using the linear-Quadrant concept to calculate BED Example Calculation Conventional Treatment Hyperfractionation • If we assume the α/β is 3 Gy for late-responding tissue and 10 • 70 fractions of 1.15 Gy given twice daily, 6 hours apart, 5 days Gy for early-responding tissue, then: per week for an overall treatment time of 7 weeks • 30 fractions of 2 Gy given one fraction per day, 5 days per week for and overall treatment times of 6 weeks: Early effects: = 80.5 1 + 1.15 E = (nd) 1 + d 10 α α/β = 89. 8 Gy10 Early effects = 60 1 + 2 Late effects: = 80.5 1 + 1.15 10 3 = 72 Gy10 = 111.4 Gy3 Late Effects = 60 1 + 2 i.e this treatment regime is more effective than the conventional 60 3 Gy for both early and late effects = 100 Gy3 4 2/25/2013 The need for retreatment Retreatment after Radiotherapy 1, Tumor recurrence 2, Second tumor ◊ bad lifestyle ◊ genetic predisposition ◊ treatment-induced Factors must be taken into account in Recovery of early and late responding retreatment tissues • Dose and volume treated in the past and the • early responding tissues recover well from overlap with initial field initial radiation and will tolerate re- • Chemotherapy in the past irradiation to almost full dose, such as skin • The time interval reaction • Critical structures involved • RT technique to be used in retreatment • animal studies showed the late responding tissues such as spinal cord do recover from • Any alternative prior radiation, probably need longer time SBRA case in an 88 year old non-smoker, Clinical experiences p16 + L Tonsil cancer recurred • 8 Gy/fraction x 5 •Spinal cord • Treatment every •Brain 3rd day • Head and neck • KPS 90%, no •Rectum weight loss, no swallowing issues •Bone • Ipsilateral tx •Breast only •lung 5 2/25/2013 Oral cavity Rapid dose fall‐off constraints SBRA is applicable for many different situations • 86 yo woman with recurrent oral cavity cancer • Treated to 40 Gy at 8 Gy/fraction • Note CT and PET 3 months post SBRA Herron DE, et al, IJROBP, Vol 75, 2009 Vargo JA, et al, Head and Neck, March 2011 Treatment response 6 2/25/2013 Alternative Radiation Modalities • Fast neutrons • Boron neutron capture •Protons •Carbon ion Putative advantages of alternative radiation modalities Fast neurons • Better physical dose distribution • Indirectly ionizing • Advantageous radiobiologic properties • Giving up energy to producing recoil protons, a- –Higher LET particles and havier nuclear fragments – Hig her RBE • Higher RBE, reduced OER, no sublethal damage –Lower OER repair, no variation of sensitivity through cell – Little sublethal damage repair cycle – Less variation of sensitivity through the • Better local control in salivary gland tumor, but cell cycle at the expense of normal tissue damage 7 2/25/2013 Protons Boron neutron capture therapy • RBE and OER of protons are not different from • To deliver a drug-containing boron that localizes that of 250-kv x-rays only in the tumor, then treat with low-energy thermal neutrons that interact with boron to • Unique depth-dose patterns and Bragg peak produce short-range, densely ionizing a-particles • Where is the magic drug? • Poor penetration with thermal neutrons Spread out of the Bragg Peak Choroidal melanoma proton therapy Carbon ion radiotherapy IMRT and proton treatment plan comparison • Similar depth-dose profile and Bragg peak as protons • Higher LET •lower OER • Loss of repair capacity • Smaller varivation in radiosensitivity through cell cycle • Increase in RBE toward the end of particle range • Target volume can be visualized by PET 8 2/25/2013 Increase in RBE toward the end of particle range 9.
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