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& a当寻找到了客户以后，买卖双方在交易磋商阶段通过函电或口头方式进行业务的洽谈.它是整个业务的关键阶段，商务英语在货物的进出口贸易的程序中.在交易磋商与签约环节上至关重要。在国际贸易的操作实务中，贸易各环节所有的交往函电都构成重要的法律依据。特别是当产生贸易纠纷时，它有可能左右纠纷解决的结果。在整个贸易过程中利用商务英语不仅可以实现贸易的全球化，不受时间和空间的限制进行面对面的洽谈和信息交流，而且还能节约成本，加快贸易开展的速度。另外.鉴于商务英语在各种信息平台上的使用也促进了对外贸易的增长，提高工作效率。商务英语为贸易双方的沟通交流搭建桥梁、准确而具体地传送双方的各类相关信息;它起着沟通买卖双方的媒介作用并涉及到对外贸易的各个环节。商 When sought after the customer, the round turns carried on the service in the transaction consultation stage through the letters and telegrams or the oral way the discussion. It is the entire service critical phase, commercial English in the cargo import-export trade procedure. On transaction consul & aThe book is thinner in 书是更加稀薄的 & a牙刷是用来刷牙的，你一天用两次，它只能用三个月，在那之后一定要买新的。你一定要有正确的方法刷牙 The toothbrush is uses for to clean the teeth, you one day use two times, it only can use for three months, after that certainly must buy newly.You must certainly have the correct method to clean the teeth & a我们的供应商需要花费至少1个星期时间来制作盒子 Our supplier needs to spend 1 week time to manufacture the box at least & a长江文艺出版社副总编辑？上海天娱传媒签约文学总监？ Yangtze River literary arts publishing house vice-editor-in-chief? Shanghai day amusement media signing literature inspector general? & aAlthough the market is not brisk at present 虽然市场当前不是轻快的 & a需要限期使用的产品，应标明生产日期和安全使用期限。 Needs to use by a set time the product, should mark the production date and the safety handling deadline. & a如果需要，我很害怕我将考不好。 正在翻译，请等待... & aKochi City,Kochi Prefecture,Japan Kochi市， Kochi专区，日本 & aWant to learn I can teach you 想要学会我可以教您 & asystem no signal 正在翻译，请等待... & aJulius De la Cruz Sol (Philippines)
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s e t t i n g s1 1 th In te r n a tio n a l C o n fe r e n c e P R IM A R Y T H E R A P Y O F E A R L Y. A d ju v a n te S tr a h le n th e r a p ie - PDF
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1 1 1 th In te r n a tio n a l C o n fe r e n c e P R IM A R Y T H E R A P Y O F E A R L Y BREAST CANCER A d ju v a n te S tr a h le n th e r a p ie M & r z , S t.g a lle n L e o n o r e H a n d l-z e lle r2 3 4 5 6 7 RED DRESS AGAI NST PI NK RI BBON In a d & q u a te D o s e n a m H e r z e n e r h & h e n d e n s p & te n H e r z to d!8 Ex a m p l e - Br ea st D o s e w a s h (K o r r e m a n e t a l)9 MINIMIERUNG DER MORBIDIT&AT DER LOKALEN BEHANDLUNG BEI10 RADI ATI ON THERAPY: AFTER BCS R T fo r a ll p ts a fte r BCS? Y: 81 % N: 1 9% A: 0% 80% 1 5% 5% S h o u ld e ld e r ly w ith E R + a n d lo n g life e x p e c ta n c y r e c e iv e RT?11 RADI ATI ON THERAPY: AFTER BCS S h o u ld e n d o c r in e th e r a p y b e u s e d w ith o u t R T fo r E + T1 N 0 cancer? (p o s tm.) C o u ld e n d o c r in e th e r a p y b e u s e d in p la c e o f R T fo r E + T 1 N 0 c a n c e r? Y: 24% N: 73% A: 3% 51 % 46% 3%12 Ef f ek t d er LR- Red. Na c h 5 Ja h r en a u f d i e Mo r t a l i t & t n a c h 1 5J13 LR BEI I NVASI VEN UND NI CHTI NVASI VEN MA - TUMOREN14 RADI ATI ON THERAPY: DCI S S h o u ld R T b e c o n s id e r e d s ta n d a r t fo r e x c is e d D C IS? C a n R T b e a v o id e d in e ld e r ly? C a n R T b e a v o id e d in lo w g r a d e D C IS? J: 81 % N: 1 9% A: 0% 61 % 39% 0% 59% 32% 1 0%15 W o n g J S, K a e lin C H, T r o y a n S L, e t a l. P r o s p e c tiv e s tu d y o f w id e e x c is io n a lo n e fo r d u c ta l c a r c in o m a in s itu o f th e b r e a s t. J C lin O n c o l 2 4 : , P a t. (m e d ia n 5 1 J, ), m it k l. (&2,5 c m ), m a m m o g r a p h is c h d e d e k tie r te m, G 1 u. 2, D C IS, m it g r o & e n R R (&1 c m ), k e in e R T 1 3 L R im N a c h b. (0,6 5,2 J.) n a c h O P J & h r l.r e z.r a te : 2,4 % 5 -J.R e z.r a te :1 2 % A K Z E P T A B L E R G R E N Z W E R T E R R E IC H T S T U D IE N A B B R U C H!!16 THE EORTC AMAROS TRIAL17 PMRT EINFL.AUF L- Rez.+ &UBERL. (25 t r i a l s o f Ma st ec t + AC& RT) 8505 p t s N+18 PMRT EINFL.AUF L- Rez.+ &UBERL. (25 t r i a l s o f Ma st,ac,& RT) p t s N-19 R. THERAPY: AFTER MASTECTOMY S h o u ld P M R T b e s ta n d a r t w ith 4 L N? S h o u ld a ll p ts. w ith N + (1-3 ) b e ir r a d.? E s p e c ia lly if y o u n g a n d w ith o th e r p o o r p r o g n o s tic fa c to r s? J: N: A: 93% 7% 0% 22% 70% 8% 72% 1 8% 1 0%20 1 5J LRR a s Fu n c t i o n o f Nu m b er o f + LN a n d PMRT21 22 23 APBI24 PHASE III MULTICENTER TRIAL Groupe Europ&en de Curietherapie European Society for Therapeutic Radiology and Oncology GEC-ESTRO APBI TRIAL25 RAD. THERAPY: ACCELERATED S h o u ld a c c e le r a te d W h o le B r e a s t R T (W B R T ) b e c o n s id e r e d a n a c c e p ta b le o p tio n? S h o u ld in tr a o p e r a tiv e p r im a r y b r e a s t R T b e c o n s id e r e d e x p e r im e n ta l? Y: N: A: 83% 1 0% 7% 84% 1 6% 0%26 27 28 29 30 1 5Y FREQUENCES OF LRR AND SURVIVAL AS A FUNCTION OF + LN AND PMRT31 Groupe Europ&en de Curietherapie European Society for Therapeutic Radiology and Oncology GEC-ESTRO APBI TRIAL32 EINFL.d.RT n a c h BET a u f L- Rez.u n d &UBERL. (1 0 t r i a l s o f BCS & RT) 6097 p t s N-33 EINFL.d.RT n a c h BET a u f L- Rez.u n d &UBERL. (1 0 t r i a l s o f BCS & RT) 6097 p t s N-34 35 Wa s b ed eu t et a d j u v a n t?& OP CHT S y s te m.t h e r a p ie n a c h O p e r a tio n CHT OP S y s te m.t h e r a p ie v o r O p e r a tio n M ETA CHT M e ta s ta s e n, k u r a tiv e r A n s a tz n ic h t m e h r m & g lic h, S y m p to m lin d e r u n g36 Regu l a t o r s o f a p o p t o t i c c el l d ea t h O n e m a s te r r e g u la to r is P 5 3 P53 bound to DNA Most of the p53 mutations that cause cancer are found in the DNAbinding domain37 Zi el d er n eo a d j u v a n t en Th er a p i e F r & h e T h e r a p ie v o n M ik r o m e ta s ta s e n T u m o r r e d u k tio n / b r u s te r h a lte n d e T h e r a p ie - E r h & h te R a te a n b r u s te r h a lte n d e n T h e r a p ie n P ie r g a e t a l ,1 % - 7 1,6 % Id e a l: p a th o lo g is c h e K o m p le ttr e m is s io n (P C R ) E in flu & a u f &U b e r le b e n s p a r a m e te r (O S ) In v iv o C h e m o s e n s itiv it& ts m e s s u n g - W ir k s a m k e it d e r B e h a n d lu n g k a n n a m A n s p r e c h e n d e s T u m o r s b e o b a c h te t w e r d e n!38 Neo a d j u v a n t e Th er a p i ebed i n gu n gen I P r & o p e r a tiv e C o r e B io p s ie G le ic h z e itig M a r k ie r u n g s c lip s H is to lo g ie m it R e z e p to r e n u n d H E R -2 -n e u39 Kl i ni s che Pr &s ent at i on40 Neo a d j u v a n t e Th er a p i ebed i n gu n gen II P a lp a tio n u n d In s p e k tio n d e r B r u s t u n d d e r A x illa v o r je d e m Z y k lu s M a m m o g r a p h ie u n d U ltr a s c h a ll z u B e g in n u n d b e i V e r d a c h t a u f P r o g r e s s io n MRI B ild g e b e n d e V e r fa h r e n n a c h 4 Z y k le n u n d u n m itte lb a r v o r d e r o p e r a tiv e n S a n ie r u n g P a th o lo g e n b e i O P in fo r m ie r e n41 Kl i n i sc h e Pr & sen t a t i o n H is to lo g ie d e r C o r e B io p s ie : In v a s iv e s M a m m a c a r c in o m, e h e r v o m d u c ta le n T y p, G 3 E R : s c h w a c h p o s, P g R : s c h w a c h p o s, H e r c e p Te s t: s ta r k p o s itiv,h e r -2 /n e u F IS H : a m p lifiz ie r t H o r m o n s ta tu s : F S H : 5 6 m U /m l, &O S tr a d io l: &1 0 p g /m l S ta g in g u n te r s u c h u n g e n : L u n g e n -R & : in tr a p u lm o n a le L & s io n e n n ic h t s ic h e r a u s s c h lie & b a r, d a r a u fh in C T d e r L u n g e : o B C T d e r L e b e r: o B S k e le tts z in tig r a p h ie : e r h & h te r K n o c h e n s to ffw e c h s e l in L W K 4, R & n tg e n z ie la u fn a h m e L W K 4 : o B42 43 44 &OR + PR In T u m o r e n w e r d e n W a c h s u m s fa k to r e n & s tr o g e n a b h & n g ig p r o d u z ie r t. M it d ie s e n k & n n e n s ic h d ie T u m o r z e lle n s e lb s t s tim u lie r e n St a r k e Ex p r essi o n d er &OR St a r k e Ex p r essi o n d er PR45 Her - 2- Rez ep t o r Hu m a n ep i d er m a l gr o wt r ec ep t o r 2 &Ub er ex p r essi o n : ~20% Agr essi ver er Ver l K& r z er e &Ub er l eb en sz ei t46 Zei t i c h er Ab l a u f d er Th er a p i e Sentinel-OP d Tumorvermessung Quadrantenresektion 7 Strahlentherapie 8 Trastuzumab 3 w f&r 1 a 12 Wochen Epirubicin + Cyclophosphamid 12 Wochen Taxan + Trastuzumab47 Chi r ur gi s che Ther api e Core Biopsie 1. Sentinel node biopsy Systemische Therapie 1. BET/Mastektomie48 Neo a d j u v a n t e Th er a p i e: CHT A n th r a z y k lin e Z y to s ta tis c h e s A n tib io tik u m S ta n d a r d Ta x a n e P fla n z e n a lk a lo id /M ito s e h e m m e r s e h r p o te n t P C R 20% P a c lita x e l (Ta x o l ) D o c e ta x e l (Ta x o te r e ) P a z ifis c h e n E ib e /Ta x u s b r e v iv o lia D e u ts c h e n E ib e /Ta x u s b a c c a ta M o n o k lo n a le r A n tik & r p e r b in d e t H E R -2 -R e z e p to r E p ir u b ic in (E p ir u b ic in ) T r a s tu z u m a b (H e r c e p tin ) 67% P C R!49 Chi r ur gi s che Ther api e 1. S e n tin e l n o d e b io p s y In v a s iv e T u m o r z e lle n b r e ite n s ic h & b e r L y m p h g e f& & e a u s L y m p h k n o te n = F ilte r s ta tio n e n 1.F ilte r = W & c h te r ly m p h k n o te n /S e n tin e l Id e n tifik a tio n m itte ls M e th y le n b la u u./o d. R a d io k o llo id Veronesi U et al, N Engl J Med 349: , 2003 Morton DL et al, Ann Surg 230: , 199950 51 Un t er sc h i ed l i c h e Th er a p i eo p t i o n en SN 2. N e o a d ju v.s y s t.t h e r a p ie 3. Q R (fa lls S N + ) + A x illa d is s52 Un t er sc h i ed l.th er a p i eo p t i o n en 1. QR + S N / A x illa d is s S y s te m.t h e r a p ie53 Un t er sc h i ed l.th er a p i eo p t i o n en 1. A b la tio + 2. S y s t.t h e r a p ie A x illa d is s.54 Un t er sc h i ed l.th er a p i eo p t i o n en 1. Neo a d j u v.sy st.th er a p i e 2. QR + Ax i l l a d i ss. 3.55 Un t er sc h i ed l.th er a p i eo p t i o n en Core Biopsie Syst. Therapie =56 Vor ber ei ung P a tie n tin M.E.: V e r k le in e r u n g d e s T u m o r s v o n 2 c m a u f 8 m m P r & o p e r a tiv e D r a h tm a r k ie r u n g d e s T u /C lip57 Ver m ei d u n g ei n es LR V e r m e id u n g e in e s L R v o n s u b s ta n tie lle r B e d e u tu n g V e r m e id u n g v o n 4 L R b e d e u te t V e r m e id u n g e in e s d u r c h B r u s tk r e b s b e d in g te n To d e s n a c h 1 5 J a h r e n58 Technique lateral and medial tangential opposed radiation fields Cobalt-60: small breast A/B CUP linear accelerator ( 6 MeV) large breast E/D CUP59 Simulation film Verification film (LINAC)60 Ver m ei d u n g ei n es LRs V e r m e id u n g e in e s L R v o n s u b s ta n tie lle r B e d e u tu n g V e r m e id u n g v o n 4 L R b e d e u te t V e r m e id u n g e in e s d u r c h B r u s tk r e b s b e d in g te n To d e s n a c h 1 5 J a h r e n61 WH - Ch i u r gi e Operative Therapie Q R + B e s tr a h lu n g s o s ic h e r w ie A b la tio B e i g r o s s e n T u m o r e n k a n n P S T e in e A b la tio o ft v e r h in d e r n S N -K onzept A x illa d is s e k tio n z u m L y m p h k n o te n s ta g in g62 WH Sy st em i sc h e Th er a p i e S ys temis che Therapie C h e m o th e r a p ie m it A n th r a c y c lin e n (u n d Ta x a n e n ) E n d o k r in e T h e r a p ie m it A r o m a ta s e h e m m e r n / Ta m o x ife n A n tik & r p e r th e r a p ie m it T r a s tu z u m a b (H e r c e p tin )63 WH Neo a d j u v a n t e Th er a p i e Neoadjuvante Therapie (PS T) In v iv o C h e m o s e n s itiv it& ts a s s a y T u m o r u n d L K N D o w n s ta g in g e r m & g lic h t V e r b e s s e r te K o s m e s is E r h & h te R a te v o n B r u s te r h a lt S o fo r tig e T h e r a p ie v o n M ik r o m e ta s ta s e n64 CUMULATIVE DOSE OF ERT AND BRACHYTHERAPY N. + ST R 100 gy 88,25 gy 75,5 gy 70,5gy 62,75 gy 57,75 gy 52,75 gy 50 gy 45 gy 40 gy 37,75 gy 25 gy LUNG R MEDIASTINUM LUNG R N.= Reference point65 66 67 68 69 70 71 72 Th e p 53 Net wo r k Stalled UV radiation replication forks & radiation p53 DNA damage repair Oncogenes Ribosomal Stress Mdm2 Apoptosis Cell cycle arrest Senescence73 P53- d ep en d en t a p o p t o si s a n d m a l i gn a n c y Defects in processes such as DNA double-strand break (DSB) repair, DNAdamage checkpoint function, and telomere maintenance, result in DSBs or exposed chromosomal ends WT p53 cells with DSBs or uncapped telomeres are predisposed to apoptosis, which limits tumorigenesis In contrast, cells with missing wt p53 can survive inappropriately, creating a permissive environment for the generation of genomic instability that can drive carcinogenesis NHEJ, non-ho HR, homologous recombination Brown & Attardi Nature Reviews Cancer 5, , 200574 PCD i m p o r t a n t a sp ec t s Programmed cell death (PCD = apoptosis) originally referred to specifically instances in which an irreversible sequence of events led to cell death Requirement for protein synthesis to initiate cell death Apoptosis is associated with a particular morphology in which the chromatin condenses and cells shrink and become denser and often fragment into several pieces Apoptotic morphology is now considered to derive from the activation of caspases, and is common to many (but not all!) cell deaths These processes are directly or indirectly genetically regulated, as opposed to necrosis or oncosis, in which the cell has no active role. Necrotic cells most typically lyse, provoking a substantial inflammatory response75 Qu a n t i t a t i ve a sp ec t s o f a p o p t o si s & Rel eva n c e f o r r esp o n se t o r a d i o t h er a p y ex a m p l es76 Di f f er en c es i n r a d i o sen si t i vi t y b et ween t wo c el l l i n es wi t h d i f f er i n g a b i l i t y t o u n d er go a p o p t o si s Kodym R et al, JBC, 200077 Ap o p t o si s q u a n t i t a t i ve ef f ec t s LY-as LY-ar Apoptosis ( 5Gy, 4h ) ~70% ~20% Survival ( 3Gy ) ~0.5% ~10% Survival 16 Gy ( 8 * 2 Gy) 6.6* *10-6 Tumor weight controlled 1.5 kg 0.4 mg Fractionated RT:78 Det er m i n a t i o n o f r a d i a t i o n c el l k i l l i n g In vivo, p r e d o m in a n t fo r m o f c e ll d e a th fo llo w in g ir r a d ia tio n o c c u r s d u r in g m ito s is a t d o s e s o f ~ 1-2 Gy A d d a k n o w n n u m b e r o f c e lls to a n e w fla s k a n d in c u b a te fo r 1-2 w e e k s E a c h s in g le c e ll w ill d iv id e s e v e r a l tim e s to fo r m c o lo n ie s th a t a r e fix e d, s ta in e d a n d c o u n te d C o u n t c o lo n ie s c o n ta in in g 5 0 c e lls (5-6 g e n e r a tio n s o f p r o life r a tio n ) to e x c lu d e c e lls th a t h a v e lim ite d g r o w th a s a r e s u lt o f s ta r tin g to d iffe r e n tia te o r b e in g s u b -le th a lly d a m a g e d79 Cl o n o gen i c c el l d ea t h T h e clonogenic cell survival assay d e te r m in e s th e a b ility o f a c e ll to p r o life r a te in d e fin ite ly, th e r e b y r e ta in in g its r e p r o d u c tiv e a b ility to fo r m a la r g e c o lo n y o r a c lo n e T h is c e ll is th e n s a id to b e clonogenic A c e ll s u r v iv a l c u r v e is th e r e fo r e d e fin e d a s a r e la tio n s h ip b e tw e e n th e d o s e o f th e a g e n t u s e d to p r o d u c e a n in s u lt a n d th e fr a c tio n o f c e lls r e ta in in g th e ir a b ility to re p ro d u c e80 Co l o n y f o r m a t i o n (c l o n o gen i c ) i n v i t r o a ssa y From: Hall - Radiobiology for the Radiologist Colony = &50 cells Small colonies?81 Ox y gen ef f ec t H y p o x ia T P 53 C hem o-& RT M a lig n a n c y82 Ox y gen ef f ec t i n Ra d i o b i o l o gy On e o f t h e m o st si gn i f i c a n t f a c t o r s a f f ec t i n g o u t c o m e83 Ox y gen t en si o n a n d r a d i o sen si t i vi t y84 eo x y gen a t i o n & f r a c t i o n a t i o n F r a c tio n a tio n S id e e ff e c ts E ffic a c y M u ltip le s m a lle r fr a c tio n s a r e b e tt e r to le r a te d th a n s in g le la r g e fr a c tio n s!85 i o l o gy o f r eo x y gen a t i o n a) In hypoxic regions, stress granules form containing HIF1mediated transcripts, sequestering the transcripts from being translated into protein. a) After radiation treatment, better oxygenated cells die and there is an increase in perfusion, leading to reoxygenation of the previously hypoxic cells. a) Macrophages are attracted to the dying tumour cells, become activated and release nitric oxide (NO), which also stabilizes HIF1. a) The increase in HIF1 activity increases vascular endothelial growth factor (VEGF) levels, promoting endothelial cell survival, angiogenesis and tumour cell survival and proliferation. Mark W. Dewhirst, Yiting Cao & Benjamin Moeller. Nature Reviews Cancer 8, , 200886 Gen es/p r o t ei n s a f f ec t i n g r a d i o sen si t i vi t y T P 53 B c l-2 fa m ily m e m b e r s D N A -r e p a ir g e n e s EGFR R O S r e la te d p r o te in s, s u c h a s S O D, c a ta la s e,... C y to k in e s : T N F -a lp h a C e ll s u r v iv a l a n d c e ll c y c le r e g u la tin g e n z y m e s : A k t, P T E N, M a p K in a s e, a n d o th e r s...87 Candi dat e genes i nvol ved i n t he pat hogenes i s of r adi at i on t oxi ci t y88 TP53, t h e m a st er r egu l a t o r o f c el l su r vi va l TP53 modulates (amongst others) Radio- and chemoresponse Cellular resistance against hypoxia Metastasis TP53 mutations in ~ 50 % of all tumors - abrogation of function of the tumor-suppressor protein p53 is one of the most common genetic alterations in cancer cells.89 Ov er v i ew c el l u l a r ef f ec t s o f i o n i z i n g r a d i a t i o n a n d c el l u l a r t a r get s n ex t sl i d e90 Membrane DNA Cellular response Genetic Instability Repair Apoptosis G1 / G2 DELAY91 Cl i n i c a l a sp ec t s o f Ra d i o b i o l o gy92 Ra d i a t i o n r esp o n se st r u c t u r a l l y u n d ef i n ed FSUs C lo n o g e n ic c e lls in th e s e s y s te m s n o t c o n fin e d to o n e p a r tic u la r F S U C e lls c a n m ig r a te fr o m o n e F S U to a n o th e r A llo w s r e p o p u la tio n o f a d e p le te d F S U E x a m p le r e -e p ith e lia liz a tio n o f a d e n u d e d a r e a o f s k in c a n o c c u r e ith e r fr o m s u r v iv in g c lo n o g e n s w ith in d e n u d e d a r e a o r b y m ig r a tio n fr o m a d ja c e n t a r e a s FSU.functional subunit93 Ti ssu e Resc u e Un i t C o n c e p t p r o p o s e d to lin k s u r v iv a l o f c lo n o g e n ic c e lls a n d fu n c tio n a l s u r v iv a l D e fin e d a s m in im u m n u m b e r o f F S U s r e q u ir e d to m a in ta in tis s u e fu n c tio n A ssum es N u m b e r o f T S U s is p r o p o r tio n a l to n u m b e r o f c lo n o g e n ic c e lls F S U s c o n ta in c o n s ta n t n u m b e r o f c lo n o g e n s F S U s c a n b e r e p o p u la te d fr o m s in g le c lo n o g e n94 Issu es wi t h FSUs S o m e tis s u e s d e fy c la s s ific a tio n C r y p ts o f je ju n u m (s tr u c tu r a lly w e ll d e fin e d b u t s u r v iv in g c r y p ts c a n /d o m ig r a te fr o m o n e c r y p t to a n o th e r to r e p o p u la te d e p le te d n e ig h b o r s95 Vo l u m e Ef f ec t i n Ra d i o t h er a p y : Ti ssu e Ar c h i t ec t u r e To ta l d o s e th a t c a n b e to le r a te d d e p e n d s o n v o lu m e ir r a d ia te d Tolerance dose is d e fin e d a s th e d o s e th a t p r o d u c e s a n a c c e p ta b le p r o b a b ility o f a tr e a tm e n t c o m p lic a tio n. In c lu d e s o b je c tiv e c r itie r a a n d s u b je c tiv e fa c to r s96 Do se vs Co m p l i c a t i o n s S p a tia l a r r a n g e m e n t o f F S U s in tis s u e is c r itic a l S e r ia lly a r r a n g e d F S U s E x a m p le : s p in a l c o r d in te g r ity o f e a c h F S U is c r itic a l to o r g a n fu n c tio n E lim in a tio n o f a n y F S U in th is s y s te m c a n r e s u lt in m e a s u r a b le p r o b a b ility o f c o m p lic a tio n R a d ia tio n d a m a g e s h o w s b in a r y r e s p o n s e th r e s h o ld b e lo w w h ic h is n o r m a l fu n c tio n, a b o v e w h ic h th e r e is lo s s o f fu n c tio n97 Do se vs. Co m p l i c a t i o n s Ex a m p l es f o r d i f f er en t t i ssu es 100 % Probability of Complications C B A Dose, (Gy) 7698 The t oxi ci t y of r adi ot her apy99 Dos e r es pons e cur ves f or r adi ot her apy100 Ea r l y (Ac u t e) a n d La t e Ef f ec t s R a d ia tio n e ffe c ts c o m m o n ly d iv id e d in to e a r ly a n d la te S h o w s d iffe r e n t p a tte r n s o f r e s p o n s e to d o s e fr a c tio n a tio n D o s e -r e s p o n s e r e la tio n s h ip s c h a r a c te r iz e d b y &/& r a tio s (m o r e o n th is la te r ) L a te e ffe c ts m o r e s e n s itiv e to c h a n g e s in fr a c tio n a tio n th a n e a r ly e ffe c ts E a r ly (a c u te ) e ffe c ts r e s u lt fr o m d e a th o f la r g e n u m b e r o f c e lls a n d o c c u r w ith in w e e k s to d a y s o f ir r a d ia tio n in tis s u e s w ith r a p id r a te o f tu r n o v e r101 Ex a m p l es o f ea r l y ef f ec t ed t i ssu es E x a m p le s : E p id e r m a l la y e r o f s k in G a s tr o in te s tin a l e p ith e liu m H e m a to p o ie tic s y s te m R e s p o n s e is d e te r m in e d b y h ie r a r c h ic a l c e ll lin e a g e c o m p o s e d o f s te m c e lls a n d d iffe r e n tia tin g o ffs p r in g. T im e o f o n s e t c o r r e la te s w ith life s p a n o f m a tu r e fu n c tio n a l c e lls102 Ex a m p l e o f l a t e- ef f ec t ed t i ssu es L a te e ffe c ts a p p e a r a fte r d e la y o f m o n th s o r y e a rs O c c u r p r e d o m in a n tly in s lo w ly p r o life r a tin g tis s u e s Lung K id n e y H e a rt C e n tr a l n e r v o u s s y s te m103 Th e p 53 Net wo r k Stalled UV radiation replication forks & radiation p53 Oncogenes Mdm2 En d DNA damage repair Ribosomal Stress Apoptosis Cell cycle arrest Senescence
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