LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 1 INTRODUCTION becomes potentially cytotoxic. Therefore the onus lies on non gap junction mediated cell communication. Evidence for some forms of bystander effect has been suggested also by conventional irradiation with low doses. One of the first studies in this field has showed a significant, unexpected increase in the frequency of sister chromatid exchanges (SCEs) after exposure of Chinese hamster ovary (CHO) cells to very low doses of alpha particles, from 0.03 to 0.25 cGy [220]. While about 1% or less of the cells were actually traversed by a particle track, 30–45% of the individual cells showed increased levels of SCE. This suggests that genetic damage following exposure to very low doses of light ions may occur also in non directly-irradiated bystander cells. The studies discussed above strongly suggest a role of extranuclear- and possibly extracellular-targets in the propagation of certain damage types after irradiation with very low doses of light ions or treatment with ICM. Experiments allowing the identification of specific targets for such phenomena can be of great help to better understand the underlying mechanisms and to quantify the relative contributions of different targets. This kind of studies is now possible due to the increasing number of microbeam facilities. Such facilities in which cells are individually irradiated by a predefined exact number of particles allow the effects of individual particle traversals to be assessed, and these methods have become a useful tool in the study of bystander responses [221, 222]. Such studies suggest a major role of cell-to-cell communication via gap-junctions [223]. 77
CHAPTER 1 INTRODUCTION 1.7 Aims and Objectives: To Study 1. Fractionated irradiation induced signaling events. The contribution of these events to the increased cell survival. 2. High LET induced signaling and variance from low LET gamma radiation. 3. Contribution of radiation induced bystander effect to cell survival and its mechanism. 78
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
Page 36 and 37: SYNOPSIS [4] Hall, E. J. Radiobiolo
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Page 40 and 41: CHAPTER 1 INTRODUCTION 15.8% 9.56%
Page 42 and 43: CHAPTER 1 INTRODUCTION far apart an
Page 44 and 45: CHAPTER 1 INTRODUCTION and are more
Page 46 and 47: CHAPTER 1 INTRODUCTION 1.3 DNA dama
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Page 50 and 51: CHAPTER 1 INTRODUCTION are unable t
Page 52 and 53: CHAPTER 1 INTRODUCTION Perhaps one
Page 54 and 55: CHAPTER 1 INTRODUCTION occurs at DS
Page 56 and 57: CHAPTER 1 INTRODUCTION related prot
Page 58 and 59: CHAPTER 1 INTRODUCTION damage must
Page 60 and 61: CHAPTER 1 INTRODUCTION At the prese
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Page 64 and 65: CHAPTER 1 INTRODUCTION provide a me
Page 66 and 67: CHAPTER 1 INTRODUCTION hypersensiti
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Page 70 and 71: CHAPTER 1 INTRODUCTION 1.4 Overview
Page 72 and 73: CHAPTER 1 INTRODUCTION 1.4.1 Radiat
Page 74 and 75: CHAPTER 1 INTRODUCTION interaction
Page 76 and 77: CHAPTER 1 INTRODUCTION p90S6 kinase
Page 78 and 79: CHAPTER 1 INTRODUCTION CD4 (formerl
Page 80 and 81: CHAPTER 1 INTRODUCTION unrepaired d
Page 82 and 83: CHAPTER 1 INTRODUCTION well to the
Page 84 and 85: CHAPTER 1 INTRODUCTION 1.6 Radiatio
Page 88 and 89: CHAPTER 2 MATERIALS AND METHODS MAT
Page 90 and 91: CHAPTER 2 MATERIALS AND METHODS 2.2
Page 92 and 93: CHAPTER 2 MATERIALS AND METHODS res
Page 94 and 95: CHAPTER 2 MATERIALS AND METHODS Arr
Page 96 and 97: CHAPTER 2 MATERIALS AND METHODS PBS
Page 98 and 99: CHAPTER 2 MATERIALS AND METHODS the
Page 100 and 101: CHAPTER 2 MATERIALS AND METHODS 2.1
Page 102 and 103: CHAPTER 3 RESULTS RESULTS 93
Page 104 and 105: CHAPTER 3 RESULTS fractionated regi
Page 106 and 107: CHAPTER 3 RESULTS On comparison of
Page 108 and 109: CHAPTER 3 RESULTS Table 3.1.2A List
Page 110 and 111: CHAPTER 3 RESULTS 80 NM_002185 IL7R
Page 112 and 113: CHAPTER 3 RESULTS SAA2 149 AU134977
Page 114 and 115: CHAPTER 3 RESULTS 221 LOC643167 RNA
Page 116 and 117: CHAPTER 3 RESULTS 299 BF244402 FBXO
Page 118 and 119: CHAPTER 3 RESULTS CDK4) 57 AU152107
Page 120 and 121: CHAPTER 3 RESULTS 134 AL045793 METT
Page 122 and 123: CHAPTER 3 RESULTS 58 AF237813 ABAT
Page 124 and 125: CHAPTER 3 RESULTS 127 AI809749 ORMD
Page 126 and 127: CHAPTER 3 RESULTS 31 BE615699 UNC84
Page 128 and 129: CHAPTER 3 RESULTS 47 AF026303 SULT1
Page 130 and 131: CHAPTER 3 RESULTS 117 BF062193 CYor
Page 132 and 133: CHAPTER 3 RESULTS 187 AL036662 ---
Page 134 and 135: CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
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CHAPTER 3 RESULTS Fig. 3.1.7 Transl
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CHAPTER 3 RESULTS 3.1.9 Stabilizati
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CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
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CHAPTER 3 RESULTS whereas only the
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CHAPTER 3 RESULTS with equal doses
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CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
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CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
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CHAPTER 3 RESULTS (7.5±0.64) (Fig.
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CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
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CHAPTER 3 RESULTS 3.3.2 Oxygen beam
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CHAPTER 3 RESULTS in all the cells.
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CHAPTER 3 RESULTS 3.3.2.3 Radiation
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CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
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CHAPTER 3 RESULTS PMA stimulated U9
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CHAPTER 3 RESULTS Fig.3.4.2. Exista
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CHAPTER 3 RESULTS up-regulation of
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CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
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CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
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CHAPTER 3 RESULTS 3.4.4 Bystander e
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CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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CHAPTER 3 RESULTS Fig.3.4.5a Gene e
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CHAPTER 4 DISCUSSION DISCUSSION 185
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CHAPTER 4 DISCUSSION directly expos
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CHAPTER 4 DISCUSSION dose is delive
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CHAPTER 4 DISCUSSION A clear cause
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CHAPTER 4 DISCUSSION 4.2 Proton bea
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CHAPTER 4 DISCUSSION Although the e
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CHAPTER 4 DISCUSSION Similar number
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CHAPTER 4 DISCUSSION the mechanism
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CHAPTER 4 DISCUSSION Thus unlike th
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CHAPTER 4 DISCUSSION different from
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CHAPTER 4 DISCUSSION upregulates ma
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CHAPTER 4 DISCUSSION Numerous studi
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CHAPTER 4 DISCUSSION inhibition of
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CHAPTER 4 DISCUSSION The survival o
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CHAPTER 5 REFERENCES [1] Khan, F. T
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CHAPTER 5 REFERENCES [19] Woo, R. A
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CHAPTER 5 REFERENCES [35] Nghiem, P
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CHAPTER 5 REFERENCES [52] McKay, B.
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CHAPTER 5 REFERENCES [69] Cary, R.
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CHAPTER 5 REFERENCES [84] Uziel, T.
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CHAPTER 5 REFERENCES [98] Liu, Y.;
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CHAPTER 5 REFERENCES [111] Fei, P.;
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CHAPTER 5 REFERENCES [127] Frank, K
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CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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CHAPTER 5 REFERENCES [171] Xia, Z.;
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CHAPTER 5 REFERENCES (MAP) kinase c
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CHAPTER 5 REFERENCES phosphorylatio
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CHAPTER 5 REFERENCES [211] Anderson
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CHAPTER 5 REFERENCES [229] Konca, K
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CHAPTER 5 REFERENCES [245] Kastan,
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CHAPTER 5 REFERENCES [261] Miralbel
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CHAPTER 5 REFERENCES [278] Weizman,
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CHAPTER 5 REFERENCES [294] Zhou, H.
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PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 729 (2012) 61-72
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S. Ghosh, M. Krishna / Mutation Res
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Cancer Invest Downloaded from infor
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1568 I. J. Radiation Oncology d Bio
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