LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 3 RESULTS Fig.3.3.2.7 Apoptosis in oxygen irradiated A549 cells. Apoptotic nuclei of A549 cells were visualized and quantified by using DAPI staining, 18 hours after 2Gy and 6Gy gamma or 2Gy oxygen irradiation. The percentage of cells with apoptotic nuclei are represented as graph. At least 100 cells per experiment were analyzed from three independent experiments. Data represents means ± SD of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. Significantly different from 6Gy gamma: # P < 0.05. 167
CHAPTER 3 RESULTS 3.4 Radiation induced bystander signaling in mammalian cells. Radiation induced bystander effect has generated a lot of interest in recent times wherein the effect of irradiating the target cell on the surrounding unirradiated bystander cells have been studied. Having established that the response of the signaling factors varied with dose, dose fractionation, time, microenvironment and radiation quality (LET), it was of interest to investigate this emerging phenomenon. An attempt has been made to investigate the underlying mechanism involved and also to determine what component of the signaling system could be altered by bystander effect and contribution of the bystander effect in the survival of the neighbouring cells. To understand bystander signaling a number of studies have been made between the same cell lines. However, not much is known whether bystander effect is extendable to dissimilar cells, particularly those cells that communicate with each other under physiological situations. The present study describes the bystander effects of radiation between similar cells and dissimilar cells in vitro. Gap junction independent signaling mechanism was looked into using human A549 cells where they were exposed to 2Gy of 60 Co γ irradiation, the medium isolated and added to fresh cells. Bystander signaling was also studied between U937 cells (human monocyte) and Lung carcinoma A549 cells. Before designing the experiment there were two aspects that had to be taken care of, one was the likelihood that the replacement of the medium itself caused transient expression of certain signaling factors and second that the components of the medium, which include proteins like growth factors, etc. which are unavoidably exposed to radiation, contribute to the changes in the bystander cell. The experimental design, therefore, consisted of the following sets: (a) control unirradiated cells, (b) γ irradiated cells, (c) A549 cells receiving medium from unirradiated A549 cells or U937 cells or 168
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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
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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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
Page 136 and 137: CHAPTER 3 RESULTS exposed to 10 Gy
Page 138 and 139: CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
Page 140 and 141: CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
Page 142 and 143: CHAPTER 3 RESULTS Fig. 3.1.7 Transl
Page 144 and 145: CHAPTER 3 RESULTS 3.1.9 Stabilizati
Page 146 and 147: CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
Page 148 and 149: CHAPTER 3 RESULTS whereas only the
Page 154 and 155: CHAPTER 3 RESULTS with equal doses
Page 156 and 157: CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
Page 158 and 159: CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
Page 160 and 161: CHAPTER 3 RESULTS (7.5±0.64) (Fig.
Page 164 and 165: CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
Page 166 and 167: CHAPTER 3 RESULTS 3.3.2 Oxygen beam
Page 168 and 169: CHAPTER 3 RESULTS in all the cells.
Page 170 and 171: CHAPTER 3 RESULTS 3.3.2.3 Radiation
Page 178 and 179: CHAPTER 3 RESULTS PMA stimulated U9
Page 180 and 181: CHAPTER 3 RESULTS Fig.3.4.2. Exista
Page 182 and 183: CHAPTER 3 RESULTS up-regulation of
Page 184 and 185: CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
Page 186 and 187: CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
Page 188 and 189: CHAPTER 3 RESULTS 3.4.4 Bystander e
Page 190 and 191: CHAPTER 3 RESULTS Fig.3.4.4b DNA da
Page 192 and 193: CHAPTER 3 RESULTS Fig.3.4.5a Gene e
Page 194 and 195: CHAPTER 4 DISCUSSION DISCUSSION 185
Page 196 and 197: CHAPTER 4 DISCUSSION directly expos
Page 198 and 199: CHAPTER 4 DISCUSSION dose is delive
Page 200 and 201: CHAPTER 4 DISCUSSION A clear cause
Page 202 and 203: CHAPTER 4 DISCUSSION 4.2 Proton bea
Page 204 and 205: CHAPTER 4 DISCUSSION Although the e
Page 206 and 207: CHAPTER 4 DISCUSSION Similar number
Page 208 and 209: CHAPTER 4 DISCUSSION the mechanism
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Page 212 and 213: CHAPTER 4 DISCUSSION different from
Page 214 and 215: CHAPTER 4 DISCUSSION upregulates ma
Page 216 and 217: CHAPTER 4 DISCUSSION Numerous studi
Page 218 and 219: CHAPTER 4 DISCUSSION inhibition of
Page 220 and 221: CHAPTER 4 DISCUSSION The survival o
Page 222 and 223: CHAPTER 5 REFERENCES [1] Khan, F. T
Page 224 and 225: 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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