LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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SYNOPSIS Fig. 3.4EDNA damage in EL-4 cells cultured for 2 h in presence of different conditioned media was measured using single cell gel electrophoresis (‘comet assay’), (A) Tail length and (B) % DNA in tail. Key: Lane 1, control unirradiated EL-4 cells; Lane 2, γ irradiated EL-4 cells; Lane 3, unirradiated EL-4 cells receiving medium from γ irradiated EL-4 cells; Lane 4, unirradiated EL-4 cells receiving medium irradiated with γ rays in the absence of cells; Lane 5, unirradiated EL-4 cells receiving medium from unirradiated EL-4 cells. Data represents means ± SE of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. Fig. 3.4F Gene expression of NF-kB (p65) and iNOS gene in EL-4 cells which had received medium from irradiated RAW 264.7 cells. EL-4 cells cultured for 2 h in presence of different conditioned media. Key: Lane 1, control EL-4 cells; Lane 2, EL-4 cells receiving medium from LPS-stimulated (500ng/ml) and γ irradiated RAW 264.7 cells; Lane 3, EL-4 cells receiving medium from γ irradiated RAW 264.7 cells without LPS-stimulation; Lane 4, EL-4 cells receiving medium from LPS-stimulated RAW 264.7 cells; Lane 5, EL-4 cells receiving medium from unirradiated RAW 264.7 cells. Data represents means ± SE of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. 23
SYNOPSIS Fig. 3.4G Gene expression of NF-kB (p65) and iNOS gene in EL-4 cells which had received medium from irradiated cells. EL-4 cells cultured for 2 h in presence of different conditioned media. Key: Lane 1, control EL-4 cells; Lane 2, γ irradiated EL-4 cells; Lane 3, EL-4 cells receiving medium from γ irradiated EL-4 cells; Lane 4, EL-4 cells receiving medium from L-NAME treated and γ irradiated EL-4 cells; Lane 5, EL-4 cells receiving medium from cPTIO treated and γ irradiated EL-4 cells; Lane 6, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), L-NAME treated and γ irradiated RAW 264.7 cells; Lane 7, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), cPTIO treated and γ irradiated RAW 264.7 cells. Data represents means ± SE of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. CHAPTER 4: DISCUSSION The work embodied in this thesis clearly shows that the fractionated doses led to a signaling response that was different from a single dose of irradiation. The work also stresses on the signaling differences between Low and High LET radiation and the fine tuning of bystander signaling. The observed results have been extensively discussed in this chapter and their significance and impact has been discussed in context with the current literature. The conclusions drawn from this study has also been included in this chapter. 4.1 Fractionated irradiation induced signaling and repair in mammalian cells. In tumor radiotherapy, radiation is given as fractionated doses [4]. This leads to development of radioresistance in the surviving tumor cells. Chronic exposure of cells to ionizing radiation induces an adaptive response that results in the increased tolerance to 24
Page 1: RADIATION INDUCED SIGNALING IN MAMM
Page 4 and 5: DECLARATION I, hereby declare that
Page 6 and 7: CONTENTS Page No. SYNOPSIS………
Page 8 and 9: 2.11 Measurement of NO production
Page 10 and 11: PREAMBLE SYNOPSIS Ionising radiatio
Page 12 and 13: SYNOPSIS Aims and Objectives: To St
Page 14 and 15: SYNOPSIS 2.6 Immunofluorescence sta
Page 16 and 17: SYNOPSIS ATM gene expression, which
Page 18 and 19: SYNOPSIS Percentage Survival 100 80
Page 20 and 21: SYNOPSIS Ratio of Rad52 to Actin Ra
Page 22 and 23: Relative Phosphorylation 45 40 35 3
Page 24 and 25: SYNOPSIS Fig. 3.3A Clonogenic Cell
Page 26 and 27: SYNOPSIS (A) Av No. of phospho BRCA
Page 28 and 29: SYNOPSIS Percentage Survival 120 10
Page 30 and 31: SYNOPSIS Fig.3.4B. Existance of cro
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Page 36 and 37: SYNOPSIS [4] Hall, E. J. Radiobiolo
Page 38 and 39: CHAPTER 1 INTRODUCTION INTRODUCTION
Page 40 and 41: CHAPTER 1 INTRODUCTION 15.8% 9.56%
Page 42 and 43: CHAPTER 1 INTRODUCTION far apart an
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Page 76 and 77: CHAPTER 1 INTRODUCTION p90S6 kinase
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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
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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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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