towards improved death receptor targeted therapy for ... - TI Pharma

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CURRICULUM VITAE Curriculum Vitae Kaamar Azijli was born on 14 september 1984 in Amsterdam. In 2002 she obtained her VWO diploma at the Hervormd Lyceum West in Amsterdam. Subsequently, she started her study Pharmaceutical Sciences at the VU University in Amsterdam. During this study she completed several internships in the group of prof.dr. Rob Leurs (Medicinal Chemistry) about Histamine H3 and H4 receptors. She also did an internship in Solvay Pharmaceuticals B.V. (now Abbott Laboratories) in the group of dr. Eric Ronken. This internship was about the Dopamine D2 receptor in the treatment of CNS diseases, such as parkinson and schizophrenia. Her literature study was written about gefitinib, the first EGFR inhibitor in the treatment of NSCLC under supervision of dr. Iwan de Esch (Medicinal Chemistry). She graduated on her Master Pharmaceutical Sciences in 2007. Next, in 2008 she started with her PhD project at the department of Medical Oncology at the VU University Medical Center in Amsterdam, entitled: “TRAIL‐induced kinase activation and apoptosis: towards improved death receptor targeted therapy for lung cancer”, which is described in this thesis. ____ (In Dutch) Kaamar Azijli is geboren op 14 september 1984 te Amsterdam. In 2002 behaalde ze haar VWO diploma aan het Hervormd Lyceum West, te Amsterdam. Vervolgens begon ze haar studie Farmaceutische Wetenschappen aan de Vrije Universiteit in Amsterdam. Tijdens deze studie werden een aantal stages verricht in de groep van prof. dr. Rob Leurs (Medicinal Chemistry) over Histamine H3 en H4 receptoren. Ook heeft ze stage gelopen in het farmaceutisch bedrijf Solvay Pharmaceuticals B.V. (tegenwoordig Abbott Laboratories) in de groep van dr. Eric Ronken. Deze stage ging over de Dopamine D2 receptor in de behandeling van ziektes in het centrale zenuwstelsel, zoals parkison en schizofrenie. Haar literatuurstudie schreef ze over gefitinib, de eerste EGFR remmer in de behandeling van niet‐kleincellige longkanker onder begeleiding van dr. Iwan de Esch (Medicinal Chemistry). Haar Master Farmaceutische Wetenschappen rondde zij af in 2007. Het jaar daarop in 2008, begon ze aan haar promotie onderzoek aan het VU medisch centrum in Amsterdam getiteld: “TRAIL‐induced kinase activation and apoptosis: towards improved death receptor targeted therapy for lung cancer”, wat beschreven staat in dit proefschrift. ‐ 155 ‐
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TRAIL-induced kinases activation an
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TRAIL‐induced kinases activation
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“In order to be irreplaceable one
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‐ 8 ‐
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Chapter 1 GENERAL INTRODUCTION Canc
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Chapter 1 OUTLINE OF THE THESIS As
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Chapter 1 Reference List 1. Jemal A
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Chapter 2 ABSTRACT Tumor necrosis f
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Chapter 2 INTRODUCTION The death li
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Chapter 2 In preclinical studies, a
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Chapter 2 Table 1| Summary of the k
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Chapter 2 proliferation could be pr
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Chapter 2 Figure 2. Canonical and n
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Chapter 2 associated with TRAIL res
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Chapter 2 adhesion molecules [109].
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Chapter 2 Reference List 1. Ashkena
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Chapter 2 37. Tolcher AW, Mita M, M
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Chapter 2 melanoma cells from TRAIL
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Chapter 2 and ERK pathways. Circula
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Chapter 3 inhibitors and TRAIL rece
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Chapter 3 of amplification of the t
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Chapter 3 P38 and JNK have opposing
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Chapter 3 Figure 2 (continued). (e)
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Chapter 3 previously established H4
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Chapter 3 effect on TRAIL‐induced
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Chapter 3 induced apoptosis in H460
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Chapter 3 40. Domina AM, Vrana JA,
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Chapter 4 role in the activation of
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Chapter 4 the tip with a diameter o
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Chapter 4 RESULTS TRAIL induces a s
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Chapter 4 vehicle control or with 5
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Chapter 4 Non‐canonical TRAIL res
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Chapter 4 A549‐shRIP1 cells clear
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Chapter 4 Figure 7. Inhibition of S
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Chapter 4 DISCUSSION The TRAIL rece
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Chapter 4 Src‐independent mechani
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Chapter 4 variants. Cell Death Dis
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Chapter 4 ‐ 82 ‐
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Chapter 5 ABSTRACT TRAIL is an inte
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Chapter 5 targets and subsequent pr
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Chapter 5 RESULTS Synergistic activ
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Chapter 5 ng/ml TRAIL (Fig. 3B). Ap
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Chapter 5 by sub‐G1 levels in the
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Chapter 5 DISCUSSION In the present
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Chapter 5 ‐ 98 ‐
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Chapter 6 ABSTRACT TRAIL is a tumor
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Chapter 6 various stress stimuli [1
Page 105 and 106: Chapter 6 Subsequently, the membran
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Page 109 and 110: Chapter 6 TRAIL‐dependent cell de
Page 111 and 112: Chapter 6 B H460 A549 C Figure 4 (c
Page 113 and 114: Chapter 6 Figure 5 (continued). Mec
Page 115 and 116: Chapter 6 regulation and checkpoint
Page 117 and 118: Chapter 6 mechanism of immune evasi
Page 119 and 120: Chapter 7 ABSTRACT Thymidine phosph
Page 121 and 122: Chapter 7 Figure 1. Schematic overv
Page 123 and 124: Chapter 7 that was measured before
Page 125 and 126: Chapter 7 RESULTS TdR conversion to
Page 127 and 128: Chapter 7 dR is secreted from the c
Page 129 and 130: Chapter 7 Figure 4. Accumulation of
Page 131 and 132: Chapter 7 angiogenic properties. Ho
Page 133 and 134: Chapter 7 activity of enzymes. Natu
Page 135 and 136: Chapter 7 ‐ 134 ‐
Page 137 and 138: Chapter 8 SUMMARIZING DISCUSSION AN
Page 139 and 140: Chapter 8 Recently, various differe
Page 141 and 142: Chapter 8 in phase II clinical tria
Page 143 and 144: Chapter 8 Reference List 1. Herbst
Page 145 and 146: Chapter 8 ‐ 144 ‐
Page 147 and 148: Chapter 9 NEDERLANDSE SAMENVATTING
Page 149 and 150: Chapter 9 waargenomen. Het gebruik
Page 151 and 152: Chapter 9 CONCLUSIE Het activeren v
Page 153 and 154: zelfs na werktijden (lees 23:45) ko
Page 155: Verder wil ik ook dr. Eric Ronken b
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