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EGFR targeted therapies in lung cancer
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    SPEAKER(S)

Dr. Pasi Janne - Dana Faber Cancer Institute and Harvard Medical School, USA

Pasi Janne received his MD and PhD from the University of Pennsylvania in 1996. He completed postgraduate training in internal medicine at Brigham and Women's Hospital and in medical oncology at DFCI in 2001. He currently works in the Lowe Center for Thoracic Oncology at DFCI. His main research interests include the study of epidermal growth factor receptor mutations in non-small cell lung cancer and their impact on the efficacy of EGFR-targeted therapeutic agents.

Talk Online Publication: Nov 2009

TOPICS COVERED IN EGFR TARGETED THERAPIES IN LUNG CANCER

Lung cancer: facts and figures - Lung cancer survival - Lung cancer burden - EGFR targeted therapeutics - EGFR mutations - Why Do EGFR inhibitors work so well in EGFR mutant cancers? - Are EGFR TKIs better than chemotherapy? - Emergence of resistance to EGFR TKIs - Mechanisms of Gefitinib/Erlotinib resistance - EGFR signaling in EGFR mutant NSCLC - Analogous kinase mutations associated with drug resistance - Irreversible EGFR inhibitors - Clinical resistance is heterogeneous - Therapeutic targeting of other oncogenes in lung cancer - Incorporating genomics into treatment

How to cite this talk:
Janne, P. (2009), "EGFR targeted therapies in lung cancer", in Heldin, C. (ed.), Signal Transduction via Protein Tyrosine Kinase Receptors: Structures, Function, Regulation, Mechanisms and Role in Disease, The Biomedical & Life Sciences Collection, Henry Stewart Talks Ltd, London (online at http://hstalks.com/bio)

Direct talk access link:
http://hstalks.com/lib.php?t=HST30.2329_1_2&c=252

    DETAILED SLIDE INDEX

1. Introduction
2. Lung cancer - facts and figures
3. Change in lung cancer survival: 1974-2001
4. Magnitude of lung cancer burden in the US: 2006
5. Non-small cell lung cancer (NSCLC) - 2009
6. EGFR inhibitors in lung cancer
7. EGFR targeted therapeutics (1)
8. Mechanisms of EGFR receptor activation
9. Structures of EGFR-TK inhibitors
10. Erlotinib vs. placebo
11. EGFR mutations
12. Somatic mutations in EGFR
13. Patients with EGFR mutations treated with TKIs
14. Prognostic information from mutant EGFR studies
15. EGFR inhibitors effect on EGFR mutant cancers
16. EGFRL858R is more sensitive to gefitinib than WT
17. EGFR mutant NSCLC cell lines depend on EGFR
18. Prevalence of EGFR mutations in cancer patients
19. Are EGFR TKIs better than chemotherapy?
20. IPASS - study design
21. Progression-free survival (PFS) in ITT population
22. The impact of EGFR mutation on response rate
23. EGFR mutation effect on progression-free survival
24. EURTAC-SLCG study design
25. Questions for treatment naive EGFR mutant
26. TRIBUTE trial: chemotherapy + erlotinib or placebo
27. CALGB 30406 phase II study: trial design
28. EGFR targeted therapeutics (2)
29. Cetuximab in NSCLC
30. FLEX clinical trial: chemotherapy +/- cetuximab
31. FLEX overall survival
32. FLEX: response rate and PFS
33. Identifying predictors of cetuximab response
34. Subsets of NSCLC cell lines produce amphiregulin
35. Amphiregulin producing EGFR WT cell lines
36. Cell cycle arrest in amphiregulin producing cells
37. Emergence of resistance to EGFR TKIs
38. Mechanisms of gefitinib/erlotinib resistance
39. EGFR signaling in EGFR mutant NSCLC
40. Development of gefitinib/erlotinib resistance
41. EGFR T790M mutation
42. Kinase mutations associated with drug resistance
43. Irreversible EGFR inhibitors
44. Irreversible EGFR TKIs affect EGFR T790M
45. Irreversible EGFR inhibitors in trials
46. Second generation EGFR TKIs
47. MET amplification
48. MET amplification and it's effect on resistance
49. Efficacy of XL184 in vitro and in vivo
50. MET inhibitors in trials
51. Clinical resistance is heterogeneous
52. Resistance mechanisms in resistant NSCLC
53. Clinical strategies for gefitinib/erlotinib resistances
54. Lung adenocarcinoma 2009 - genetically diverged
55. Somatic mutations in NSCLC
56. Targeting of other lung cancer oncogenes
57. Lung cancer therapy in 2009
58. END