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Checkpoint Blockade in Cancer Immunotherapy
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    SPEAKER(S)

Prof. James Allison - Memorial Sloan-Kettering Cancer Center, USA

James P. Allison is the David H. Koch Chair in Immunologic Studies at the Sloan-Kettering Institute. Dr. Allison began his career in basic science at the University of Texas, Austin, where he received his BS in microbiology and his PhD in biological sciences. He is a leader in the field of immunology, particularly in developing ways to help the immune system recognize and destroy cancer cells. His research is focused on the mechanisms that regulate the immunological responses of T lymphocytes, especially strategies to manipulate those responses in clinically relevant areas, including autoimmunity, allergies, vaccinations and tumor therapy. Dr. Allison is a member of the National Academy of Sciences and an Investigator in the Howard Hughes Medical Institute.

Talk Online Publication: Oct 2007

TOPICS COVERED IN CHECKPOINT BLOCKADE IN CANCER IMMUNOTHERAPY

Activation of naive T-cells - CD28 and CTLA-4 - Differential regulation of T-cell responses - Responding repertoire - Biological role of CTLA-4 - Tumor-specific immune responses - Treg activity - CTLA-4/GVax - Immunotherapies - Conventional therapies - Ipilumumab - Clinical studies: melanoma - Reversible immune mediated toxicity

How to cite this talk:
Allison, J. (2007), "Checkpoint Blockade in Cancer Immunotherapy", in Waldmann, H. (ed.), Monoclonal Antibodies as Therapeutic Agents: Fundamentals, Therapeutic Applications and Latest Advances, 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=HST47.1385_1_3&c=252

    DETAILED SLIDE INDEX

1. Introduction
2. Checkpoint blockade In cancer immunotherapy
3. Two signals are required for naive T cells activation
4. Many molecules shape the immune response
5. Functional asymmetry of CD28 and CTLA-4
6. Integration of TCR and costimulatory signals
7. Localization of CD28/CTLA-4 in migrating T cells
8. The movement of CD28 and CTLA-4
9. Do B7-1 or/and B7-2 dimerize?
10. B7-1 may dimerizes,while B7-2 appear monomeric
11. CD28 and CTLA-4 signaling complexes
12. Signaling processes on the T cell - APC junction
13. The role of CD28 and CTLA-4 cytoplasmic tails
14. Effect of agonists' strength on CTLA-4 localization
15. CD28 and CTLA- 4 trafficking
16. Differential regulation of T cell responses
17. CTLA-4 preferentially inhibits the best-fit response
18. Models for biological role of CTLA-4
19. How does CTLA-4 broaden responding repertoire?
20. Biological role of CTLA-4
21. Effect of CTLA-4 blockade
22. Effect of anti-CTLA-4 on transplantable tumor
23. Anti-CTLA-4 and GM-CSF synergise
24. Side effects following rejection of B16 melanoma
25. Effect of anti-CTLA-4/GVax
26. CTLA-4 has a cell-autonomous activity
27. Effect of exposure to anti-CTLA-4 in vivo
28. Effect of exposure to anti-CTLA-4 in vitro
29. Anti-CTLA-4 does not block Treg activity in vitro
30. Anti-CTLA-4/GVax increases Teff/Treg ratio
31. Summary: effective combinations of anti-CTLA-4
32. Chimeric murine CTLA-4 transgene
33. Effect of anti-CTLA-4 on MC38 tumor growth
34. MDX-010 (Ipilumumab)
35. Clinical response to a single dose of Ipilumumab
36. MDX-010-05 study design
37. Trial results: complete responder - patient 11
38. Example: CTLA-4 blockade effects on tumors
39. Reversible immune mediated toxicity
40. MDX010-020: Pivotal Phase III Trial
41. Autologous GVAX followed by MDX-010
42. Trial results: melanoma patient 15
43. Ovarian GVAX and Anti-CTLA-4 Ab - single dose
44. Reduction in tumor nodules following MDX-010 Rx
45. "Lupus-like" rash in ovarian cancer
46. Ovarian GVAX and Anti-CTLA-4 Ab effects
47. Research contributors
48. GVAX immunotherapy and Ipilimumab for HRPC
49. Trial results: PSA curves at dose-level 3
50. Trial results: bone scan improvement in patient 8
51. Checkpoint blockade works
52. Many questions still to be answered
53. Acknowledgements
54. Current lab members
55. END