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Changing Therapeutic Landscape in ALL, CLL, and NHL

Panelists: John C. Byrd, MD, Ohio State University; Dan Douer, MD, MSKCC;Stephen P. Hunger, MD, University of Colorado; Brad S. Kahl, MD, University
Published: Friday, Jun 20, 2014
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In the last segment of the series, moderator Gary J. Schiller, MD, asks each panelist to share their final thoughts on the changing therapeutic landscape in acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), and non-Hodgkin lymphoma (NHL).

For young adult patients with ALL, a genetic subtype is emerging that behaves similarly to Philadelphia chromosome-positive disease, notes Stephen P. Hunger, MD. This new subtype is characterized by a number of fusion genes that affect tyrosine kinases, such as ABL-1/2, JAK2, CSF-1, and PDGFR. Anecdotally, this subtype behaves similarly to BCR-ABL fusion-positive ALL and has shown promising responses to imatinib, Hunger suggests. This realization could lead to further genomic profiling of younger patients with ALL in order to identify subsets that could benefit from tyrosine kinase inhibitors.

Many of these novel treatments would not have been possible without research into basic biology, suggests Michael C. Lill, MD. These findings have led to promising small molecular inhibitors and immune-based therapies. Along these lines, while many of these therapies apply to specific populations or molecular drivers, some may have application in broader populations, believes Dan Douer, MD. The bispecific monoclonal antibody blinatumomab could be affective across ALL populations, Douer believes.

Despite the dramatic efficacy seen with many of the new targeted agents in CLL, resistance inevitably emerges, Brad S. Kahl, MD, notes. In order to prevent or delay this resistance, research will focus on rational combinations. Adding to this, John C. Byrd, MD, feels that many of these novel targeted therapies have the potential to expand to other diseases, outside of blood cancer, especially in combination with immunologic agents.
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For High-Definition, Click
In the last segment of the series, moderator Gary J. Schiller, MD, asks each panelist to share their final thoughts on the changing therapeutic landscape in acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL), and non-Hodgkin lymphoma (NHL).

For young adult patients with ALL, a genetic subtype is emerging that behaves similarly to Philadelphia chromosome-positive disease, notes Stephen P. Hunger, MD. This new subtype is characterized by a number of fusion genes that affect tyrosine kinases, such as ABL-1/2, JAK2, CSF-1, and PDGFR. Anecdotally, this subtype behaves similarly to BCR-ABL fusion-positive ALL and has shown promising responses to imatinib, Hunger suggests. This realization could lead to further genomic profiling of younger patients with ALL in order to identify subsets that could benefit from tyrosine kinase inhibitors.

Many of these novel treatments would not have been possible without research into basic biology, suggests Michael C. Lill, MD. These findings have led to promising small molecular inhibitors and immune-based therapies. Along these lines, while many of these therapies apply to specific populations or molecular drivers, some may have application in broader populations, believes Dan Douer, MD. The bispecific monoclonal antibody blinatumomab could be affective across ALL populations, Douer believes.

Despite the dramatic efficacy seen with many of the new targeted agents in CLL, resistance inevitably emerges, Brad S. Kahl, MD, notes. In order to prevent or delay this resistance, research will focus on rational combinations. Adding to this, John C. Byrd, MD, feels that many of these novel targeted therapies have the potential to expand to other diseases, outside of blood cancer, especially in combination with immunologic agents.
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