Dr. Daver on Immune Checkpoint Pathways in AML

Naval Daver, MD
Published Online: Wednesday, Dec 28, 2016



Naval Daver, MD, assistant professor, Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, discusses research evaluating different immune checkpoint pathways in patients with acute myeloid leukemia (AML).

Since nivolumab (Opdivo) and other immune checkpoint drugs have shown exciting results in a number of other solid tumors, researchers are now turning their attention toward these different immune checkpoint pathways in the treatment of patients with AML.

Daver provides an overview of a study in which the investigators collected bone marrow tissue samples and blood from patients with AML. After analyzing those samples, they found that the 2 checkpoint pathways that seemed to be overexpressed in the bone marrow were PD-1 and OX40.

Based on those findings, he says, multiple clinical trials began in different patient populations—including those with AML, myelodysplastic syndrome, and chronic lymphocytic leukemia—to see if the researchers could target this overexpression of PD-1 in the bone marrow, increase T cell activity, and improve responses—or durability of responses—in these patients. Moreover, these results ultimately provide a strong rationale for further research into immune checkpoint pathways in AML and other hematologic malignancies.


Naval Daver, MD, assistant professor, Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, discusses research evaluating different immune checkpoint pathways in patients with acute myeloid leukemia (AML).

Since nivolumab (Opdivo) and other immune checkpoint drugs have shown exciting results in a number of other solid tumors, researchers are now turning their attention toward these different immune checkpoint pathways in the treatment of patients with AML.

Daver provides an overview of a study in which the investigators collected bone marrow tissue samples and blood from patients with AML. After analyzing those samples, they found that the 2 checkpoint pathways that seemed to be overexpressed in the bone marrow were PD-1 and OX40.

Based on those findings, he says, multiple clinical trials began in different patient populations—including those with AML, myelodysplastic syndrome, and chronic lymphocytic leukemia—to see if the researchers could target this overexpression of PD-1 in the bone marrow, increase T cell activity, and improve responses—or durability of responses—in these patients. Moreover, these results ultimately provide a strong rationale for further research into immune checkpoint pathways in AML and other hematologic malignancies.



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