Dismantling myeloid blood cancer at its core

Scientists know the primary genetic determinants of myeloid blood cancers and yet treatment options have remained largely unchanged for 50 years. One challenge is how to rid the body of cancer-carrying gene cells without harming other cells. Dr. Shannon Elf is dissecting the unique nature of these cells and what they need to survive in order to develop targeted treatments for intervention. View Halo Profile >>

Tell me about your research…

Although the genes that drive the development of myeloid blood cancers have largely been defined, there are currently few effective targeted treatments for these diseases. My research focuses on identifying unique molecular dependencies in myeloid blood cancers that can be targeted for therapeutic intervention, with the long­-term goal of improving upon current treatment regimens for these diseases. Currently, we are focused on understanding the role of the unfolded protein response in myeloproliferative neoplasms and acute myeloid leukemia. We are working to dissect the molecular mechanisms underlying UPR activation in specific subsets of MPN and AML, and to use this mechanistic insight to develop rationally designed therapies to target the UPR in these challenging diseases.

My research focuses on identifying unique molecular dependencies in myeloid blood cancers that can be targeted for therapeutic intervention, with the long­-term goal of improving upon current treatment regimens for these diseases.

Can you explain that to a non-scientist?

Although we know most of the genes that cause blood cancers, we still haven’t found effective ways to specifically kill blood cancer cells carrying those genes without affecting the normal cells our body needs to function. To do this, we need to first identify plausible targets for therapy, meaning genes that are required only by blood cancer cells to grow and survive, but not by normal cells. We then need to understand how those genes work, and what they do to promote survival in blood cancer cells. Using this understanding, we can then design drugs that specifically interfere with the function of those genes, which would culminate in targeted killing of cancer cells but not normal cells, resulting in far fewer side effects than cytotoxic treatments like chemotherapy.

Although we know most of the genes that cause blood cancers, we still haven’t found effective ways to specifically kill blood cancer cells carrying those genes without affecting the normal cells our body needs to function.

My lab is approaching this problem by investigating a pathway called the unfolded protein response, which appears to be required specifically by a subtype of blood cancer cells called myeloid blood cancer cells. We are working to understand how this pathway functions in myeloid blood cancer cells so we can then design drugs that specifically target this pathway.

How could it someday impact patient lives?

Treatment for myeloid blood cancers has remained largely unchanged for the past 50 years. Standard of care for these patients includes chemotherapy and bone marrow transplantation, both of which severely impact quality of life, and neither of which are curative. Identifying new targets for therapeutic intervention, understanding the molecular mechanisms underlying those targets, and using that mechanistic insight to rationally design specific, targeted therapies has the potential to not only improve quality of life for patients undergoing treatment, but to eventually cure these diseases.

Identifying new targets for therapeutic intervention, understanding the molecular mechanisms underlying those targets, and using that mechanistic insight to rationally design specific, targeted therapies has the potential to not only improve quality of life for patients undergoing treatment, but to eventually cure these diseases.