Role of Cohesin Mutations in Acute Myelogenous Leukemia

  • Crispino, John D (PD/PI)

Project: Research project

Project Details


Heartland Blood Centers provides critical support in the form of blood and blood products to patients with leukemia and has supported important organizations like the Leukemia and Lymphoma Society (LLS). Hematologists and Oncologists at Northwestern and the Lurie Cancer Center in Chicago are known internationally for their care of patients with leukemia and blood disorders as well as for their research focus on blood cancers. In addition, the Blood Research Institute, now a part of Heartland, has built a research team of physicians and scientists that is focused on the causes of leukemia, the abnormalities in leukemia stem cells, the treatment for leukemia, and ways to potentially prevent leukemia. The goal of the work described in this proposal is to provide an additional level of support in the form of research aimed at understanding the fundamental defects in forms of leukemia, leading to new ways to treat and cure leukemia. The research links scientists in the Division of Hematology-Oncology and the Lurie Cancer Center at Northwestern with scientists at the Blood Research Institute. The focus of the work is on something called the cohesin complex, which is a group of proteins that regulate gene expression. Mutations in the cohesin complex are a prevalent cause of acute myeloid leukemia, one of the most devastating forms of leukemia. These mutations appear to increase the ability of the cells to self renew, leading to one of the hallmarks of leukemia – too many cells. Outcomes of this work can be expected to better integrate our mission based blood research into the Chicago area, provide an important conceptual model for that integration, strengthen relationships with one of our leading customers, help our patients with blood cancers, and establish Heartland Blood Centers as the premier blood center in greater Chicago.
Effective start/end date10/1/159/30/17


  • Heartland Blood Centers (AGMT-12/18/15)


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