Prognostic Marker for Acute Myeloid Leukemia (AML) Relapse
Acute myeloid leukemia regeneration enriched cells identified as a means to determine treatment options to predict patient relapse
Background
Acute Myeloid Leukemia (AML) is an aggressive and heterogeneous cancer characterized by abnormal differentiation of myeloid blood cells. While considerable advancements in AML treatment have been made, the long-term survival rate of AML is still less than 50% in younger patients and only around 15% for older adults today. A key challenge is that surviving leukemic cells contribute to relapse post-chemotherapy, but little is known about these enduring leukemic cells and how they reinitiate disease, leading to a lack of methods to monitor disease post-intervention and lack of therapies to combat AML relapse.
Technology Overview
Researchers from McMaster University have identified a new population of cells defined by CD74/CD68 expression, termed AML regeneration enriched cells (RECs), which play a crucial role in the regeneration of AML following chemotherapy. Based on this discovery, a prognostic method has been developed for prediction of patient survival and treatment failure in AML.
Further details:
Identification of cells of leukemic stem cell origin with non-canonical regenerative properties. Cell Rep Med. 2024 Apr 16;5(4):101485. doi: 10.1016/j.xcrm.2024.101485.
Stage of Development
Proof of principle data available (Cell Reports Medicine, 2024).
Benefits
- Improved understanding of AML relapse mechanisms.
- Establishment of prognostic markers to predict whether a patient will relapse.
- Help clinicians navigate treatment options and disease management to administer personalized approaches for AML patients.
Applications
- Discovery of targets and pathways within the REC population to serve as markers and indicators of AML relapse.
- Diagnostic metrics and tool for AML treatment planning and prognosis.
- Development of targeted therapies aimed at reducing leukemia regeneration via RECs and their associated pathways.