Acute Myeloid Leukemia Could Have a New Treatment

            Leukemia is a cancer of the blood. Acute Myeloid Leukemia (AML) is one of the many forms of the disease, and it is the most common leukemia in adults. AML is notorious for its deteriorating progression, and how the cancer can quickly interfere with typical systems in our body. AML, specifically, has been identified as originating in bone marrow, and it actively prevents the normal production and development of blood cells. 

 When cells are immature, they do not have a “job” or a “role” in the body yet. The function of the cell is developed as it matures and “differentiates” into the career the body tells it to follow. However, sometimes, as cells mature, they can mature abnormally, and this often results in tumors— large, atypical cell growth that can either be benign (harmless) or malignant (cancerous). Immature blood cells are commonly found in bone marrow, where AML originates. Cancerous cells, or even immature cells that will become cancerous, can prolong the disease in people and remain even after copious amounts of treatment. They can do so by simply proliferating rapidly, but also by impacting other body systems.

 Relapsing AML can occur when not all cancerous cells are eliminated during treatment, and this, unfortunately, is common. Immature leukemic cells can develop and damage immune system pathways that would otherwise target these abnormal cells, ensuring that they continue to grow and spread. 

Prior research determined a specific enzyme (a protein) in the body that affects the dysfunctions of the immune pathways. This enzyme, called “UBE2N “, could present researchers with a target to stop the harm brought to immune pathways by cancerous cells, and this is precisely what some researchers have been focusing on. 

This photo from the Leukemia & Lymphoma Society of Canada depicts normal blood from bone marrow and blood affected by AML

    

            While earlier research found a general connection between damage to immune pathways and abnormalities in blood cells, research focused on AML pathways was still infantile. Recently, researchers have identified how immature blood cells in AML patients can influence immune pathways, and how restricting UBE2N can be a potential therapy. 

These are fluorescent-stained UBE2N-antibodies: they are used to make proteins appear fluorescent by attaching to the targeted enzyme; in this case, UBE2N

This recent research established just how essential UBE2N is to promoting leukemic cells to manipulate immune pathways. Using patient-cell lines means that this finding was corroborated in human cells, as well as being confirmed in mice. After establishing UBE2N’s malignant role, the researchers then used small molecules to inhibit the ability of the UBE2N enzyme to function. Inhibiting UBE2N resulted in some major positive detections: not only did the body’s immune pathways regain normal function, but leukemic cells were terminated as a result. All this was accomplished without harming normal cells, as some cancer therapies unfortunately do. 

But what does this mean for AML patients?

The researchers hope that this finding can contribute to future research on inhibiting harmful enzymes in cancer patients. There is no guarantee that inhibiting one enzyme will be a “cure”, but it is a definitive step in a promising direction. Meanwhile, the inhibiting of UBE2N can still have therapeutic effects, and researchers think that, in tandem with other therapies, targeting UBE2N will open a new door to beating diseases like AML, with limited relapse.