 Let's look at the myeloid leukemias. The first one we'll talk about is the acute myelogenous leukemia or AML. AML typically shows up at the age of around 65 years of age or older. The most common subtype that's tested on the USMLE is your M3 subtype. More recently they've decided to change up the naming system of this, so you might see this as APL or acute pro-myelogenous leukemia. That and M3 subtype are the same thing, they are interchangeable and that's the most commonly tested one. You see on these our rods, so as you can see in this photo here on the left, these little our rods look like needles or splinters all throughout each leukemia cell and you'll see several of them in this picture here. Those our rods are what can actually cause DIC. Those are can be released from the cell and cause DIC within the the body of an individual that has AML. The M3 subtype is also commonly associated with a translocation 1517 and it is treatable. We treat this with an all trans retinoic acid as well as arsenic. Risk factors for AML include Down syndrome, so this is your Trisomy 21, chemotherapy, a history of chemotherapy, so people that have had chemotherapy way in the past can develop this cancer. Radiation, once again similar to chemotherapy, if you've had a past history of radiation therapy, you can develop AML and then myeloproliferative disorders are a risk factor. For development of AML and finally the last of the myelogenous leukemia that we're going to discuss today is chronic myelogenous leukemia also known as CML. The age of onset for CML is anywhere from 45 to 85 years of age with the median age of about 64 years. CML is associated with the translocation 922 or the Philadelphia chromosome and it is BCR-ABL. CML also is seen as potentially having a blast crisis and what you're seeing in CML are all of these circulating leukemia cells and they're very immature and that blast crisis can actually be an acceleration of the CML into or transforming into AML or ALL. Obviously these increased granulocytes of the immature granulocytes that you're seeing in CML can lead to splinomegaly because those white blood cells are going to be backing up in the spleen as the spleen tries to destroy them and it will cause the spleen to enlarge. We do see a very low level of leukocyte alanine phosphatase. This is a result of low activity in malignant neutrophils, whereas if you have a benign neutrophilia such as a lukemoid reaction, you're going to see the leukocyte alkaline phosphatase stay about normal and maybe decrease a little bit with a neutrophilia in response to those stressors like infections, medications, or severe hemorrhage. To treat CML we use a BCR-ABL tyrosine kinase inhibitor and specifically for CML we're going to use a matinib.