It has taken me a long time to understand what AML is, and I still have much more to learn. I thought I'd compile some of my thoughts about what I've learned. So much of what I've studied doesn't make sense because I don't know what all of the scientific terms mean. But, I've tried to understand what I feel is important and I thought I'd share some of it with you. I hope that it makes sense to you and that it helps you understand more about AML.
AML stands for Acute Myeloid Leukemia. Leukemia is a broad term for several types of blood or bone marrow cancers. Some Leukemias are: Acute Myeloid Leukemia (AML), Acute Lymphoblastic Leukemia (ALL), Cronic Lympoblastic Leukemia (CLL), Cronic Myeloid Leukemia (CML). In acute leukemia, the cells grow very rapidly. A single Leukemia cell can divide from 1 cell into 2 billion cells in roughly 16 days.
Erin had AML type M7. There are 8 types of AML: M0 - M7. M7 means that she had Megakaryocytic Leukemia. Let me explain. Please look at the chart below that I copied from my sister's high school Physiology book. I guess high school was more useful than I thought. Everything made so much more sense once I studied this chart.
Looking to the development of blood I first saw that a stem cell (the top blob that looks like a pink fried egg) will either divide into a myeloid stem cell (the left arrow) or a lymphoid stem cell (the right arrow). In Erin's case, I looked at the myeloid stem cell (left arrow). It then turns into a Megakaryblast (the biggest pink blob on the left side) which turns into a platelet (they look like jelly beans).
In Erin's case of AML, the stem cells in her bone marrow (specifically, the Megakaryoblasts) made many abnormal cancerous cells instead of platelets. The cancer cells are called blasts because they look similar to normal immature blast cells. Instead of becoming normal mature platelets, the cancerous cells divided rapidly and uncontrollably, they were unable to mature and work like normal blast cells, and they don't die easily. Eventually, these megakaryoblasts filled up Erin's bone marrow, preventing normal cells from being made. Then, they built up in her bloodstream. They can also invade the lymph nodes, brain, skin, liver, kidneys, and other organs. Thankfully, we caught Erin's leukemia early enough on that it hadn't spread past her bone marrow and blood.
Her pale skin and her many bruises were what made us have Erin's blood work checked out in the first place. The picture below is what a smear of her blood work might have looked like. The purple blobs are the mixed up megakaryoblasts (cancer).
One third of children with AML type M7 have a chromosome translocation t(1;22)(p13;q13). Another third are Down Syndrome and the last third are heterogeneous. In looking even deeper into Erin's chromosomes, 10% of the cells counted in a chromosome analysis done on her bone marrow sample had this t(1;22)(p13;p13) translocation, the other 90% of the cells showed a normal female chromosome complement. The translocation involved a fusion of the RBM15 and MKL1 genes. Did you understand that? Ha ha, neither did I. To the 1% out there that understood that, please give yourself a pat on the back.
I wish I knew more about genetics, I really don't understand any of the translocation, but from what I was told, recent data showed that patients with this translocation respond well to intensive AML chemotherapy. The most important thing to me was helping Erin fight AML. And, if her genetics say that she'll respond well, that is good enough understanding for me.