How do I know the stage of my acute myeloid leukemia?

How do I know the stage of my AML? We don't typically think of AML as having a staging system. Because it's a blood cancer circulating around the whole body almost from the point of its inception, there isn't the same type of staging you might be used to in hearing about for lung cancer or breast cancer or colon cancer. It is important in trying to understand each person's AML to try to understand what is driving it. So when we do the tests that I mentioned, the genetics, the molecular testing, etc., to subcategorize the AML, it helps us understand the prognosis. It helps us understand the likelihood of standard chemotherapy helping that patient to attain first a remission and potentially a durable remission or cure. And so there are certain factors such as genetic and molecular changes that specifically tell us that the patient is high risk or poor risk and standard chemotherapy is not likely to help them as much versus at the other extreme of a patient who is likely to have a leukemia that is more sensitive to chemotherapy and thus be considered good risk versus most people which fall in the middle to intermediate risk. What is the difference between good, intermediate, and adverse risk AML? The common probes we look for in AML would be too numerous to elucidate in a setting such as this. But in general, if someone were to be considered to have a good risk or better risk AML, what we mean is usually that is a patient who has a disease that's driven by mutations in core binding factors. And there's a couple of specific mutations that have those driving characteristics. To that group, you add in patients where we don't see genetic changes on the standard fish or cytogenetics, but we see from the molecular testing that we discussed certain things that show us that patient's leukemia is likely more sensitive to the standard chemotherapy. Certain mutations, for instance, in nucleophosamine or CEBPA may indicate that that patient's leukemia is more likely treatable with standard chemotherapy. On the flip side, there's changes which speak to the patient's leukemia being tougher to treat, not as responsive to standard chemotherapy. Certain genetic changes like monosomy 7, but genetic mixed with and complemented with molecular changes can highlight people such as those with an FLT3 or FLT3 mutation. Certain but not all FLT3 mutations speak to a higher risk of standard chemotherapy not helping that patient. Mutations in P53, we understand, are tough to treat with regular chemotherapy. And things such as that would help us better understand the risk strategy that we talked about earlier and then potentially direct the options for therapy.