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Know Your Diagnosis: How Do AML Cells Change Over Time?

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Published on March 28, 2018

How do acute myeloid leukemia (AML) cells arise and interact with the body? How do these cancer cells typically evolve over time?  AML experts Dr. Ross Levine and Dr. Gwen Nichols joined Patient Power to discuss the fundamental biology patients should know about their condition, how AML cells can change, and the latest research on genetic predispositions to the disease. Watch now to learn more about the AML disease course. 

This is a Patient Empowerment Network program produced by Patient Power, in partnership with The Leukemia & Lymphoma Society (LLS). We thank Astellas, Celgene Corporation, Novartis, Pfizer and Seattle Genetics for their support.

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Transcript | Know Your Diagnosis: How Do AML Cells Change Over Time?

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That's how you’ll get care that's most appropriate for you.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

Andrew Schorr:

So you may be watching this because, maybe very recently, you or a loved one were told you have AML. 

And you said oh, my God. So, Ross, could you just define it for us a little bit? First of all, I’m aware that some people with myelofibrosis can transform or be seen to transform. And I know a wonderful gentleman with the MPN Research Foundation. He’s had polycythemia vera for years, quickly switched to myelofibrosis, and I think he’s even having a transplant in New York right now. Things can change. So what’s happening with the cells? What’s going on and from myelodysplastic syndrome, too?

Dr. Levine:            

A lot of great questions. I would say a couple of things. First thing I’d say is that acute myeloid leukemia, or AML, is really a disease where very immature blood cells get stuck. And instead of becoming all of the different types of blood cells you need, in your body, red cells to carry oxygen, platelets to help clot, white cells to fight infections, instead of those stem cells, which normally replenish those cells on an ongoing basis, the changes in the DNA sequence and other biological events in the wiring get that cell stuck in a stem cell like state.

And it, basically, overtakes everything. It becomes a mass of undifferentiated leukemia cells. So when people ask me what leukemia is, that’s what an acute leukemia is. It’s important to understand though that that’s not what MDS or a disease like polycythemia myelofibrosis fundamentally is. There are some similarities. MDS patients can have the same inability to make all of the cells. But, usually, you still make some of the cells. It’s just they’re not quite made right or at the same rate.

And a situation like polycythemia vera and, to some degree, myelofibrosis, you actually make too many cells. And so, that means that there is a switch that gets flipped when the disease goes from a myelodysplasia or polycythemia vera or myelofibrosis to AML.

Where there’s another thing where those cells get stuck even earlier or further. And that’s important because we don’t really, fundamentally, believe or understand yet that the people that come in and have AML as their first thing, probably it’s different subtypes of those 20 than the people that start with MDS or MPN. So if you look at those 20 subtypes, the people that go from MDS to AML or from MPN to AML, they don’t spread out into all of those subtypes. They’re, actually, almost subtypes in and of themselves.

And we think those we’ll need in the long term, ultimately, different treatments than the other flavors where people walk in and have it at the beginning. And there are molecular reasons why that we, at least partially, understand.

So, going back to something you said earlier, it’s really so important to understand what version of AML do you have. What was your history? How did you get there? 

So, Gwen, do we have any idea where this comes from? Let’s just say, you walk in, if you will, AML, de Novo, did I do something to develop it?

Dr. Nichols:         

So, the majority of patients, we have no idea, at the current time, what predisposes them to get leukemia. We’re learning some very interesting data, especially for AML and the elderly, that there may be clones that all of us have, as we age, that start to—are harbored in your bone marrow for a length of time. But we still don’t know what that switch is or that trigger that makes those clones stop maturing, as Ross has talked about, and get arrested at an early stage and become leukemia. We’re supporting a lot of research to try and look at that because, if we understood that switch, we could try and prevent the change from one to another.

And I think we have been behind a lot of other types of cancers in understanding predisposition in this disease. It’s usually only very significant other medical illnesses like myelodysplastic syndrome that we know transfer, or toxic exposures that the great majority of people do not have. So we’re also looking at environmental and genetic predispositions. But I think there’s some fundamental biology that we still need to understand.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

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