DR COLE: So this is a lady that I am currently taking care of. She is 44. She works at one of the casinos in Oklahoma. She had very poor health insurance when she was diagnosed, and she was kind of bounced around from different emergency rooms for her menorrhagia and ultimately settled in our hospital with circulating blasts. So we brought her into the hospital, biopsied her. Her bone marrow had 43% blasts. She has a KIT mutation. She went on to have 7 + 3 with cytarabine and idarubicin. And she also went into complete remission on day 14 and day 28 bone marrows.

So she’s been kind of interesting as far as what to do next for her. Because of her health insurance issues, she was not eligible to be seen by any transplant person in the state of Oklahoma, because they didn’t accept her insurance. And until she was able to secure other type of insurance, that wasn’t on the table for her.

And I don’t think this is unique to just where I live in the country, but there are a lot of people with different ethnicities. She happens to be adopted and of Native American descent. So that kind of plays into what kind of match would be available for her, if and when she is able to get a transplant.

So we went ahead and started consolidation for her, and she has done very well. She has magically been able to get on Oklahoma Medicaid and now is eligible for a transplant. And she is being considered for a haplo.

DR STONE: What are her chromosomes?

DR COLE: She was normal except for the KIT mutation.

DR CORTES: She has children?

DR COLE: She has 3 children, yes.

DR STONE: I think, again, this is a patient that the KIT mutation is — in normal chromosome patients doesn’t really factor into the prognosis right now. Although, I assume she has no FLT3 or NPM1 mutation?

DR COLE: Yes. Those were all negative.

DR STONE: Yeah. So she falls in the same kind of category of a normal chromosome patient without an NPM1 mutation, in whom I would transplant in first CR. Not because of the KIT mutation but because of the absence of the NPM1 mutation, basically. And I think your management has been very great. I would use at least some form of high-dose ara-C-based consolidation, not necessarily 3 grams but at least 1.5 grams/m². I like the CALGB dosing, because that’s the best prospective data. That’s a day 1, 3 and 5 dosing twice a day.

Anyway, I think this bring up a key issue about access to healthcare in America that transcends the management of AML but a very important one as stewards of our healthcare dollars. We don’t want to waste money, but we also want to make sure that people have access to care. And it’s really sad to learn that there are citizens in this country, due to the foibles or our politicians, who don’t have access to healthcare when they should, immediately. It’s something to consider.

DR LOVE: Any comment, Jorge, on strategies that target patients with KIT mutations?

DR CORTES: There have been several attempts at looking into that, because we, of course, have many drugs that are inhibitors of KIT. We talked about some of the FLT3 inhibitors that are c-KIT inhibitors. And many of the ABL kinase inhibitors are KIT inhibitors. So there were trials some time ago with imatinib and with dasatinib. For the most part, those trials were not positive. So in the general patient that has a c-KIT mutation, as Rich mentioned, prognostic implications are probably not relevant, and there’s no good strategy. So I wouldn’t use it.

It’s been a little bit more of a debate on the good-prognostic cytogenetic abnormalities in the translocation 8;21s, where there does seem to be that there is a prognostic implication. Some groups, like ours, have not shown that, but many others have. So I think that there is possibly something there. But the intervention is still questionable. We certainly don’t use, routinely, any of these drugs, because they haven’t been shown to — like, any of these KIT inhibitors. So for the moment, that remains an open question.

DR STONE: But there was a nonrandomized trial led by the Alliance, Guido Marcucci of adding dasatinib to 3 + 7 chemo in patients who had inversion 16 and 8;21, because they have both — about 25% have a c-KIT mutation, which is a bad prognostic feature in that subgroup. And also, the other ones have overexpression of c-KIT, which may be bad. The results, noncontrolled fashion, were encouraging. And the Germans are doing a randomized trial right now in CBF patients of chemo plus or minus dasatinib.

Module 1: Current and future approaches to targeted therapy for acute myeloid leukemia (AML)

Module 2: Other clinical issues in AML management

Module 3: Case discussions