What is AML?
AML stands for Acute Myeloid Leukemia — a cancer of the blood and bone marrow. In a healthy body, the bone marrow produces blood cells in an orderly way: red cells to carry oxygen, white cells to fight infection, and platelets to help blood clot. In AML, that process goes wrong. Abnormal, immature white blood cells (called blasts) multiply rapidly and crowd out the healthy cells the body needs to function.
“Acute” means it moves fast. This is not a slow-growing cancer. It requires treatment quickly.
AML is different in a specific way that’s worth understanding: because leukemia is a cancer of the blood itself, there is nothing to surgically remove. The disease is systemic from the start, and treatment has to match that — which is why induction chemotherapy for AML involves weeks inpatient, intentionally wiping out the entire bone marrow, healthy cells and cancer alike, and waiting for it to rebuild. It is not more or less hard than what others have faced — it’s simply a different kind of hard at the start.
What is a Mutation?
Every cancer has a genetic fingerprint — specific changes in the DNA of cancer cells that influence how the disease behaves and how it should be treated. These changes are called mutations. They’re not inherited or contagious; they happen in the cancer cells themselves. Identifying a patient’s mutations helps doctors choose the right drugs and predict how the disease will respond to treatment.
AML has several known mutations. The one most relevant to Kevin’s care is FLT3 — a mutation that causes cancer cells to grow and divide more aggressively. It is associated with higher-risk disease and is one of the primary reasons a bone marrow transplant is required for long-term cure.
Kevin’s Mutation: FLT3-Positive
Kevin’s AML is FLT3-positive. This means his cancer carries the FLT3 mutation, which drives more aggressive cell growth and makes the disease harder to control with chemotherapy alone.
Kevin’s AML is FLT3-positive. This means his cancer carries the FLT3 mutation, which drives more aggressive cell growth and makes the disease harder to control with chemotherapy alone.
This is significant for two reasons:
- It is why a bone marrow transplant is the recommended path to cure — chemotherapy can achieve remission, but it cannot hold it indefinitely in FLT3-positive AML.
- It opens the door to targeted therapy. Drugs called FLT3 inhibitors are specifically designed to interfere with the FLT3 mutation’s ability to drive cancer growth. Kevin has been taking one of these — Midostaurin (also known as Rydapt) — alongside his chemotherapy. This class of drug has significantly improved outcomes for patients with FLT3-positive AML compared to chemotherapy alone.
Why a Transplant?
With FLT3-positive AML, the goal of chemotherapy is to achieve and maintain remission long enough to get to transplant. The transplant itself does something chemotherapy cannot: it replaces the bone marrow entirely with donor cells, giving the immune system a fresh start. Those donor cells don’t just rebuild the immune system — they also actively continue to fight any remaining cancer cells. This is called the graft-versus-leukemia effect, and it’s a core reason transplant offers a path to cure rather than just control.
The goal of everything Kevin’s team is doing — every cycle of chemotherapy, every infusion, every carefully timed step — is to get him to transplant in the strongest possible position.