What is Chronic Myeloid Leukemia?
Chronic myeloid leukemia (CML) starts with an abnormal change, or mutation, in a cell’s DNA that creates a chromosome known as the Philadelphia (Ph) chromosome.
- When the Ph chromosome is present in cells, a protein known as BCR-ABL is produced
- The BCR-ABL protein causes the bone marrow to produce abnormal white blood cells
- These abnormal cells are CML cells. Over time, they overtake healthy white blood cells in the bone marrow to cause leukemia
In CML, abnormal cells crowd out healthy cells in the bone marrow
CML is a progressive disease
There are 3 phases, or stages, of CML that represent different levels of progression. Ranging from least severe to most severe, the phases are:
Treating CML with TKI therapy
Many people with CML are treated with a type of targeted therapy known as a tyrosine kinase inhibitor, or TKI. The protein that causes CML, BCR-ABL, is a tyrosine kinase protein. The TKIs used to treat CML specifically inhibit BCR‑ABL. They help stop abnormal white blood cells, or CML cells, from forming in the body.
Monitoring your response to treatment
The goal of CML treatment is to keep your levels of BCR-ABL as low as possible. This can help reduce the number of CML cells in your body. Your doctor may do molecular or cytogenetic tests on cells from your bone marrow or blood to see how well a treatment is working.
One term your doctor may use to describe the results of these tests is log reduction. This is a measure of how much BCR-ABL levels have been lowered. Log reductions typically mean that a treatment is working well to control CML.
Not an actual doctor. / Not an actual patient.
Understanding BCR-ABL mutations, including T315I, and how they affect treatment
Why and how to get tested for BCR-ABL mutations
Sometimes medications start to lose their effectiveness over time. If you see your BCR-ABL levels rise, this may be due to treatment resistance. One reason your treatment may become resistant is that over time, your CML has developed a mutation. A mutation is a change in a gene. For CML, it is a change in the BCR-ABL protein. This may cause a particular treatment to stop working.
T315I is the most common BCR-ABL mutation. Your doctor should test your blood for the BCR-ABL protein, specifically the T315I mutation, and monitor your BCR-ABL levels every 3, 6, and 12 months when you're on treatment.
There are only a few CML treatments that have been specifically designed to treat people with a T315I mutation. ICLUSIG was the first FDA-approved TKI to treat people with the T315I mutation.
Your mutation status may change throughout your treatment journey. The presence of mutations plays an important role in your next treatment decision. Ask your doctor about mutation testing to ensure you are on the right track for your therapy.
How mutations may affect your treatment journey
When your TKI treatments along with other genetic factors cause the T315I mutation, ask your doctor about ways to regain your treatment effectiveness. Your doctor may recommend that you change to a different TKI that works better against the mutation.
How ICLUSIG benefits adults with mutations, including the T315I mutation
The goal of treating your CML is to reduce the levels of BCR-ABL and keep them low.
If your BCR-ABL levels rise, this may be due to treatment resistance caused by a mutation. The T315I mutation in particular is present in a significant number of patients who are resistant to therapy. ICLUSIG was the first TKI to be approved to treat people with the T315I mutation.