Internal Diseases and Therapy · MU Sofia

67. Chronic myeloid leukemia

Covers chronic myeloid leukaemia, beginning with a comparison of myeloid and lymphoid lineages and a brief overview of the main leukaemia types by lineage and onset. It then describes the disease's epidemiology, the BCR-ABL fusion and Philadelphia chromosome t(9;22), the progression to blast or accelerated phase, typical clinical features such as splenomegaly, and the expected blood and smear findings. It closes with imatinib as the tyrosine kinase inhibitor used for management.

Inside: 1 section · 3 labelled pictures · 12 flashcards · 2 min

Topic 67 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 352 words (2 min of reading), with 12 flashcards.

In this note

  1. Chronic myelogenous leukemia

Chronic myelogenous leukemia

Leukemia is a group of cancers, originating in the bone marrow, that cause high numbers of (immature) white blood cells.

First, we need to remember, what are myeloid and lymphoid cells, and more specifically, what are myeloblasts and lymphoblasts?

Right, types of leukemia

  • We can divide based on the lineage affected:
  • Myeloid
  • Lymphoid
  • And based on onset
  • Chronic
  • Acute

First, let’s take an overall look at the four main types of leukemia.

OK, chronic myeloid leukaemia (CML), this is an uncontrolled proliferation of myeloid cells and it accounts for 15% of leukaemias. It is a type of myeloproliferative disorder (unlike multiple myeloma, which is a plasma cell disorder) and generally affects those aged 40-60 yrs of age with an incidence of about 1 in 100000.

CML sees marked myeloid hyperplasia of the bone marrow, with dysregulation of haematopoiesis due to BCR-ABL gene fusion that causes an abnormal expansion of myeloid cells in the bone marrow and peripheral blood. This gene fusion is known as the so-called Philadelphia chromosome, present in >90% of those with CML, formed by the translocation of chromosome 9 and 22 (t(9;22)).

Image: “Schematic of the Philadelphia Chromosome” by Aryn89, CC BY-SA 4.0, via Wikimedia Commons.

CML is predominantly a chronic condition with slow progression, however around 10% of patients will go through a blast or accelerated phase despite treatment, which eventually results in acute myeloid or acute lymphoblastic leukaemia.

The typical presentation of a CML patient is that of weight loss, tiredness, fever, sweats, along with symptoms such as abdominal fullness. Splenomegaly is found in 75% of patients, and it is often massive, hepatomegaly, anemia and bruising may all also be found.

Tests will show a marked increase in WBC (often >100x10*9) with an increase in all myeloid cells. Hb will be decreased or normal while platelets are variable. The peripheral blood smear will show a marked increase in granulocytes at all stages of maturation (blasts <10%) while cytogenetic analysis should reveal t(9;22).

Management of CML is with the tyrosine kinase inhibitor imatinib, which is well tolerated in most patients with an 8 year survival of about 90%.

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