Internal Diseases · MU Sofia

Theory · 49. Chronic myeloid leukemia

Covers the definition of chronic myeloid leukaemia as a BCR-ABL driven myeloproliferative neoplasm, then its three phases: chronic, accelerated and blast crisis. Also outlines risk factors, the Philadelphia chromosome, pathogenesis, symptoms including leukostasis-related eye findings, physical signs, and blood, marrow and cytogenetic or molecular tests. Finishes with treatment by phase, mainly tyrosine kinase inhibitors, and prognosis with monitoring by BCR-ABL PCR.

Inside: 10 sections · 4 labelled pictures · 15 flashcards · 3 min

Topic 46 of 88 in the MU Sofia syllabus for Internal Diseases (Dental Medicine, Year 4). The free AceMed note covers it in 10 sections, about 373 words (3 min of reading), with 15 flashcards.

In this note

  1. Chronic Myeloid Leukemia (CML)
  2. Definition:
  3. Classification (Phases of CML):
  4. Etiology:
  5. Pathogenesis:
  6. Symptoms:
  7. Diagnosis:
  8. Laboratory Tests:
  9. Treatment:
  10. Prognosis:

Definition:

Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm characterized by:

  • Excessive proliferation of mature and maturing granulocytes (especially neutrophils, eosinophils, basophils)
  • Caused by a reciprocal translocation t(9;22) → Philadelphia chromosome, resulting in the BCR-ABL fusion gene, which encodes a constitutively active tyrosine kinase.
  • Accounts for ~15% of all leukemias, affecting mostly adults between 40–60 years.

Classification (Phases of CML):

  1. 1. Chronic phase (CP):
  • Most patients present in this phase (often asymptomatic or mild symptoms)
  1. 2. Accelerated phase (AP):
  • Worsening symptoms, increased blasts, cytopenias
  1. 3. Blast crisis (BC):
  • Resembles acute leukemia (AML or ALL) with >20% blasts in blood/marrow

Etiology:

General Risk Factors:

  • Ionizing radiation: DNA damage to hematopoietic precursors
  • Chemical exposure: Benzene
  • Genetic predispositions
  • Viruses: HTLV-1 (more relevant to T-cell leukemia but mentioned as general risk)

Specific Etiology:

  • Philadelphia chromosome (t(9;22)):
  • ABL gene on chromosome 9 fuses with BCR gene on chromosome 22
  • Forms BCR-ABL fusion gene → constitutive activation of tyrosine kinase
  • Drives uncontrolled proliferation and resistance to apoptosis

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