Acute Myelogenous Leukemia (AML) in Children

Acute Myelogenous Leukemia in Children

Key Points:

  • Acute Myelogenous Leukemia (AML) is a rapidly progressing cancer of the blood and bone marrow
  • It accounts for about 20% of childhood leukemias
  • Most common in children under 2 years and teenagers
  • Characterized by overproduction of immature myeloid cells
  • Requires prompt diagnosis and intensive treatment

Acute Myelogenous Leukemia (AML) is a rapidly progressing malignancy of the blood and bone marrow, characterized by the overproduction of immature myeloid cells. In children, AML accounts for approximately 20% of all leukemias, making it the second most common type after Acute Lymphoblastic Leukemia (ALL). AML is most frequently diagnosed in children under 2 years of age and in teenagers, with a slight predominance in males. The disease results from genetic alterations in hematopoietic stem cells, leading to uncontrolled proliferation and impaired differentiation of myeloid progenitor cells.



Acute Myelogenous Leukemia in Children
  1. What percentage of childhood leukemias are Acute Myelogenous Leukemia (AML)?
    Approximately 15-20%
  2. Which AML subtype is most common in children with Down syndrome?
    Acute megakaryoblastic leukemia (AMKL or M7)
  3. What is the characteristic genetic abnormality in acute promyelocytic leukemia (APL)?
    t(15;17) PML-RARA fusion
  4. Which presenting symptom is more common in AML compared to ALL?
    Bleeding or bruising
  5. What is the name of the chromosome abnormality associated with a favorable prognosis in AML?
    t(8;21)
  6. Which drug is used for induction therapy in acute promyelocytic leukemia?
    All-trans retinoic acid (ATRA)
  7. What is the typical number of cycles of intensive chemotherapy used in AML treatment?
    4-5 cycles
  8. Which AML subtype is associated with Auer rods on peripheral blood smear?
    Acute promyelocytic leukemia (APL)
  9. What is the overall cure rate for childhood AML?
    Approximately 60-70%
  10. Which gene is commonly mutated in core-binding factor AML?
    KIT gene
  11. What is the name of the life-threatening complication associated with APL treatment?
    Differentiation syndrome
  12. Which chemotherapy drug is the backbone of AML induction therapy?
    Cytarabine
  13. What is the most common site of extramedullary involvement in AML?
    Skin (leukemia cutis)
  14. Which molecular marker is associated with poor prognosis in AML?
    FLT3-ITD mutation
  15. What is the name of the AML subtype associated with inv(16) or t(16;16)?
    Acute myelomonocytic leukemia with eosinophilia
  16. Which test is used to detect minimal residual disease in AML?
    Multiparameter flow cytometry or PCR
  17. What is the role of hematopoietic stem cell transplantation in childhood AML?
    Indicated for high-risk patients in first remission or any patient in second remission
  18. Which syndrome is associated with an increased risk of developing AML?
    Fanconi anemia
  19. What is the name of the AML subtype characterized by monocytic differentiation?
    Acute monocytic leukemia (M5)
  20. Which chromosome abnormality is associated with therapy-related AML?
    11q23 (MLL) rearrangements
  21. What is the typical duration of maintenance therapy in childhood AML?
    Maintenance therapy is not routinely used in AML
  22. Which organ is most commonly affected by granulocytic sarcoma in AML?
    Orbit (eye)
  23. What is the name of the gene commonly mutated in AML with normal cytogenetics?
    NPM1
  24. Which laboratory finding is characteristic of acute promyelocytic leukemia?
    Disseminated intravascular coagulation (DIC)
  25. What is the name of the AML subtype associated with bilineage or biphenotypic features?
    Mixed phenotype acute leukemia (MPAL)
  26. Which targeted therapy is used in FLT3-mutated AML?
    Midostaurin
  27. What is the most common late effect of anthracycline therapy in AML survivors?
    Cardiomyopathy
  28. Which imaging modality is used to detect CNS involvement in AML?
    MRI of the brain and spine
  29. What is the name of the phenomenon where AML cells infiltrate the gums?
    Gingival hypertrophy
  30. Which epigenetic modifier is commonly mutated in childhood AML?
    DNMT3A


Disclaimer

The notes provided on Pediatime are generated from online resources and AI sources and have been carefully checked for accuracy. However, these notes are not intended to replace standard textbooks. They are designed to serve as a quick review and revision tool for medical students and professionals, and to aid in theory exam preparation. For comprehensive learning, please refer to recommended textbooks and guidelines.





Powered by Blogger.
For mobile users: Use horizontal view or desktop mode for best experience. Please click on an ad before leaving.