Chronic Myeloid Leukemia
Also written as CML.
chronic myeloid leukemia.\nWhen patients with acute promyelocytic leukemia Airway obstruction refers to a blockage at the level of the
What our notes say
- chronic myeloid leukemia.\nWhen patients with acute promyelocytic leukemia Airway obstruction refers to a blockage at the level of the (Harrisons Pulmonary and Critical Care Medicine)
- *Reciprocal translocation* — exchange of segments between two non-homologous chromosomes (e.g., t(9;22) BCR-ABL in chronic myeloid leukemia). (Genetic Disorders CAT: Key Terms & Inheritance Patterns Explained — CAT)
- Chromosomal translocations — Chronic myeloid leukemia (BCR-ABL, t(9;22)) (Cytopathology vs Histopathology CAT: Definitions & Lab Basics — CAT)
- A 45-year-old woman develops chronic myeloid leukemia (CML). (General Pathology MCQs: Cancer, Tumors & Molecular Path Review — MCQ Bank)
- This creates the Philadelphia chromosome associated with chronic myeloid leukemia, producing the BCR-ABL fusion gene. (Oncopathology And Genetic Disorders End Semester Cat — CAT)
Practice questions on Chronic Myeloid Leukemia
A 45-year-old woman develops chronic myeloid leukemia (CML). Cytogenetic analysis reveals a reciprocal translocation between chromosomes 9 and 22. The resultant fusion gene codes for a protein with which abnormal activity?
- Inhibition of tyrosine kinase activity
- Constitutive activation of tyrosine kinase activity
- Inhibition of serine/threonine kinase activity
- Constitutive activation of serine/threonine kinase activity
Answer: B. The translocation between chromosomes 9 and 22 creates the Philadelphia chromosome, resulting in the BCR-ABL fusion gene. This fusion gene encodes a constitutively active tyrosine kinase, which drives the uncontrolled proliferation of myeloid cells seen in CML.
A 45-year-old woman with chronic myeloid leukemia (CML) is found to have a reciprocal translocation between chromosomes 9 and 22. The resultant fusion gene codes for a protein with which abnormal activity?
- Inhibition of apoptosis
- Decreased DNA repair
- Constitutive tyrosine kinase activity
- Autocrine growth factor production
Answer: C. The Philadelphia chromosome (t(9;22)) in CML results in the fusion of the BCR and ABL genes, creating the BCR-ABL fusion gene. This gene encodes a constitutively active tyrosine kinase that drives uncontrolled cell proliferation, a hallmark of CML.
In chronic myeloid leukemia, the BCR-ABL fusion protein drives malignancy primarily by
- Enhancing DNA repair mechanisms
- Increasing p53-mediated apoptosis
- Constitutive tyrosine kinase activity without regulation
- Blocking cyclin D synthesis
Answer: C. The BCR-ABL fusion results from t(9;22) translocation and causes loss of the regulatory region controlling tyrosine kinase activity, leading to continuous mitogenic signaling.
In chronic myeloid leukemia (CML), the BCR-ABL fusion protein drives malignancy primarily by:
- Inhibiting apoptosis
- Increasing tyrosine kinase activity
- Binding to p53
- Inducing DNA damage
Answer: B. The t(9;22) Philadelphia chromosome creates the BCR-ABL fusion gene, which encodes a constitutively active tyrosine kinase that promotes uncontrolled proliferation.