A 34-year-old man presents with symptoms of fatigue, weakness, nose bleeds, and palpitations with exertion. On examination he is pale, blood pressure 110/70 mm Hg, pulse 100/min, heart sounds are normal, lungs are clear, and he has multiple petechiae and bruises on his legs. His blood count is abnormal: hemoglobin 8.5 g/dL white blood cells (WBCs) 4000/mL, platelets 50,000/mL, and there are blast cells in the peripheral blood. He is diagnosed with acute promyelocytic leukemia (AML-M3). Which of the following is a characteristic of this acute myelogenous leukemia? (See Fig. below.)
A 34-year-old man presents with symptoms of fatigue, weakness, nose bleeds, and palpitations with exertion. On examination he is pale, blood pressure 110/70 mm Hg, pulse 100/min, heart sounds are normal, lungs are clear, and he has multiple petechiae and bruises on his legs. His blood count is abnormal: hemoglobin 8.5 g/dL white blood cells (WBCs) 4000/mL, platelets 50,000/mL, and there are blast cells in the peripheral blood. He is diagnosed with acute promyelocytic leukemia (AML-M3). Which of the following is a characteristic of this acute myelogenous leukemia? (See Fig. below.)
💡 Explanation
## **Core Concept**
Acute promyelocytic leukemia (APL), also known as AML-M3, is a subtype of acute myeloid leukemia (AML) characterized by the abnormal promyelocytes in the bone marrow and peripheral blood. APL is associated with a specific chromosomal translocation, t(15;17), which leads to the formation of the PML-RARA fusion gene. This genetic abnormality plays a crucial role in the pathogenesis of APL.
## **Why the Correct Answer is Right**
The correct answer, , is associated with the presence of the t(15;17) chromosomal translocation and the PML-RARA fusion gene, which is a hallmark of acute promyelocytic leukemia (AML-M3). This translocation results in the disruption of the normal function of the retinoic acid receptor-alpha (RAR-alpha) and promyelocytic leukemia (PML) genes, leading to the accumulation of immature promyelocytes in the bone marrow and peripheral blood. The presence of this specific genetic abnormality is diagnostic for APL and guides the targeted therapy with all-trans retinoic acid (ATRA) and arsenic trioxide.
## **Why Each Wrong Option is Incorrect**
- **Option A:** This option is incorrect because it does not specifically relate to the characteristic genetic abnormality or the typical morphological features of APL.
- **Option B:** This option is incorrect as it does not accurately represent the specific chromosomal translocation or the fusion gene associated with APL.
- **Option C:** Although not explicitly listed, any option not associated with the t(15;17) translocation and PML-RARA fusion gene would be incorrect.
## **Clinical Pearl / High-Yield Fact**
A key clinical pearl for APL (AML-M3) is the association with disseminated intravascular coagulation (DIC), which is a life-threatening complication. The presence of the t(15;17) translocation and the PML-RARA fusion gene makes APL highly responsive to treatment with all-trans retinoic acid (ATRA) and arsenic trioxide, which can induce complete remission in many patients.
## **Correct Answer: C.**
✓ Correct Answer: D. Auer bodies in blast cells
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