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Clinical and laboratory features of seven patients with acute myeloid leukemia (AML)-M2/M3 and elevated myeloblasts and abnormal promyelocytes.

He G, Wang C, Li Q, Tan H, Chen F, Huang Z, Yu B, Zheng L, Zheng R, Liu D - Cancer Cell Int. (2014)

Bottom Line: The PML/RARα fusion gene was present in six patients and two patients presented a mixed PML/RARα and AML1/ETO genotype.Five cases achieved CR and two cases did not achieve remission and one case transform into AML-M2 after CR1.The clinical and laboratory features of seven patients with AML-M2/M3 are demonstrated in the present study, providing information on the FAB sub-classification.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, The First Affiliated Hospital of Guangzhou Medical University, No. 1 Kangda Road, Haizhu District, 510000 Guangzhou, China.

ABSTRACT

Background: There is limited information on a special subtype of Acute myeloid leukemia (AML) characterized by >20% myeloblasts and >20% abnormal promyelocytes in bone marrow and peripheral blood.

Objective: The objective of the present investigation was to explore the clinical and laboratory features of seven patients with AML-M2/M3.

Method: We retrospectively assessed cell morphology, cytochemistry, immunophenotype, cytogenetics, and clinical features of seven patients with this rare subtype of AML.

Results: All seven cases had thrombocytopenia, coagulation abnormalities, >20% myeloblasts and abnormal promyelocytes. The PML/RARα fusion gene was present in six patients and two patients presented a mixed PML/RARα and AML1/ETO genotype. Five cases achieved CR and two cases did not achieve remission and one case transform into AML-M2 after CR1.

Conclusions: The clinical and laboratory features of seven patients with AML-M2/M3 are demonstrated in the present study, providing information on the FAB sub-classification.

No MeSH data available.


Related in: MedlinePlus

Y:Nested RT-PCR for Case 7: M: marker. 1 − 7: PML/RARа fusion gene. 1: mutation, type S positive control; 2: patient type S PCR products; 3: type S positive control; 4: healthy control, type S PCR products; 5: type L positive control; 6: patient type L PCR products; 7: healthy control, type L PCR products. 8-10: AML1/ETO fusion gene; 8: positive control; 9: patient PCR products; 10: healthy control PCR products.
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Fig3: Y:Nested RT-PCR for Case 7: M: marker. 1 − 7: PML/RARа fusion gene. 1: mutation, type S positive control; 2: patient type S PCR products; 3: type S positive control; 4: healthy control, type S PCR products; 5: type L positive control; 6: patient type L PCR products; 7: healthy control, type L PCR products. 8-10: AML1/ETO fusion gene; 8: positive control; 9: patient PCR products; 10: healthy control PCR products.

Mentions: Bone marrow smears revealed 49% myeloblasts and 13% abnormal promyelocytes, while the cells in the PB smear were 14% myeloblasts and 13% promyelocytes. The BM cells harbored both the PML/RARа fusion gene, S type, and the AML1/ETO fusion gene. Immunophenotyping by FCM revealed two groups of blast cells. The SSC lower cell group was approximately 44.9% of the total and this population was 13.5% CD11b(+), 90.8% CD13(+), 40.3% CD15(+), 82.6% CD33(+), 62.3% CD34(+), 12.4% CD56(+), 40.3% CD64(+), 88.0% CD117(+), 85.9% HLA-DR (+), and 97.8% cMPO(+), while no antigens of other lineages were expressed. The SSC lower cell group was approximately 48.3% of the total and this population was 46.6% CD11b(+), 94.9% CD13(+), 17.3% CD14(+), 95.3% CD15(+), 83.0% CD33(+), 26.1%(+) CD56, 70.4% CD64(+), 43.8% CD117(+), 35.0% HLA-DR(+), and 98.9% cMPO(+). Antigens of other lineages were not expressed (Figure 3).Figure 3


Clinical and laboratory features of seven patients with acute myeloid leukemia (AML)-M2/M3 and elevated myeloblasts and abnormal promyelocytes.

He G, Wang C, Li Q, Tan H, Chen F, Huang Z, Yu B, Zheng L, Zheng R, Liu D - Cancer Cell Int. (2014)

Y:Nested RT-PCR for Case 7: M: marker. 1 − 7: PML/RARа fusion gene. 1: mutation, type S positive control; 2: patient type S PCR products; 3: type S positive control; 4: healthy control, type S PCR products; 5: type L positive control; 6: patient type L PCR products; 7: healthy control, type L PCR products. 8-10: AML1/ETO fusion gene; 8: positive control; 9: patient PCR products; 10: healthy control PCR products.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325959&req=5

Fig3: Y:Nested RT-PCR for Case 7: M: marker. 1 − 7: PML/RARа fusion gene. 1: mutation, type S positive control; 2: patient type S PCR products; 3: type S positive control; 4: healthy control, type S PCR products; 5: type L positive control; 6: patient type L PCR products; 7: healthy control, type L PCR products. 8-10: AML1/ETO fusion gene; 8: positive control; 9: patient PCR products; 10: healthy control PCR products.
Mentions: Bone marrow smears revealed 49% myeloblasts and 13% abnormal promyelocytes, while the cells in the PB smear were 14% myeloblasts and 13% promyelocytes. The BM cells harbored both the PML/RARа fusion gene, S type, and the AML1/ETO fusion gene. Immunophenotyping by FCM revealed two groups of blast cells. The SSC lower cell group was approximately 44.9% of the total and this population was 13.5% CD11b(+), 90.8% CD13(+), 40.3% CD15(+), 82.6% CD33(+), 62.3% CD34(+), 12.4% CD56(+), 40.3% CD64(+), 88.0% CD117(+), 85.9% HLA-DR (+), and 97.8% cMPO(+), while no antigens of other lineages were expressed. The SSC lower cell group was approximately 48.3% of the total and this population was 46.6% CD11b(+), 94.9% CD13(+), 17.3% CD14(+), 95.3% CD15(+), 83.0% CD33(+), 26.1%(+) CD56, 70.4% CD64(+), 43.8% CD117(+), 35.0% HLA-DR(+), and 98.9% cMPO(+). Antigens of other lineages were not expressed (Figure 3).Figure 3

Bottom Line: The PML/RARα fusion gene was present in six patients and two patients presented a mixed PML/RARα and AML1/ETO genotype.Five cases achieved CR and two cases did not achieve remission and one case transform into AML-M2 after CR1.The clinical and laboratory features of seven patients with AML-M2/M3 are demonstrated in the present study, providing information on the FAB sub-classification.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, The First Affiliated Hospital of Guangzhou Medical University, No. 1 Kangda Road, Haizhu District, 510000 Guangzhou, China.

ABSTRACT

Background: There is limited information on a special subtype of Acute myeloid leukemia (AML) characterized by >20% myeloblasts and >20% abnormal promyelocytes in bone marrow and peripheral blood.

Objective: The objective of the present investigation was to explore the clinical and laboratory features of seven patients with AML-M2/M3.

Method: We retrospectively assessed cell morphology, cytochemistry, immunophenotype, cytogenetics, and clinical features of seven patients with this rare subtype of AML.

Results: All seven cases had thrombocytopenia, coagulation abnormalities, >20% myeloblasts and abnormal promyelocytes. The PML/RARα fusion gene was present in six patients and two patients presented a mixed PML/RARα and AML1/ETO genotype. Five cases achieved CR and two cases did not achieve remission and one case transform into AML-M2 after CR1.

Conclusions: The clinical and laboratory features of seven patients with AML-M2/M3 are demonstrated in the present study, providing information on the FAB sub-classification.

No MeSH data available.


Related in: MedlinePlus