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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 7  |  Issue : 1  |  Page : 115-120

Acute myeloid leukemia: Comparing French–American–British classification with immunophenotype and cytogenetics


1 Department of Pathology, Shri Dharmasthala Manjunatheshwara University, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India
2 Department of Hematology, Shri Dharmasthala Manjunatheshwara University, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka, India

Date of Submission20-Dec-2021
Date of Decision20-Mar-2022
Date of Acceptance22-Mar-2022
Date of Web Publication27-Jun-2022

Correspondence Address:
Dr. Girish Kamat
Department of Hematology, Shri Dharmasthala Manjunatheshwara University, SDM College of Medical Sciences and Hospital, Dharwad, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjhs.bjhs_138_21

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  Abstract 


BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease as it affects multiple lineages of hematopoietic cells.
AIMS AND OBJECTIVES: This study aims to (1) evaluate the immunophenotypic findings of AML patients, (2) correlate the morphological subtypes of AML according to French–American–British classification with immunophenotypic findings, and (3) correlate the immunophenotypic findings in AML patients with findings in cytogenetic studies.
MATERIALS AND METHODS: The present study was a cross sectional study. Seventy three patients with a final diagnosis of AML, whose immunophenotyping and/or cytogenetic study results were available, were included in the study.
RESULTS: Twenty one (31.81%) out of 66 patients with AML aberrantly expressed lymphoid antigens. The lymphoid antigens expressed were CD7, CD19, TdT, and CD5 which were found in 13 (19.69%), 9 (13.6%), 2 (3%), and 1 (1.51%) patient, respectively. Two out of three patients with t(8;21)(q22;q22) had CD19 aberrant expression. This association was found to be statistically significant with the Fisher exact test, with a statistic value of 0.0277 (P < 0.05). Co expression of two lymphoid antigens such as CD7 and CD19 was associated with monosomy 7 and was found to be statistically significant with a Fisher exact test, with a statistic value of 0.0217 (P < 0.05). In our study, t(8;21) (q22;q22) was found in AML M2 and AML M1. Many of the patients in our study were diagnosed as acute leukemia by morphological evaluation and were not diagnosed as AML. However, immunophenotyping and cytogenetics helped in getting final diagnosis of such patients.
CONCLUSION: In conclusion, this study highlights the importance of morphological, immunophenotypic, and cytogenetic evaluations in the diagnosis of AML.

Keywords: Acute myeloid leukemia, cytogenetics, immunophenotyping


How to cite this article:
Rao M, Kamat G, Goni D, Balikai G. Acute myeloid leukemia: Comparing French–American–British classification with immunophenotype and cytogenetics. BLDE Univ J Health Sci 2022;7:115-20

How to cite this URL:
Rao M, Kamat G, Goni D, Balikai G. Acute myeloid leukemia: Comparing French–American–British classification with immunophenotype and cytogenetics. BLDE Univ J Health Sci [serial online] 2022 [cited 2022 Aug 16];7:115-20. Available from: https://www.bldeujournalhs.in/text.asp?2022/7/1/115/348265



Acute myeloid leukemia (AML) is a group of malignant hematopoietic neoplasms.[1] It is a heterogeneous disease, as it affects multiple lineages of hematopoietic cells.[2] AML most commonly affects adults.[3] In 1976, pathologists from France, the United States, and Great Britain suggested a classification system for AML and acute lymphoblastic leukemia. This was called French, American, and British (FAB) classification. This classification was an effort to improve concordance among different pathologists in an era when morphological examination was the only available tool for the diagnosis of AML. Because of this classification system, pathologists were able to subclassify AML into clinically and biologically distinct subtypes.[4] However, this classification was not objective and failed to identify AML cases when morphology was not typical. Immunophenotyping played a major role in the diagnosis of AML, when morphological interpretation was difficult.[5] Furthermore, some markers had prognostic significance. Cytogenetic analysis helps us to know the molecular basis of the disease. Present WHO classification stresses on Immunophenotyping and cytogenetic studies along with morphological evaluation for exact categorization of AML. However, because of lack of facilities, FAB classification continues to be used by many pathologists across India.[6]

This study aims to (1) evaluate the immunophenotypic findings of AML patients, (2) correlate the morphological subtypes of AML according to FAB classification and immunophenotypic findings, and (3) correlate the immunophenotypic findings in AML patients with findings of cytogenetic studies.


  Materials and Methods Top


The present study was a cross-sectional study. Seventy-three patients with a final diagnosis of AML, whose immunophenotyping and/or cytogenetic reports were available, were included in the study. Patients in blast crises of chronic myeloid leukemia and biphenotypic leukemia were excluded from the study. Patients diagnosed between January 2017 and December 2020 were included in the present study.

The medical records of these 73 patients were reviewed to collect patient details such as age and sex. Bone marrow (BM) aspirate smears were available for morphologic evaluation. They were stained with Wright-Giemsa stain for microscopic evaluation.

BM aspirate samples of 66 patients were studied by flow cytometry using the machine BD FACSDiva 8.0.2. BM samples of the remaining seven patients were not subjected to flow cytometry analysis, as patients declined further evaluation or treatment due to financial constraints. An acute leukemia panel included the markers, CD7, CD19, CD79a, CD11c, CD11b, CD13, CD15, CD14, CD33, CD64, CD117, MPO, CD34, CD45, HLA-DR, CD5, TdT, CD14, CD71, CD41a, CD61, and CD38. Staining of more than 20% of cells with a particular marker was considered to be positive.

Cytogenetic reports of 46 patients were available for analysis. Reports of the remaining 27 patients were not available, either because of failure of getting metaphases or lack of testing due to financial constraints. Cytogenetic analysis was done on 24 h unstimulated cultures on RPMI 1640, Hi-Karyol media. Metaphases were captured at banding resolution of 450–550 with “G bands by Trypsin and Giemsa” banding technique.

For real-time polymerase chain reaction (RT-PCR), peripheral blood samples were sent in 27 patients. This was done in only those patients who were willing for treatment. Peripheral blood was sent, as a repeat, BM aspiration procedure was not possible. This analysis was not done in 46 patients, as they were not willing for further evaluation due to financial constraints. Blood was sent in ethylenediaminetetraacetic acid anticoagulant to detect specific gene rearrangements and mutations associated with AML such as PML-RARA, NPM1 mutation, t(8;21), Inv (16), FLT3-ITD mutation, and BCR-ABL1. These tests were done by in-house developed assay designed as per Europe Against Cancer protocol. In brief, the 5′ nuclease assay (TaqMan technology) uses a single internal oligonucleotide probe bearing a 5′ reporter fluorophore (e.g., 6-carboxyfluorescein) and 3′ quencher fluorophore (e.g., 6-carboxytetramethylrhodamine). During the extension phase, the TaqMan probe is hydrolyzed by the nuclease activity of the Taq polymerase, resulting in the separation of the reporter and quencher fluorochromes and consequently in an increase in fluorescence. All the PCR reactions were performed on a 7700 ABI platform (Applied Biosystems, Foster City, USA) using primers and TaqMan probes kindly provided by Applied Biosystems in conjunction with the TaqMan Universal Master Mix purchased from the same manufacturer. The number of amplification cycles was 50.

Statistical analysis was done by calculating mean and proportions. Fisher exact test was done to calculate statistically significant association considering a P < 0.05.


  Results Top


There were a total of 73 patients with a final diagnosis of AML. The mean age was 39.27 years (range: 4 years–83 years). Thirty-nine (53.42%) patients were males. Thirty-four (46.57%) patients were females. The male-to-female ratio was 1.14:1. AML was further subclassified based on morphology in BM aspirate smears [Table 1].
Table 1: Classification of 73 patients with acute myeloid leukemia based on morphology in bone marrow aspirate smears

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Immunophenotyping

Immunophenotyping by flow cytometry was done in 66 patients. In remaining patients, flow cytometry was not possible due to financial constraints. The most common antigens that were positive were CD13, CD33, CD45, MPO, CD117, CD64, CD34, and HLA-DR, which were found in 96.96%, 93.93%, 89.39%, 87.87%, 80.3%, 63.63%, 60.6%, and 48.48% of patients, respectively.

Aberrant expression of lymphoid antigens

Twenty (31.81%) patients out of 66 patients aberrantly expressed lymphoid antigens. Four (6.06%) patients expressed two lymphoid antigens. Rest of the 17 (25.75%) patients expressed a single lymphoid antigen. The lymphoid antigens expressed were CD7, CD19, TdT, and CD5 which were found in 13 (19.69%), 9 (13.6%), 2 (3%), and 1 (1.51%) patient, respectively. M1 was the most common subtype associated with aberrant expression of lymphoid antigens, followed by AML with myelodysplasia-related changes (AML-MRC), AML (unclassified), and M2 and M3 in decreasing order. M4 and M5 were not associated with the expression of lymphoid antigens.

Acute myeloid leukemia-M1

Thirteen (19.69%) patients were morphologically classified under this group. The most frequently expressed antigens were CD33 (92.3%), CD13 (84.61%), CD117 (84.61%), CD45 (84.61%), CD34 (61.5%), HLA-DR (46.15%), and CD64 (46.15%). 7.6% of the cases expressed CD71. Lymphoid antigens, CD7 and CD19 were expressed in 38.46% and 23.07% patients, respectively.

Acute myeloid leukemia-M2

Five (7.57%) patients were put in this category. All patients expressed CD13, CD33, CD117, CD45, MPO, and CD34. Lymphoid antigens such as CD19 (40%), CD7 (20%), and TdT (20%) were expressed.

Acute myeloid leukemia-M3

Thirteen (19.69%) patients in this category were evaluated with immunophenotyping, as morphology of this disorder is very distinct, and the final diagnosis is based on demonstration of PML-RARA fusion gene. All of these cases were positive for CD13, CD33, CD64, and CD45. 7.69% of the patients showed aberrant CD7 expression.

Acute myeloid leukemia-M4

Three (4.54%) patients were included in this category. All patients expressed CD13, CD33, CD64, CD117, CD45, MPO, CD14, and CD36. 66.66% of the cases expressed CD36, CD11c, CD15, and HLA-DR. 33.33% of the cases expressed CD41a and CD61. 33.33% of the cases expressed CD71.

Acute myeloid leukemia-M4Eo

One (1.5%) patient was put into this category. Immunophenotyping revealed positivity for CD11b, CD13, CD33, CD64, CD117, CD45, CD38, CD15, and MPO.

Acute myeloid leukemia-M5

Four (6%) patients belonged to this category. One patient had M5a morphology and was positive for CD36 and CD64 co-expression, CD11b, CD13, CD33, CD64, and CD38. Patients with M5b were positive for CD13, CD33, CD64, MPO, HLA-DR, and CD34. 66.66% of the patients showed CD36 and CD64 co-expression and CD14 positivity. 33.33% of the cases were positive for CD11c, CD11b, and CD36.

Acute myeloid leukemia with myelodysplasia related changes

Ten (15.15%) patients belonged to this category. All were positive for MPO and CD13. Other frequently expressed markers were CD33 (90%), CD117 (90%), HLA-DR (90%), and CD34 (80%). Ten percentage of the patients expressed CD71 and CD41a. Seventy percentage of the patients showed aberrant expression of lymphoid antigens such as CD7 (20%), TdT (20%), and CD19 (30%).

Acute myeloid leukemia, unclassified

Seventeen (25.75%) patients were included in this category. These patients could be diagnosed only as acute leukemias in BM aspirates and after immunophenotyping were found to have AML. The most frequently encountered antigens were CD13 (100%), CD33 (88.2%), CD45 (88.2%), CD15 (47%), and HLA-DR (47%). CD71 was expressed by 17.64% of the patients. One (5.88%) patient showed CD36 and CD64 co-expression. Five (29.4%) patients aberrantly expressed lymphoid antigens including CD7 (11.7%), TdT (5.88%), CD19 (5.88%), and CD5 (5.88%).

Comparing morphological subtypes of acute myeloid leukemia with findings of genetic studies

Cytogenetic reports of 46 cases were available for analysis. The most common finding was PML-RARA fusion gene which was detected in 19 (41.3%) patients, and all the 19 patients were morphologically diagnosed to be AML-M3. Normal karyotype was found in 12 (26%) patients. Trisomy 8 was found in five (10.86%) patients. t(8;21)(q22;q22) and FLT3-ITD mutation was found in three (6.5%) patients each [Figure 1]. Inv (16)(p13.1q22) and del (5)(q13q31) were found in two (4.34%) patients each. One (2.17%) patient each had monosomy 7, NPM1 mutation, add (15)(q26), t(16;21)(p11.2;q22), and high hyperdiploidy (51, XY, +8, +10, +13, +14, +21) [Table 2].
Figure 1: Karyogram showing t(8;21)(q22;q22)

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Table 2: Comparing morphological subtypes with genetic findings in 46 patients

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Acute myeloid leukemia-M1

Cytogenetic study was done in four patients with AML-M1 morphology. Three (75%) patients had normal karyotype, and one (25%) patient had 45, X,-Y, and t(8;21)(q22;q22) karyotype [Figure 2].
Figure 2: Karyogram showing 45, X,-Y, t(8;21)(q22;q22)

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Acute myeloid leukemia-M2

RT-PCR of 1 AML-M2 patient showed t(8;21)(q22;q22) and FLT3-ITD mutation. Genetic studies were not done for the rest.

Acute myeloid leukemia-M3

All 19 cases of AML-M3 diagnosed by morphology were positive for PML-RARA fusion gene either by PCR or by cytogenetics.

Acute myeloid leukemia-M4

Cytogenetic study was done in three patients. One (33.33%) patient each had normal karyotype, Inv (16)(p13.1q22), add (11)(p15), and trisomy 8 with additional marker chromosome.

Acute myeloid leukemia-M4Eo

One patient had AML-M4Eo and he had trisomy 8 on cytogenetic analysis.

Acute myeloid leukemia-M5b

Cytogenetic study was done in two patients and both had normal karyotype.

Acute myeloid leukemia with myelodysplasia related changes

Cytogenetic study was done in six patients. Three (50%) patients had a normal karyotype. One (16.66%) patient had monosomy 7. Two (33.33%) patients had trisomy 8 with two additional marker chromosomes and monosomy 21 in one patient.

Acute myeloid leukemia, unclassified

Cytogenetic study was done in ten patients. Three (30%) had normal karyotype. Two (20%) patients showed del (5)(q13q31). Two patients had trisomy 8, and one patient had t(8;21)(q22;q22) along with loss of chromosome Y. One patient had high hyperdiploidy. Inv (16)(p13.1;q22) was found in one patient. One patient had add (15)(q26), t (16;21)(p11.2;q22).

Comparing immunophenotypic findings with genetic studies

Genetic study was done in 11 out of 21 AML patients expressing aberrant lymphoid antigens. Three (60%) of the CD7-positive cases were having a normal karyotype, and one (20%) patient each had trisomy 8 and PML-RARA fusion gene. Two (50%) patients with CD19 expression had t(8;21)(q22;q22), and one patient each had normal karyotype and add (15)(q26), t(16;21)(p11.2;q22). One patient with TdT expression had trisomy 8, monosomy 21, and two additional marker chromosomes. One patient with aberrant expression of two lymphoid antigens including CD7 and CD19 showed monosomy 7 [Table 3].
Table 3: Comparing aberrant lymphoid antigen expression and cytogenetic finding

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Two out of three patients with t (8;21)(q22;q22) had CD19 aberrant expression and was found to be statistically significant when compared with other AML without t(8;21) (q22;q22) with the Fisher exact test statistic value of 0.0277 (P < 0.05).

Co-expression of two lymphoid antigens such as CD7 and CD19 was associated with monosomy 7 and was found to be statistically significant with a Fisher exact test statistic value of 0.0217 (P < 0.05).


  Discussion Top


In the present study, 23.28% of patients were not diagnosed as AML by morphological assessment. This is because of the inability to differentiate AML and acute lymphoblastic leukemia, due to the absence of granules or  Auer rods More Details in the blasts and hence a diagnosis of “acute leukemia” was made in BM aspirate smears. However, after immunophenotyping, all these cases could be diagnosed as AML. Out of these cases, 5.88% of the cases expressed monocytic markers and showed del (5q) in cytogenetics which is known to occur in AML-M4.[7] Another 5.88% of the cases which were categorized as AML-unclassified, had del (5q) suggesting a possibility of AML with MRC. 5.88% of patients with AML-unclassified, were found to have inv (16)(p13.1q22). There is no specific cytogenetic abnormality associated with AML-M1.[4] 5.88% of the cases of AML-unclassified, had thrombocytosis. According to published literature, AML with Inv (3) (q21.3q36.2) is associated with thrombocytosis.[8] However, in our study, AML with thrombocytosis had normal karyotype. 5.88% of the patients belonging to AML-unclassified category had both NPM1 and FLT3-ITD mutation and also were negative for HLA-DR which is known to occur in AML with NPM1 mutation. Secondary mutations such as FLT3-ITD are frequently encountered in AML with NPM1 mutation. Furthermore, AML with NPM1 mutation has a favorable response to therapy even with FLT3-ITD mutation. However, the coexistence of these two mutations has a poorer prognosis than NPM1 mutation alone.[8]

Expression of lymphoid antigens was seen most commonly with AML-M1 in our study. In a study conducted by Khalidi HS et al., AML which could not be classified had the highest proportion of cases with aberrant lymphoid antigens.[9] In a study conducted by Basharat M et al., AML-M2 was the most common morphological subtype showing aberrant lymphoid antigens such as CD7 or CD19.[5] In a study conducted by Khalidi HS et al., AML was associated with CD2, CD3, CD8, CD10, and CD20 expression in addition to those expressed in our cases. CD19 aberrant expression was found in 71.4% of the cases with t(8;21)(q22;q22) in a study conducted by Andrieu V et al.[10] In our study, 66.66% of the cases with t(8;21)(q22;q22) demonstrated CD19 aberrant expression and was found to be statistically significant association when compared with other AML without t(8;21)(q22;q22).

In a study conducted by Zheng J et al., 63.63% of the AML-M4 cases had a normal karyotype. 9.09% of the M4 cases had Inv (16)(p13.1q22).[11] 9.09% of the M4 cases in a study conducted by Khalidi HS et al. had Inv (16)(p13.1q22).[9] In our study, 33.33% of the M4 cases had Inv16 (p13.1;q22) and 33.33% of the cases had normal karyotype.

Eighty percentage of the cases with M4Eo morphology had Inv (16) in a study conducted by Khalidi HS et al., whereas trisomy 8 was found in the patient with M4Eo in our study.[9]

Both the patients with M5 had a normal karyotype in our study, whereas 61.5% of the patients had a normal karyotype in a study conducted by Zheng J et al.[11]

In our study, t (8;21) was found in AML-M2 and AML-M1. This was found in one out of four cases of AML-M1. In a study conducted by Andrieu V, t(8;21) was found in 3% of AML-M1 cases.[10]

In our study, one out of three patients with AML-M4 had expression of CD41a and CD61. CD41a and CD61 are markers for megakaryoblasts but maybe misinterpreted to be positive when the platelets adhere to blasts. Thus, a cytoplasmic expression of these antigens is more specific for acute megakaryoblastic leukemia.[8]

CD71 is not a specific marker for acute erythroid leukemia.[12] In our study, 7.6%, 33.33%, and 10% of the M1, M4, and AML with MRC cases had the expression of this marker, respectively.

The presence of t (8;21) is usually associated with good prognosis and was found in 6.6% of the AML cases in our study.[13] Furthermore, Inv (16) is associated with a good prognosis and was found in 4.3% of the patients in our study.[14] There are conflicting reports regarding the prognostic significance of trisomy 8 in AML.[15] In our study, trisomy 8 was the most common cytogenetic abnormality detected after t (15;17) and was found in 10.86% of the patients.


  Conclusion Top


Morphology along with immunophenotyping and genetic studies helps in categorizing the patients for treatment purposes. Morphology helps in making a provisional diagnosis before obtaining immunophenotyping and results of genetic studies. We found a significant association between aberrant expression of certain lymphoid antigens and certain cytogenetic abnormalities. Many of the patients with acute leukemia were morphologically unclassified in our study, and immunophenotyping plays a major role in categorizing a patient as AML. Further studies on the prognostic significance of trisomy 8 in AML are suggested, as this is the second most frequently found cytogenetic abnormality in our patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Demichelis-Gómez R, Zapata-Canto N, Leyto-Cruz F, Terreros-Muñoz E, Carrillo A, Montaño-Figueroa E, et al. Acute myeloid leukemia in Mexico: The specific challenges of a developing country. Results from a Multicenter National Registry. Clin Lymphoma Myeloma Leuk 2020;20:e295-303.  Back to cited text no. 1
    
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Voigt AP, Brodersen LE, Alonzo TA, Gerbing RB, Menssen AJ, Wilson ER, et al. Phenotype in combination with genotype improves outcome prediction in acute myeloid leukemia: A report from Children's Oncology Group protocol AAML0531. Haematologica 2017;102:2058-68.  Back to cited text no. 2
    
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Preethi CR. Clinico-hematological study of acutemyeloid leukemias. J Clin Diagn Res 2014;8:FC14-7.  Back to cited text no. 3
    
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Schiffer CA, Stone RM. Morphologic classification and clinical and laboratory correlates. In: Holland-Frei Cancer Medicine. 6th ed. Hamilton: BC Decker; 2003. Available from: https://www.ncbi.nlm.nih.gov/books/NBK13452/. [Last accessed on 2022 Jun 10].  Back to cited text no. 4
    
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Basharat M, Khan SA, Din NU, Ahmed D. Immunophenotypic characterisation of morphologically diagnosed cases of Acute Myeloid Leukaemia (AML). Pak J Med Sci 2019;35:470-6.  Back to cited text no. 5
    
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Ghosh S, Shinde SC, Kumaran GS, Sapre RS, Dhond SR, Badrinath Y, et al. Haematologic and immunophenotypic profile of acute myeloid leukemia: An experience of Tata Memorial Hospital. Indian J Cancer 2003;40:71-6.  Back to cited text no. 6
[PUBMED]  [Full text]  
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Singh T. Atlas and Text of Hematology. 4th ed. New Delhi: Avichal Publishing Company; 2018.  Back to cited text no. 7
    
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Khalidi HS, Medeiros LJ, Chang KL, Brynes RK, Slovak ML, Arber DA. The immunophenotype of adult acute myeloid leukemia: High frequency of lymphoid antigen expression and comparison of immunophenotype, French-American-British classification, and karyotypic abnormalities. Am J Clin Pathol 1998;109:211-20.  Back to cited text no. 9
    
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Andrieu V, Radford-Weiss I, Troussard X, Chane C, Valensi F, Guesnu M, et al. Molecular detection of t(8;21)/AML1-ETO in AML M1/M2: Correlation with cytogenetics, morphology and immunophenotype. Br J Haematol 1996;92:855-65.  Back to cited text no. 10
    
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Zheng J, Wang X, Hu Y, Yang J, Liu J, He Y, et al. A correlation study of immunophenotypic, cytogenetic, and clinical features of 180 AML patients in China. Cytometry B Clin Cytom 2008;74:25-9.  Back to cited text no. 11
    
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Liu Q, Wang M, Hu Y, Xing H, Chen X, Zhang Y, et al. Significance of CD71 expression by flow cytometry in diagnosis of acute leukemia. Leuk Lymphoma 2014;55:892-8.  Back to cited text no. 12
    
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Reikvam H, Hatfield KJ, Kittang AO, Hovland R, Bruserud Ø. Acute myeloid leukemia with the t(8;21) translocation: Clinical consequences and biological implications. J Biomed Biotechnol 2011;2011:104631.  Back to cited text no. 13
    
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Eghtedar A, Borthakur G, Ravandi F, Jabbour E, Cortes J, Pierce S, et al. Characteristics of translocation (16;16)(p13;q22) acute myeloid leukemia. Am J Hematol 2012;87:317-8.  Back to cited text no. 14
    
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Elliott MA, Letendre L, Hanson CA, Tefferi A, Dewald GW. The prognostic significance of trisomy 8 in patients with acute myeloid leukemia. Leuk Lymphoma 2002;43:583-6.  Back to cited text no. 15
    


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