P–414 HLA-G expression as a new prognostic marker of successful implantation

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
M Bakleicheva ◽  
O Bespalova ◽  
T Ivashchenko ◽  
T Tral ◽  
G Tolibova
Keyword(s):  
Cytogenetic Study ◽  
Normal Karyotype ◽  
Induced Abortion ◽  
Laser Scanning Microscopy ◽  
Qualitative Assessment ◽  
Extravillous Trophoblast ◽  
Relative Area ◽  
Missed Abortion ◽  
Histological Picture ◽  
Villous Trophoblast

Abstract Study question Is the low HLA-G expression a determinant of early reproductive loss? Summary answer Low expression of HLA-G is associated with pregnancy complications and can be one of the reasons of spontaneous abortion (such as RPL). What is known already The dysregulated maternal immune responses to invading embryos may play role in RIF, RPL, and second- and third-trimester obstetrical conditions. HLA-G is a molecule that was first known to confer protection to the fetus from destruction by the immune system of its mother, thus critically contributing to fetal–maternal tolerance due to inducing displacement of pro-inflammatory to Th1 cell-mediated response of Th2, has a positive influence on the process of implantation. HLA-G is mainly restricted to the fetal–maternal interface on the extravillous cytotrophoblast, to placenta, amnion. Study design, size, duration It was a prospective complex cohort study from 2016–2020 years with pathomorphological investigations. The purpose of this study is to investigate the HLA-G and KIR2DL4 expression in chorionic villous among 3 groups (study included 118 cases of abortion material): group 1 – 36 cases after missed abortion with normal karyotype, group 2 – 36 cases after missed abortion with polyploidy and group 3 – 46 cases after induced abortion group (normal pregnancy). Participants/materials, setting, methods Criteria of inclusion: abortive material from 3 groups of women with missed or after induced abortion; 6–12 weeks, singleton pregnancy, cytogenetic of chorionic villous was obligatorily - normal fetal karyotype and polyploidy of fetus. Pathomorophological investigation included H&E stain, IHC and confocal laser scanning microscopy. Immunohistochemical examination included quantitative and qualitative assessment of the expression of Anti-HLA-G (mouse monoclonal) in an extra villous trophoblast and Anti-KIR2DL1+KIR2DL3 + KIR2DL4 + KIR2DS4 (rabbit polyclonal) in chorionic villi. Main results and the role of chance The immunohistochemical study showed homogenous distribution HLA-G expression in extravillous trophoblast cells (EVT) and KIR2DL4 expression in chorion villous both in missed abortion groups and in induced abortion group. HLA-G expression average relative area in 1 and 2 groups was not statistically different (in 1 group with normal karyotype 33,9±3,5 and in 2 group 38,6±2,8). But the expression of HLA-G in 3 group was strictly higher (55,6 ±2,4). The average relative area of KIR2DL4 receptor wasn’t statistically different among 3 groups. However, the histological picture both missed abortion groups (for the genetic\immunological reasons for rejection) is the only one - this is a missed abortion of an early terms of gestation. In a histological study of missed abortion, as our study shows, the histological picture is similar in 1 and 2 groups. Thus, in 1 group with a normal karyotype of the fetus (before conducting the chorion cytogenetic study in the genetics laboratory) in 59.2% the histological examination determined a picture of an impaired early pregnancy with signs of trophoblast chromosomal pathology. Thus, without a cytogenetic study of the chorion, it is impossible to clearly determine whether the chromosomal pathology of the fetus is the cause of missed abortion. Limitations, reasons for caution There is no limitations, reasons for caution. Wider implications of the findings: Thus, HLA-G molecule has a leading role in the onset and successful prolongation of pregnancy, implantation, placentation and fetal development. Trial registration number 98–2019

Mutations of the Nucleophosmin (NPM1) Gene Are Common in Adult Acute Myeloid Leukemia and Associated with Favorable Prognosis If Present without FLT3-ITD Mutation.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 224-224 ◽  
Author(s):  
Christian Thiede ◽  
Sina Koch ◽  
Eva Creutzig ◽  
Christine Steudel ◽  
Thomas Illmer ◽  
...  
Keyword(s):  
Disease Free Survival ◽  
Normal Karyotype ◽  
Clinical Impact ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Lower Probability ◽  
Novel Mutations ◽  
Npm1 Mutation ◽  
Specific Subset ◽  
Acute Myeloid

Abstract Nucleophosmin (NPM1) is a nucleo-cytoplasmic shuttling protein with multiple functions, including regulation of the p53-ARF pathway. Rearranged NPM1 has been found in a small subgroup of AML patients with t(5;17). Recently, mutations of NPM1 have been described in patients with acute myeloid leukaemia, especially in patients with normal karyotype (Falini et al, NEJM 2005). These mutations lead to an elongated protein which is retained in the cytoplasm. The precise prevalence as well as the long term clinical impact of this mutation is currently unclear. Patients and methods: We investigated 1485 samples from adult patients with newly diagnosed AML and advanced MDS for mutations in exon 12 of the NPM1 gene. The majority of these individuals were treated in the AML96 protocol of the DSIL (former SHG). Mutations in NPM1 exon 12 were screened using genomic DNA from the time of diagnosis and Genescan analysis. In a subgroup, mutations were confirmed by sequencing. In addition, confocal laser scanning microscopy was performed to investigate the localization of mutant NPM1 in cases with novel mutations. Results: A 4-bp insert in the genomic sequence was detected in 408/1485 patients (27.5%). In 229 cases sequenced so far the most common change was the previously reported Type A (80.3%), followed by B (9.2%) and D (3.1) and 13 novel mutations, which showed cytoplasmic localization of NPM1 in all five analyzed cases. The NPM1-mutations were most prevalent in patients with normal karyotype (324/709; 45.7%) compared to 58/686 with karyotype abnormalities (8.5%) (P<.0001). NPM1 mutations were rarely seen in cases with good risk abnormalities [t(8;21): 2/57; inv(16: 2/73; t(15;17): 0/47] but also rarely detected together with high risk cytogenetics [-5/5q-: 3/94;-7/7q-: 5/122; complex: 4/185]. The mutation was found to be associated with high WBC counts, high BM blasts and higher platelet counts (P <.0001). Mutant NPM1 was also more prevalent in females compared to males (33.1 vs 22.9%; P<.00001). Most NPM1 mutations were found in cases with de novo AML, mainly in FAB subgroups M5a, M5b, and M4, and were absent or rare in M3, M0, M6, and M7. Patients with NPM1 alterations had significantly more FLT3-ITD mutations, even if restricted to patients with normal karyotype (NPM1-mut: 43.8% vs. NPM1-wt: 19.9%; p<.0001), whereas a significantly lower rate of MLL-PTD mutations was found (NPM1-mut: 0/207 vs. NPM1-wt: 39/549; P<.0001). To assess the clinical impact, 4 groups were defined based on the NPM1 and FLT3-ITD status for patients with normal karyotype: NPM1-mut/FLT3-ITD neg; NPM1-mut/FLT3-ITD pos; NPM1-wt/FLT3-ITD pos; NPM1-wt/ FLT3-ITD neg. Among these groups, patients having only an NPM1-mutation had significantly better overall survival (OS), disease free survival (DFS) and a lower probability of relapse, compared to all other groups. This was confirmed in a multivariate analysis (HR NPM1-mut/FLT3-ITD neg for OS: 0.76 95% CI: 0.587–.992; DFS: 0.661, 95% CI: 0.449–0.973). In addition, these patients had a significantly lower cumulative incidence of relapse (CIR at 40 months: 37.2%; P = .009). Conclusion: With more than 27%, NPM1-mutations represent the most frequent genetic abnormality in adult AML identified so far. They characterize a specific subset in patients with normal karyotype. If not associated with FLT3-ITD mutations, NPM1 abnormalities appear to identify a subgroup with improved response towards treatment. The mechanistic background remains to be determined.

Clinical Relevance of Cytogenetics Abnormalities in Adult Patients with Acquired Aplastic Anaemia.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3748-3748
Author(s):  
Vikas Gupta ◽  
Carol Brooker ◽  
Jennifer A. Tooze ◽  
Qi-long Yi ◽  
Deborah Sage ◽  
...  
Keyword(s):  
Aplastic Anaemia ◽  
Clinical Relevance ◽  
Cytogenetic Study ◽  
Cumulative Risk ◽  
Normal Karyotype ◽  
Similar Response ◽  
Trisomy 8 ◽  
Abnormal Karyotype ◽  
Monosomy 7 ◽  
Poor Prognostic Factor

Abstract The clinical relevance of cytogenetics abnormalities in aplastic anaemia (AA) patients at time of diagnosis is unclear. We evaluated the clinical course of 81 AA patients with successful cytogenetics at diagnosis and treated with immunosuppressive therapy (IST) from January 1993 to March 2004. A cytogenetic study was considered to be successful if there were a minimum of 15 evaluable metaphases in the absence of a clonal abnormality. Response to IST, survival and later clonal complications in patients with an abnormal karyotype (n=10) was compared to those with a normal karyotype (n=71). The cytogenetic abnormalities at diagnosis consisted of trisomy 6 (n=2), trisomy 8 (n=2), trisomy 15 (n=2), monosomy 7 (n=1), add(10) (n=1), t(3;11) (n=1) and t(4;6) (n=1). Four out of five evaluable patients with a trisomy responded to a first or subsequent course of IST. One patient with monosomy 7 achieved a complete response and later developed haemolytic PNH but with no recurrence of the monosomy 7. None of the patients with a non-numerical karyotypic abnormality responded to IST. No significant differences in 4-year event-free survival (EFS) (54% vs. 30%, p=0.15), overall survival (OS) (84% vs. 80%, p=0.33) or later clonal disorders (PNH, MDS and AML) were observed between the patients with a normal karyotype and those with an abnormal karyotype. Advanced age (≥60 years) was the only independent poor prognostic factor for survival in a multivariate analysis. Among the patients with a normal karyotype (n=71), 6 patients later developed a clonal cytogenetic abnormality with a cumulative risk of 10% at 4 years. These abnormalities were trisomy 15 (n=2), trisomy 6(n=1), monosomy 7 (n=2) and t(13;15) (n=1). None of the three patients who acquired trisomies developed any clinically significant problem, while acquisition of monosomy 7 was associated with a transformation to MDS/AML. Our data show that AA patients with a trisomy cytogenetic clone at diagnosis show a similar response to IST, evolution to later clonal abnormalities and survival, compared to those AA patients with a normal karyotype.

scholarly journals Human endogenous retrovirus-W envelope (syncytin) is expressed in both villous and extravillous trophoblast populations

2006 ◽  
Vol 87 (7) ◽  
pp. 2067-2071 ◽  
Author(s):  
A. Muir ◽  
A. M. L. Lever ◽  
A. Moffett
Keyword(s):  
Cell Lines ◽  
First Trimester ◽  
Endogenous Retrovirus ◽  
Endogenous Retroviruses ◽  
Extravillous Trophoblast ◽  
Human Endogenous Retrovirus ◽  
Human Trophoblast ◽  
Human Endogenous Retroviruses ◽  
Normal Tissues ◽  
Villous Trophoblast

The placenta is unique amongst normal tissues in transcribing numerous different human endogenous retroviruses at high levels. In this study, RT-PCR and immunohistochemistry were used to investigate the expression of syncytin in human trophoblast. Syncytin transcripts were found in first-trimester trophoblast cells with both villous and extravillous phenotypes and also in the JAR and JEG-3 choriocarcinoma cell lines. Syncytin protein was detected in villous trophoblast and in all extravillous trophoblast subpopulations of first- and second-trimester placental tissues. It was also present in ectopic trophoblast from tubal implantations. This study confirms that syncytin is expressed widely by a variety of normal human trophoblast populations, as well as choriocarcinoma cell lines.

scholarly journals The Distribution of Laminins and Fibronectins Is Modulated During Extravillous Trophoblastic Cell Differentiation and Decidual Cell Response to Invasion in the Human Placenta

1997 ◽  
Vol 45 (4) ◽  
pp. 569-581 ◽  
Author(s):  
Matti Korhonen ◽  
Ismo Virtanen
Keyword(s):  
Cell Differentiation ◽  
Basement Membrane ◽  
Human Placenta ◽  
Cell Response ◽  
Extravillous Trophoblast ◽  
Decidual Cell ◽  
Trophoblastic Cell ◽  
Trophoblastic Cells ◽  
Villous Trophoblast

We studied the distribution of laminin (Ln) α1–α3, β1–β3, and γ1 chains, and of the extradomain-A (EDA) and EDB and the oncofetal epitope of fibronectin (Onc-Fn) in extravillous trophoblastic cells and decidua in the human placenta by immunohistochemistry. We found that the transition from villous to extravillous trophoblast was accompanied by emergence of immunoreactivity for EDA-, EDB-, and Onc-Fn among the cells. Furthermore, whereas the villous trophoblastic basement membrane (BM) contains Ln α1, α2, β1, β2, and γ1 chains, immunoreactivity for Ln α1, β1, and γ1, but not for Ln α2 and β2 chains, was detected in association with extravillous trophoblastic cells. Interestingly, although immunoreactivity for the Ln α1, α2, β1, β2, and γ1 chains was detected in all decidual cell BMs, EDB-Fn and Onc-Fn were detected only in decidua that had been invaded by the trophoblast. In summary, our results describe distinct changes in the distribution of Ln and Fn isoforms during the differentiation of villous trophoblast into extravillous trophoblastic cells. Furthermore, EDB- and Onc-Fn are preferentially found in decidua that has been invaded by the trophoblast, indicating that the deposition of these Fn isoforms reflects a decidual cell response to invasion.

scholarly journals Intrauterine Growth Retardation Fetus with Trisomy 16 Mosaicism

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Takol Chareonsirisuthigul ◽  
Suchin Worawichawong ◽  
Rachanee Parinayok ◽  
Patama Promsonthi ◽  
Budsaba Rerkamnuaychoke
Keyword(s):  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Fetal Heart ◽  
Cytogenetic Study ◽  
Normal Karyotype ◽  
Internal Organs ◽  
Normal Morphology ◽  
Trisomy 16 ◽  
Intrauterine Growth ◽  
Mosaic Trisomy

Fetal trisomy 16 is considered uniformly lethal early in gestation. It has been reported to be associated with the variability of clinical features and outcomes. Mosaic trisomy 16 leads to a high risk of abnormality in prenatal cases. Intrauterine growth retardation (IUGR) is a common outcome of mosaic trisomy 16. Herein, we report on the case of Thai male IUGR fetus with trisomy 16 mosaicism. The fetal body was too small. Postmortem investigation of placenta revealed the abnormality including small placenta with furcated cord insertion and single umbilical cord artery. Cytogenetic study demonstrated trisomy 16 that was found 100% in placenta and only 16% in the fetal heart while other organs had normal karyotype. In addition, cardiac and other internal organs examination revealed normal morphology.

scholarly journals Trisomy 12 in chronic lymphocytic leukemia: an interphase cytogenetic study

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 775-779
Author(s):  
AP Losada ◽  
M Wessman ◽  
M Tiainen ◽  
AH Hopman ◽  
HF Willard ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Chronic Lymphocytic Leukemia ◽  
Karyotype Analysis ◽  
Cytogenetic Study ◽  
Normal Karyotype ◽  
Lymphocytic Leukemia ◽  
Metaphase Chromosomes ◽  
Interphase Cytogenetics ◽  
Trisomy 12

Interphase cytogenetics by means of in situ hybridization with the chromosome 12-specific biotinylated alpha satellite DNA probe pSP 12–1 was used for the study of trisomy 12, the most common chromosomal abnormality in chronic lymphocytic leukemia. In situ hybridization was performed on methanol/acetic acid fixed cells of conventional cytogenetic preparations from eight patients and on morphologically and immunologically classified cells of cytospin preparations from seven patients. The results show that trisomy 12 is more common than assumed on the basis of karyotype analysis of metaphase chromosomes: 2 of 13 patients with a normal karyotype in G-banding analysis were shown to have trisomy 12 by interphase cytogenetics. Immunophenotyping of the cells of one patient showed that the trisomy was restricted to cells with Ig light chain clonality. For the evaluation of the prognostic, therapeutic, and biologic significance of trisomy 12, in situ hybridization should be used in parallel with karyotype analysis because it allows the study of all cell populations of both interphase and mitotic cells, whether neoplastic or normal.

Comparative analysis of chromosomal aberrations in children with acute leukemia

2020 ◽  
Vol 5-6 (215-216) ◽  
pp. 7-14
Author(s):  
Zhansaya Nessipbayeva ◽  
◽  
Minira Bulegenova ◽  
Meruert Karazhanova ◽  
Dina Nurpisova ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Leukemia ◽  
Chromosomal Aberrations ◽  
Cytogenetic Study ◽  
Normal Karyotype ◽  
Blast Cell ◽  
Bone Marrow Blast ◽  
Scientific Center ◽  
Blast Cells ◽  
Medical Histories

Leukemia is a hematopoetic tissue tumor with a primary lesion of the bone marrow, where the morphological substrate is the blast cell. Chromosomal and molecular genetic aberrations play a major role in the acute leukemia pathogenesis, determing the morphological, immunological and clinical features of the disease. Our study was aimed to to analyze retrospectively the structure and frequency of chromosomal aberrations in children with initially diagnosed acute leukemia. Material and methods. Medical histories retrospective analysis of children charged to oncohematology department of the «Scientific Center of Pediatrics and Pediatric Surgery» in Almaty for the period 2015 - 2017 was carried out. 310 histories with primary diagnosed acute leukemia were studied. Results and discussion. Among 310 patients different chromosome aberrations were isolated in 158 patients (51%) during cytogenetic and molecular cytogenetic (in situ hybridization) studies of bone marrow blast cells. A normal karyotype was observed in 102 patients (33%). Conclusion. The lymphoblastic variant of acute leukemia was determined in 75.5%, that indicates its leading role in AL structure among the children of different ages. AML was determined in 22.6% of all OL cases. The most frequent chromosomal rearrangement in ALL patients was blast cell chromosome hyperdiploidy (10,6%) and t(12;21)(p13;q22)/ETV6-RUNX1,which was detected in 37 (16%) patients. The most frequent AML abberation was t (8;21) (q22;q22)/RUNX1-RUNX1T1, identified in 15 (21.4%) patients. Keywords: acute leukemia, bone marrow, blast cells, karyotype, chromosomal aberrations, cytogenetic study.

scholarly journals Genotype-Phenotype Characterization of Wolf-Hirschhorn Syndrome Confirmed by FISH: Case Reports

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
F. Sheth ◽  
O. R. Akinde ◽  
C. Datar ◽  
O. V. Adeteye ◽  
J. Sheth
Keyword(s):  
Cytogenetic Study ◽  
Case Reports ◽  
Normal Karyotype ◽  
Comparative Genomic ◽  
Molecular Cytogenetic ◽  
Contiguous Gene ◽  
Multiple Malformation ◽  
Molecular Cytogenetic Techniques

The Wolf-Hirschhorn syndrome (WHS) is a multiple malformation and contiguous gene syndrome resulting from the deletion encompassing a 4p16.3 region. A microscopically visible terminal deletion on chromosome 4p (4p16→pter) was detected in Case 1 with full blown features of WHS. The second case which had an interstitial microdeletion encompassingWHSC 1andWHSC 2genes at 4p16.3 presented with less striking clinical features of WHS and had an apparently “normal” karyotype. The severity of the clinical presentation was as a result of haploinsufficiency and interaction with surrounding genes as well as mutations in modifier genes located outside the WHSCR regions. The study emphasized that an individual with a strong clinical suspicion of chromosomal abnormality and a normal conventional cytogenetic study should be further investigated using molecular cytogenetic techniques such as fluorescencein situhybridization (FISH) or array-comparative genomic hybridization (a-CGH).

Congenital Diaphragmatic Hernia and Chromosomal Anomalies: Autopsy Study

2004 ◽  
Vol 7 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Dariusz Borys ◽  
Jerome B. Taxy
Keyword(s):  
Congenital Diaphragmatic Hernia ◽  
General Hospital ◽  
Diaphragmatic Hernia ◽  
Cytogenetic Study ◽  
Normal Karyotype ◽  
The Other ◽  
Chromosomal Anomalies ◽  
Unbalanced Translocation ◽  
Autopsy Study ◽  
Heart Abnormalities

In a 10-year review of autopsy records from Lutheran General Hospital (1992–2002), 13 cases of congenital diaphragmatic hernia (CDH) were found. The fetuses ranged between 21 and 35 wk of gestation. Four were born alive and five were diagnosed prenatally. The defect was left-sided in 11 cases. Cytogenetic study revealed five cases with normal karyotype and three cases with complex karyotypes. In five cases, no karyotype was performed. The three complex karyotypes were: 46,XX,del(8)(p23.1), 47,XX,+i(12)(p10)[6]/46XX[14] (Pallister-Killian syndrome), and 47,XY,+der(22)t(11:22) (q23.3:q11.2). The unbalanced translocation of chromosomes 11 and 22 in congenital diaphragmatic hernia has not been previously described. Three fetuses had heart abnormalities, including one which was associated with the 8p deletion. The other two had no karyotype study. Neither in this study, nor in the literature, is there a consistent or prevailing association between a specific chromosomal anomaly and CDH. The embryologic closure of the diaphragmatic leaflets may be mediated by a nonstructural chromosomal defect, more than one gene, and/or may be related to abnormalities not currently detectable.

Comparison of Cytogenetic and Molecular Genetic Detection of t(8;21) and inv(16) in a Prospective Series of Adults With De Novo Acute Myeloid Leukemia: A Cancer and Leukemia Group B Study

2001 ◽  
Vol 19 (9) ◽  
pp. 2482-2492 ◽  
Author(s):  
Krzysztof Mrózek ◽  
Thomas W. Prior ◽  
Colin Edwards ◽  
Guido Marcucci ◽  
Andrew J. Carroll ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
False Positive ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Cytogenetic Study ◽  
Molecular Genetic ◽  
False Negative ◽  
Normal Karyotype ◽  
Rt Pcr ◽  
Acute Myeloid

PURPOSE: To prospectively compare cytogenetics and reverse transcriptase–polymerase chain reaction (RT-PCR) for detection of t(8;21)(q22;q22) and inv(16)(p13q22)/t(16;16)(p13;q22), aberrations characteristic of core-binding factor (CBF) acute myeloid leukemia (AML), in 284 adults newly diagnosed with primary AML. PATIENTS AND METHODS: Cytogenetic analyses were performed at local laboratories, with results reviewed centrally. RT-PCR for AML1/ETO and CBFβ/MYH11 was performed centrally. RESULTS: CBF AML was ultimately identified in 48 patients: 21 had t(8;21) or its variant and AML1/ETO, and 27 had inv(16)/t(16;16), CBFβ/MYH11, or both. Initial cytogenetic and RT-PCR analyses correctly classified 95.7% and 96.1% of patients, respectively (P = .83). Initial cytogenetic results were considered to be false-negative in three AML1/ETO-positive patients with unique variants of t(8;21), and in three CBFβ/MYH11-positive patients with, respectively, an isolated +22; del(16)(q22),+22; and a normal karyotype. The latter three patients were later confirmed to have inv(16)/t(16;16) cytogenetically. Only one of 124 patients reported initially as cytogenetically normal was ultimately RT-PCR–positive. There was no false-positive cytogenetic result. Initial RT-PCR was falsely negative in two patients with inv(16) and falsely positive for AML1/ETO in two and for CBFβ/MYH11 in another two patients. Two patients with del(16)(q22) were found to be CBFβ/MYH11-negative. M4Eo marrow morphology was a good predictor of the presence of inv(16)/t(16;16). CONCLUSION: Patients with t(8;21) or inv(16) can be successfully identified in prospective multi-institutional clinical trials. Both cytogenetics and RT-PCR detect most such patients, although each method has limitations. RT-PCR is required when the cytogenetic study fails; it is also required to determine whether patients with suspected variants of t(8;21), del(16)(q22), or +22 represent CBF AML. RT-PCR should not replace cytogenetics and should not be used as the only diagnostic test for detection of CBF AML because of the possibility of obtaining false-positive or false-negative results.

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