00019606-201212000-00005ArticleDiagnostic Molecular PathologyDiagnostic Molecular Pathology© 2012 Lippincott Williams & Wilkins, Inc.21December 2012
p 225–233Reduction in WT1 Gene Expression During Early Treatment Predicts the Outcome in Patients With Acute Myeloid LeukemiaOriginal ArticlesAndersson, Charlotta MD*,†,‡; Li, Xingru MD*,†; Lorenz, Fryderyk MD§; Golovleva, Irina MD, PhD*,∥; Wahlin, Anders MD, PhD§; Li, Aihong MD, PhD*,†Departments of *Medical Biosciences†Clinical Chemistry‡Pathology§Radiation Sciences∥Medical and Clinical Genetics, Umeå University, Umeå, SwedenSupported by the Children’s Cancer Foundation in Sweden, the Lion’s Cancer Research Foundation, Umeå, Sweden, and the County Council of Västerbotten, Umeå, Sweden.The authors declare no conflict of interest.Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website, www.molecularpathology.com.Reprints: Aihong Li, MD, PhD, Department of Medical Biosciences, Clinical Chemistry, By 6M, 2nd floor, Umeå University, SE-90185 Umeå, Sweden (e-mail:
[email protected]).AbstractWilms tumor gene 1 (WT1) expression has been suggested as an applicable minimal residual disease marker in acute myeloid leukemia (AML). We evaluated the use of this marker in 43 adult AML patients. Quantitative assessment of WT1 gene transcripts was performed using real-time quantitative-polymerase chain reaction assay. Samples from both the peripheral blood and the bone marrow were analyzed at diagnosis and during follow-up. A strong correlation was observed between WT1 normalized with 2 different
control genes (β-actin and ABL1, P<0.001). WT1 mRNA level at diagnosis was of no prognostic relevance (P>0.05). A≥1-log reduction in WT1 expression in bone marrow samples taken <1 month after diagnosis significantly correlated with an improved overall survival (P=0.004) and freedom from relapse (P=0.010) when β-actin was used as control gene. Furthermore, a reduction in WT1 expression by ≥2 logs in peripheral blood samples taken at a later time point significantly correlated with a better outcome for overall survival (P=0.004) and freedom from relapse (P=0.012). This result was achieved when normalizing against both β-actin and ABL1. These results therefore suggest that WT1 gene expression can provide useful information for minimal residual disease detection in adult AML patients and that combined use of
control genes can give more informative results.Acute myeloid leukemia (AML) is a heterogeneous disease with a wide spectrum of phenotypes. Cytogenetic alterations, molecular genetic defects, and minimal residual disease (MRD) are patient-related prognostic factors. Current treatment protocols are based on these prognostic factors, which contribute to individualized therapy and risk-adapted intensification.1 In Sweden, considerable progress in patient survival has been reported, but the majority of AML patients die of the disease.2 Studies have shown that detection of MRD in AML is prognostically relevant.3–5Multicolor flow cytometry (MFC) and polymerase chain reaction (PCR) are the methods of choice in the quantification of MRD, with their advantage of high sensitivity.6,7 MFC allows the detection of 1 leukemic cell in 103 to 104 normal cells,4 but standardization of MRD detection by this method is problematic.8 Furthermore, aberrant blast immunophenotypes may shift during treatment9 or may represent a preceding myelodysplastic clone rather than the transformed acute leukemic clone.10In parallel with the development of MFC, there have been developments in the use of molecular markers with real-time quantitative-PCR (RQ-PCR) in MRD assessments. Leukemia-specific gene mutations (eg, NPM1), gene rearrangement transcripts due to chromosome translocations (eg, PML-RARA or CBFB-MYH11), and overexpressed gene transcripts in AML can be useful molecular markers in monitoring MRD.11 However, NPM1 mutations could be identified only in about 35% of AML patients.12 More than 40 subsets of mutations have been identified, and 17 different approaches to detection of NPM1 mutations have been developed for RQ-PCR, indicating that the methodology is complex.13 Similarly, the use of transcripts (eg, PML-RARA or CBFB-MYH11) for MRD detection is also limited to subtypes of AML.14,15Wilms tumor gene 1 (WT1) has been evaluated for use as a suitable molecular marker of MRD in AML.3,16–18 However, some issues must be considered when using WT1 as an MRD marker. One pertains to the fact that WT1 is expressed in normal tissues and can never be “undetectable” in the way that fusion genes or gene mutations can be. WT1 expression in the normal bone marrow (BM) is confined to the primitive CD34+ population of precursor cells,19 and normal precursor cells are seen in peripheral blood (PB) only in exceptional cases. Therefore, different criteria have to be applied for the interpretation of results from BM and PB. Another issue to be considered is differences in the performance of the assay concerning the amplification region of the WT1 transcript and normalization against different
control genes (CGs).3Our main goal was to investigate the importance of WT1 gene expression regarding outcome prediction at diagnosis and during follow-up, in both BM and PB. Furthermore, we wanted to determine whether WT1 expression levels may be influenced by the use of different CGs for normalization of WT1 expression.MATERIALS AND METHODSPatientsForty-three adult patients (median age 61 y, range 23 to 85 y) who were diagnosed with AML between 1996 and 2002 were included in the study. These patients were treated at the Department of Hematology, Umeå University Hospital, according to standard protocols. Patients with severe comorbidity precluding the initiation of intensive induction chemotherapy were excluded. BM and PB samples were obtained at diagnosis and during treatment. Informed consent was obtained in accordance with the recommendations of the Declaration of Helsinki and institutional regulations, including approval by the local ethical committee.The diagnosis and classification of AML were based on criteria according to the revised French-American-British (FAB) classification. Expression levels of WT1 mRNA were quantified in BM at diagnosis in 34 patients. Additional follow-up samples from 9 patients were analyzed, yielding a total of 43 patients. WT1 gene expression levels in PB could be quantified at diagnosis and during follow-up in 14 patients. The total number of samples was 202 and the median number of follow-up samples per patient was 3 (range 1 to 7). The median follow-up time was 22 months (range 1 to 141).The cytogenetic analyses were performed on BM samples taken at diagnosis at the Department of Medical and Clinical Genetics, Umeå University Hospital. At least 20 cells were analyzed. Risk group stratification based on cytogenetic findings was evaluated retrospectively. Cytogenetic risk group stratification was performed as described by Grimwade et al.20 The risk was categorized into favorable, intermediate, or adverse. Molecular data were not available and were therefore not incorporated in the risk stratification. Myelodysplastic syndrome (MDS) was defined as an antecedent hematological disorder if diagnosed at least 2 months before the diagnosis of leukemia.Treatment RegimensPatients, except those with acute promyelocytic leukemia (FAB M3), were treated according to the standard antracycline-based and cytarabine-based protocols. After achieving complete remission (CR), the patients received standard consolidation therapies. Patients who failed to achieve CR were assigned to salvage regimens. Patients with acute promyelocytic leukemia were treated with a combination of all-trans retinoic acid and conventional chemotherapy. Fourteen patients underwent hematopoietic stem cell transplantation (HSCT).Quantitative Assessment of WT1 Transcript ExpressionTotal RNA was extracted using the TRIzol method (Invitrogen AB, Stockholm, Sweden). After extraction and isolation, the RNA concentration was determined by measurement of the optical density at 260 nm, and the RNA was stored at −80°C until use.cDNA was synthesized by reverse transcription with the Superscript II Reverse Transcriptase kit according to the manufacturer’s protocol (Invitrogen). In brief, reverse transcription was carried out on 0.5 µg of total RNA in a total volume of 10 µL of a mixture containing 0.5 µL oligo p(dT) 12-18 primer, 0.5 µL 10 mM dNTP mix, 2 µL 5× first-strand buffer, 1 µL 0.1 M DTT, 0.5 µL RNaseOUT recombinant ribonuclease inhibitor, and distilled water. According to the manufacturer’s instructions, the reverse transcriptase was finally inactivated at 70°C for 15 minutes and the cDNA was stored at −20°C for RQ-PCR.RQ-PCR using TaqMan technology was performed to quantify WT1 mRNA expression. RQ-PCR reactions were carried out in a 25 µL volume containing 12.5 µL universal PCR master mix, each primer at a concentration of 0.5 µM, probe at 0.1 µM, and 50 ng of cDNA. The amplification was carried out in the ABI Prism 7000 Sequence Detection System (Applied Biosystems, Foster City, CA). Triplicate assays were run in parallel for each sample. WT1 transcription values were normalized against the expression of CGs β-actin and ABL1, to adjust for variations in RNA and cDNA synthesis.Primers and probes for the WT1 gene and the 2 CGs (the β-actin gene and the ABL1 gene) were described previously.21–23 The amplification conditions were an initial 2 minutes of incubation at 50°C (to destroy any contaminating template), 10 minutes at 95°C (to activate AmpliTaq Gold enzyme), followed by 50 cycles of denaturation at 95°C for 15 seconds and annealing/extension at 62°C for 1 minute. Standard curves were generated using a series of dilutions of plasmid DNA carrying the WT1, β-actin, or ABL1 genes with copy numbers from 100 to 106. A log line was generated with at least 5 points during the logarithmic phase of PCR amplification. The average of the slope and R2 of standard curves were −3.494±0.06189 and 0.997±0.0038, respectively, showing that the RQ-PCR used in this study was efficient. The mean of triplicates of the WT1 gene copy numbers was divided by the mean of duplicates of copy numbers of the CG.RNA from K562 cells was reverse transcribed into cDNA and was used as an internal experimental control for the RQ-PCR assay. The reproducibility of the method was found to be stable [between-run imprecision on cycle threshold (Ct) was 2.4% for β-actin, 3.4% for WT1, and 5.6% for ABL1].Statistical AnalysisThe Mann-Whitney U test was used to compare differences in WT1 gene expression between 2 independent variables and the Kruskal-Wallis 1-way analysis of variance was used for groups. Correlations between 2 variables were tested according to Spearman correlation tests. The Kaplan-Meier method was used to estimate the distribution of freedom from relapse (FFR) and overall survival (OS). The log-rank test was used to determine differences in the probability of FFR and survival between groups (WT1 expression levels or log reduction). For patients who achieved CR, FFR was measured from the date of diagnosis until the day of relapse of the disease. Patients were censored at the date of last clinical follow-up or death in remission. Any P-value of <0.05 was taken to represent a statistically significant difference. SPSS software version 18.0 for Windows (SPSS, Chicago, IL) was used for all statistical analysis.RESULTSCorrelation of WT1 Transcript Levels Normalized Against 2 Different CGsThe β-actin gene has been used as CG for WT1 expression in previous MRD studies.22,24,25 More recently, several studies have used the ABL1 gene as CG for normalizing WT1 transcripts.3,23,26 To compare the usefulness of the β-actin gene and the ABL1 gene as CGs for normalization of WT1 expression levels, we performed an analysis on the WT1 expression using these 2 CGs in a total of 202 samples including 48 diagnostic (14 PB and 34 BM) and 154 follow-up samples (65 PB and 89 BM). WT1 transcripts were detectable in 133 of 202 samples. We found significant agreement of WT1 gene expression levels normalized with the β-actin gene and the ABL1 gene (r=0.96, P<0.001, Fig. 1) (Supplemental Digital Content 1, http://links.lww.com/PDM/A31). We also found a significant association for a subset of samples with lower expression levels for WT1 (r=0.72, P<0.001, Fig. 1).JOURNAL/dimp/04.03/00019606-201212000-00005/figure1-5/v/2021-02-17T200047Z/r/image-jpegPositive correlation between Wilms tumor gene 1 (WT1) mRNA expression levels normalized against those of β-actin (y-axis) and those of ABL1 (x-axis). Samples with low expression levels for both WT1/β-actin (≤0.1) and WT1/ABL1 (≤100) also showed a similar trend.Expression Levels of WT1 Gene mRNA and Clinical Characteristics at DiagnosisWe analyzed a total of 34 BM samples from newly diagnosed adult patients with AML. At diagnosis, the median ratio of WT1 gene expression was 10.57/10000 β-actin (0.11 to 76.54) and 1268/10000 ABL1 (11 to 14151). The WT1 gene expression and its relation to clinical characteristics are shown in Table 1. No significant differences in WT1 expression were observed regarding age or sex. Regarding FAB classification, the highest expression levels of WT1 mRNA at diagnosis were observed in the FAB M3 subtype and the lowest levels were seen in the FAB M5 subtype. The small number of patients in each group made the statistics for individual subgroups uncertain, and no significant differences were found between groups (P=0.261 for WT1/β-actin, P=0.171 for WT1/ABL1). No significant difference was shown between patients with a history of MDS and patients with de novo AML. The CD34 antigen expression assessed by FACScan analysis and reported as negative or positive did not correlate with WT1 transcription levels (P=0.592 for WT1/β-actin, P=0.394 for WT1/ABL1).JOURNAL/dimp/04.03/00019606-201212000-00005/table1-5/v/2021-02-17T200047Z/r/image-tiffWT1 Gene Expression Levels and Clinical Characteristics at Diagnosis in Patients With Acute Myeloid LeukemiaTo determine the prognostic relevance of WT1 expression levels at diagnosis, the patients were divided into 2 groups according to the median of the initial WT1 transcript ratio. There was no difference in WT1 mRNA expression at diagnosis between patients who relapsed and those who did not relapse. According to cytogenetics, the highest expression was observed in the favorable group (P=0.070 for WT1/β-actin, P=0.042 for WT1/ABL1). This could be explained by the fact that patients with FAB M3 who had high WT1 expression belonged to the favorable cytogenetic group.Prognostic Significance of Reduction in WT1 Gene Expression During TreatmentTo determine the prognostic relevance of WT1 gene expression levels in both BM and PB for OS and FFR during follow-up, different intervals were evaluated as follows. Interval 1: <1 month, samples taken between 3 and 4 weeks after diagnosis (median 25 d, range 19 to 30 d); and interval 2: between 1 and 6 months (median 2.7 mo, range 1.03 to 5.7 mo). We analyzed the effect of a ≥1-log reduction and a ≥2-log reduction in WT1 mRNA expression, and found that in interval 1, the achievement of ≥1-log reduction in BM was associated with improved OS and FFR when β-actin was used as CG (P=0.004 for OS and P=0.010 for FFR, Fig. 2). No significant result was achieved regarding a ≥2-log reduction or when ABL1 was used as CG (data not shown). PB could not be analyzed because very few follow-up samples were available at this interval. In interval 2, the achievement of a ≥2-log reduction in PB was associated with improved OS (P=0.004, Fig. 3) and FFR (P=0.012, Fig. 4) when both β-actin and ABL1 were used as CGs. Similarly, a ≥1-log reduction in PB was also associated with improved OS and FFR (data not shown). No significant results were achieved when we analyzed BM samples during this interval (data not shown).JOURNAL/dimp/04.03/00019606-201212000-00005/figure2-5/v/2021-02-17T200047Z/r/image-jpegKaplan-Meier plot of overall survival (A) and freedom from relapse (B). Acute myeloid leukemia patients were divided into groups on the basis of a ≥1-log or a ≤1-log reduction in Wilms tumor gene 1 WT1 expression (relative to expression of the β-actin gene) in bone marrow at <1 month.JOURNAL/dimp/04.03/00019606-201212000-00005/figure3-5/v/2021-02-17T200047Z/r/image-jpegKaplan-Meier plot of the overall survival of acute myeloid leukemia patients with a reduction in Wilms tumor gene 1 (WT1) gene expression in peripheral blood of above or below 2 logs, between 1 and 6 months. A, WT1 gene expression normalized against β-actin gene expression. B, WT1 gene expression normalized against ABL1 gene expression.JOURNAL/dimp/04.03/00019606-201212000-00005/figure4-5/v/2021-02-17T200047Z/r/image-jpegKaplan-Meier plot of freedom from relapse of acute myeloid leukemia patients with a reduction in Wilms tumor gene 1(WT1) gene expression in peripheral blood of above or below 2 logs, between 1 and 6 months. A, WT1 gene expression normalized against β-actin gene expression. B, WT1 gene expression normalized against ABL1 gene expression.Correlations Between WT1 Gene Expression and the Clinical Course of the DiseaseA median WT1 gene expression level of 0.0279/10000 β-actin and 17.38/10000 ABL1 was observed in BM samples at first CR in 23 patients with AML. Interestingly, 1 patient at the first morphologic CR at day 97 showed a discrepancy of 0.68-log reduction in WT1/β-actin ratio but a 5.8-log increase in WT1/ABL1 ratio in BM.Thirteen patients had BM relapse during follow-up. One patient (case 884) was diagnosed with AML M1 at the age of 58 years and had no known history of MDS. At diagnosis, the WT1 gene expression level was 8.35/10000 β-actin and 900.62/10000 ABL1 and the percentage of blasts was 38%. CR was achieved after 1 induction treatment, and expression of the WT1 gene became undetectable in both PB and BM. Two months later, after first CR, the patient had relapse in BM (blasts >90%) and the WT1 gene expression level was higher than at diagnosis (39.69/10000 β-actin and 1431.33/10000 ABL1). This patient died of the disease 9 months after diagnosis.Fourteen patients received HSCT. In 5 of these patients, BM samples were available for quantitative assessment of WT1 expression at diagnosis and during follow-up before and after transplantation. Two induction treatment courses had been given to all patients except for 1 patient (case 2253) who was treated with only 1 induction course. Before transplantation, all patients were in CR and showed significantly lower expression of the WT1 gene than at diagnosis. After transplantation, a very low level of WT1 expression was found in 2 patients and the WT1 transcript was undetectable in 3 patients (Table 2).JOURNAL/dimp/04.03/00019606-201212000-00005/table2-5/v/2021-02-17T200047Z/r/image-tiffWT1 Gene Expression Before and After Hematopoietic Stem Cell Transplantation in Cases With Acute Myeloid LeukemiaDISCUSSIONSeveral authors have reported that expression of the WT1 gene at diagnosis may be predictive of outcome.16,27,28 However, other studies,3,5,29 including the present study, have not been able to confirm these findings. These contradictory reports may reflect differences in (1) the performance of assays (TaqMan or SYBR green dye) and standardized approaches (absolute or relative quantitative RQ-PCR analysis); (2) patient materials (BM or PB); (3) treatment protocols and length of follow-up; or (4) different WT1 cut-off levels used for defining the status of MRD.WT1 mRNA expression has been shown to be a good candidate for the evaluation of MRD, especially in AML patients in the absence of FACScan or DNA MRD markers.11,30–32 However, widespread implementation of WT1 MRD measurements has been hampered by the lack of knowledge of how and when to measure MRD levels. It is notable that some RQ-PCR assays that amplify 3′ regions of the WT1 gene, where mutations occur in 14% of AML patients, may give rise to false-negative results.33 Cilloni et al3 recently undertook a systematic evaluation of 9 published and “in-house” RQ-PCR assays in a quality-control study involving 11 European LeukemiaNet laboratories. There were marked differences in the assay performance, and the best, which used primers located in the 5′ region of the gene away from the mutational hotspot, was ultimately selected.3 In the present study, specific primers and probes were designed to measure the transcription of WT1 in the region (between exon 1 and exon 2) in which a lower frequency of mutations has been reported.34–36 The assay had a high efficiency with an average slope of −3.494 and sensitivity of being able to amplify at least 10 copies (data not shown). It has been shown that patients with a WT1 expression higher than 20 WT1 copies/10000 ABL1 copies after induction and consolidation chemotherapy have a shorter OS.37 In a recent pediatric MRD study by Lapillonne et al,38 the WT1 copy number was normalized against TATA box-binding protein gene transcripts and expressed as WT1/TBP×1000 ratio. WT1 ratio >50 after induction was found to be an independent prognostic risk factor of relapse. Cilloni et al3 showed that PB can be used for MRD assessment during treatment in 46% of AML cases. In these informative patients, WT1 transcripts with a <2-log reduction after induction were found to have a significantly increased risk of relapse, and WT1 transcripts at a level exceeding the upper normal values by the end of consolidation predicted a significantly increased risk of relapse.In the present study, we found that there was a significant correlation between a ≥1-log reduction in WT1 transcripts in BM samples taken <1 month (usually 3 or 4 wk) after diagnosis and a better outcome regarding OS and FFR when β-actin was used as CG. Furthermore, when we analyzed WT1 expression levels in PB samples taken at a later time point (between 1 and 6 mo), both ≥2-log and ≥1-log reductions predicted the outcome. This result was obtained when normalizing against either β-actin or ABL1. Despite the limited number of patients in this study, our observations are in agreement with previous studies showing that early MRD measurements can provide predictive information on the patient outcome.3,39WT1 gene expression analysis on PB is likely to be the most informative, given the low background level of WT1 with PB relative to BM.HSCT is a potentially curative approach for AML, and monitoring of MRD is routinely performed after BM transplantation. Quantitative assessment of WT1 mRNA expression after allogeneic stem cell transplantation has recently been demonstrated to be a useful tool for monitoring MRD in AML.40,41 In the present study, we could not prove the usefulness of WT1 gene expression as a predictor of relapse after BM transplantation because of the restricted patient material. However, all samples after BM transplantation showed reduced WT1 gene expression compared with the degree of gene expression before transplantation.Several genes have been suggested as internal CGs for RQ-PCR to correct for variations in the quality and quantity of RNA. β-glucuronidase has been shown as an optimal CG for molecular monitoring of chronic myelogenous leukemia.42,43 Tamaki et al44 demonstrated a strong correlation between WT1 gene transcription values normalized against β-actin, ABL1, and GAPDH as CGs. In 2003, a study group within the Europe Against Cancer program identified suitable CGs for diagnosis and detection of MRD in patients with leukemia.26 Only ABL1 was proposed for use as a CG as its mRNA expression was not significantly different in normal and leukemic samples at diagnosis. β-actin was excluded after the first round of the study as the presence of pseudogenes was a major criterion for exclusion and further analysis. The ABL1 gene is ubiquitously expressed at a desirable level and has no pseudogenes, but some primers for ABL1 can also yield amplification of ABL1 transcripts from translocations in Philadelphia-positive leukemia.31β-actin has been documented to have pseudogenes, but primer combinations have been described that were claimed to be RNA-specific, thus preventing amplification of contaminating genomic DNA.44,45 Another argument against β-actin as a CG in AML patients would be that monosomy 7 occurs in 4% of AML patients20 and the functional β-actin gene is located on chromosome 7. In our study cohort, 3 patients had monosomy 7 in diagnostic BM samples and the expression of β-actin was in the same range as in other patients. One patient had a relatively high expression of β-actin (data not shown). Recent studies have found that repair of gene transcriptional activity induced by chemotherapy in vivo was in the order β-actin> p53> N-ras> d-globin.46 Levels of β-actin and ubiquitin mRNAs were relatively constant in the same RNA samples posthypoxia.47 These findings suggest that β-actin transcripts are probably less affected by chemical-induced or stress-induced damage to gene activity. Similarly, at the protein level, β-actin is used as a standard loading control for western blots without reflecting this issue. Interestingly, in our cohort, 1 patient in the first CR showed a log reduction in WT1 mRNA expression when WT1 was normalized against β-actin, but an unrealistic log increase when WT1 was normalized against ABL1. The reason for this is unclear. Unfortunately, no single RNA has constant expression in all situations during development and experimental treatment.48,49 Every researcher should first demonstrate a satisfactory degree of the CGs used in their specific application. We found that there was a strong agreement between the WT1 gene expression levels normalized against the β-actin gene and against the ABL1 gene as internal CGs, and we believe that the results achieved with β-actin as CG are informative. The study also shows that a combination of 2 CGs can yield more informative results, but larger patient numbers will be necessary to confirm these data.In conclusion, we have found (1) a good correlation between WT1 expression levels normalized against β-actin and against ABL1; (2) that expression levels of WT1 mRNA at diagnosis are of no prognostic relevance; (3) that reduction in WT1 gene expression in BM (≥1-log) <1 month after diagnosis can predict the outcome (regarding OS and FFR) when β-actin is used as CG; and (4) that reduction in WT1 expression in PB (≥2-log) between 1 and 6 months of treatment can predict the outcome (regarding OS and FFR) irrespective of the CG used. Taken together with previous MRD studies,3,4,18,37,40,50 the data collected here suggest that the analysis of WT1 expression may be a useful tool for monitoring of MRD in AML.ACKNOWLEDGMENTSThe authors thank the doctors and nurses at the Hematology Section, Department of Oncology, Umeå University Hospital, for sample handling and continuous updating of the clinical data. They also thank the laboratory technicians at the Department of Clinical Genetics, Umeå University Hospital, for sample preparation.REFERENCES1. Dohner H, Estey EH, Amadori S, et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European LeukemiaNet. Blood. 2010;115:453–474[Context Link][CrossRef][Medline Link]2. Derolf AR, Kristinsson SY, Andersson TM, et al. Improved patient survival for acute myeloid leukemia: a population-based study of 9729 patients diagnosed in Sweden between 1973 and 2005. Blood. 2009;113:3666–3672[Context Link][CrossRef][Medline Link]3. Cilloni D, Renneville A, Hermitte F, et al. Real-time quantitative polymerase chain reaction detection of minimal residual disease by standardized WT1 assay to enhance risk stratification in acute myeloid leukemia: a European LeukemiaNet study. J Clin Oncol. 2009;27:5195–5201[Context Link][Full Text][CrossRef][Medline Link]4. Kern W, Voskova D, Schoch C, et al. Determination of relapse risk based on assessment of minimal residual disease during complete remission by multiparameter flow cytometry in unselected patients with acute myeloid leukemia. Blood. 2004;104:3078–3085[Context Link][CrossRef][Medline Link]5. Weisser M, Kern W, Rauhut S, et al. Prognostic impact of RT-PCR-based quantification of WT1 gene expression during MRD monitoring of acute myeloid leukemia. Leukemia. 2005;19:1416–1423[Context Link][Full Text][CrossRef][Medline Link]6. Li AH, Forestier E, Rosenquist R, et al. Minimal residual disease quantification in childhood acute lymphoblastic leukemia by real-time polymerase chain reaction using the SYBR green dye. Exp Hematol. 2002;30:1170–1177[Context Link][CrossRef][Medline Link]7. Thorn I, Forestier E, Botling J, et al. Minimal residual disease assessment in childhood acute lymphoblastic leukaemia: a Swedish multi-centre study comparing real-time polymerase chain reaction and multicolour flow cytometry. Br J Haematol. 2011;152:743–753[Context Link][Full Text][CrossRef][Medline Link]8. Kern W, Bacher U, Haferlach C, et al. The role of multiparameter flow cytometry for disease monitoring in AML. Best Pract Res Clin Haematol. 2010;23:379–390[Context Link][CrossRef][Medline Link]9. Oelschlagel U, Nowak R, Schaub A, et al. Shift of aberrant antigen expression at relapse or at treatment failure in acute leukemia. Cytometry. 2000;42:247–253[Context Link][CrossRef][Medline Link]10. Westers TM, Alhan C, Chamuleau ME, et al. Aberrant immunophenotype of blasts in myelodysplastic syndromes is a clinically relevant biomarker in predicting response to growth factor treatment. Blood. 2010;115:1779–1784[Context Link][CrossRef][Medline Link]11. Grimwade D, Vyas P, Freeman S. Assessment of minimal residual disease in acute myeloid leukemia. Curr Opin Oncol. 2010;22:656–663[Context Link][Full Text][CrossRef][Medline Link]12. Scholl S, Mugge LO, Landt O, et al. Rapid screening and sensitive detection of NPM1 (nucleophosmin) exon 12 mutations in acute myeloid leukaemia. Leuk Res. 2007;31:1205–1211[Context Link][CrossRef][Medline Link]13. Schnittger S, Kern W, Tschulik C, et al. Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML. Blood. 2009;114:2220–2231[Context Link][CrossRef][Medline Link]14. Grimwade D, Jovanovic JV, Hills RK, et al. Prospective minimal residual disease monitoring to predict relapse of acute promyelocytic leukemia and to direct pre-emptive arsenic trioxide therapy. J Clin Oncol. 2009;27:3650–3658[Context Link][Full Text][CrossRef][Medline Link]15. Corbacioglu A, Scholl C, Schlenk RF, et al. Prognostic impact of minimal residual disease in CBFB-MYH11-positive acute myeloid leukemia. J Clin Oncol. 2010;28:3724–3729[Context Link][Full Text][CrossRef][Medline Link]16. Inoue K, Sugiyama H, Ogawa H, et al. WT1 as a new prognostic factor and a new marker for the detection of minimal residual disease in acute leukemia. Blood. 1994;84:3071–3079[Context Link][CrossRef][Medline Link]17. Cilloni D, Messa F, Arruga F, et al. Early prediction of treatment outcome in acute myeloid leukemia by measurement of WT1 transcript levels in peripheral blood samples collected after chemotherapy. Haematologica. 2008;93:921–924[Context Link][CrossRef][Medline Link]18. Ostergaard M, Olesen LH, Hasle H, et al. WT1 gene expression: an excellent tool for monitoring minimal residual disease in 70% of acute myeloid leukaemia patients—results from a single-centre study. Br J Haematol. 2004;125:590–600[Context Link][Full Text][CrossRef][Medline Link]19. Baird PN, Simmons PJ. Expression of the Wilms’ tumor gene (WT1) in normal hemopoiesis. Exp Hematol. 1997;25:312–320[Context Link][Medline Link]20. Grimwade D, Walker H, Oliver F, et al. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1612 patients entered into the MRC AML 10 trial. The Medical Research Council Adult and Children’s Leukaemia Working Parties. Blood. 1998;92:2322–2333[Context Link][CrossRef][Medline Link]21. Sitaram RT, Degerman S, Ljungberg B, et al. Wilms’ tumour 1 can suppress hTERT gene expression and telomerase activity in clear cell renal cell carcinoma via multiple pathways. Br J Cancer. 2010;103:1255–1262[Context Link][CrossRef][Medline Link]22. Ogawa H, Tamaki H, Ikegame K, et al. The usefulness of monitoring WT1 gene transcripts for the prediction and management of relapse following allogeneic stem cell transplantation in acute type leukemia. Blood. 2003;101:1698–1704[Context Link][CrossRef][Medline Link]23. Willasch AM, Gruhn B, Coliva T, et al. Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study. Leukemia. 2009;23:1472–1479[Context Link][Full Text][CrossRef][Medline Link]24. Kreuzer KA, Saborowski A, Lupberger J, et al. Fluorescent 5′-exonuclease assay for the absolute quantification of Wilms’ tumour gene (WT1) mRNA: implications for monitoring human leukaemias. Br J Haematol. 2001;114:313–318[Context Link][Full Text][CrossRef][Medline Link]25. Inoue K, Ogawa H, Sonoda Y, et al. Aberrant overexpression of the Wilms tumor gene (WT1) in human leukemia. Blood. 1997;89:1405–1412[Context Link][CrossRef][Medline Link]26. Beillard E, Pallisgaard N, van der Velden VH, et al. Evaluation of candidate
control genes for diagnosis and residual disease detection in leukemic patients using “real-time” quantitative reverse-transcriptase polymerase chain reaction (RQ-PCR)—a Europe against cancer program. Leukemia. 2003;17:2474–2486[Context Link][Full Text][CrossRef][Medline Link]27. Trka J, Kalinova M, Hrusak O, et al. Real-time quantitative PCR detection of WT1 gene expression in children with AML: prognostic significance, correlation with disease status and residual disease detection by flow cytometry. Leukemia. 2002;16:1381–1389[Context Link][CrossRef][Medline Link]28. Bergmann L, Miething C, Maurer U, et al. High levels of Wilms’ tumor gene (WT1) mRNA in acute myeloid leukemias are associated with a worse long-term outcome. Blood. 1997;90:1217–1225[Context Link][CrossRef][Medline Link]29. Schmid D, Heinze G, Linnerth B, et al. Prognostic significance of WT1 gene expression at diagnosis in adult de novo acute myeloid leukemia. Leukemia. 1997;11:639–643[Context Link][CrossRef][Medline Link]30. Inoue K, Ogawa H, Yamagami T, et al. Long-term follow-up of minimal residual disease in leukemia patients by monitoring WT1 (Wilms tumor gene) expression levels. Blood. 1996;88:2267–2278[Context Link][CrossRef][Medline Link]31. Cilloni D, Gottardi E, De Micheli D, et al. Quantitative assessment of WT1 expression by real time quantitative PCR may be a useful tool for monitoring minimal residual disease in acute leukemia patients. Leukemia. 2002;16:2115–2121[Context Link][CrossRef][Medline Link]32. Kern W, Haferlach C, Haferlach T, et al. Monitoring of minimal residual disease in acute myeloid leukemia. Cancer. 2008;112:4–16[Context Link][Full Text][CrossRef][Medline Link]33. King-Underwood L, Pritchard-Jones K. Wilms’ tumor (WT1) gene mutations occur mainly in acute myeloid leukemia and may confer drug resistance. Blood. 1998;91:2961–2968[Context Link][CrossRef][Medline Link]34. Summers K, Stevens J, Kakkas I, et al. Wilms’ tumour 1 mutations are associated with FLT3-ITD and failure of standard induction chemotherapy in patients with normal karyotype AML. Leukemia. 2007;21:550–551[Context Link][Full Text][CrossRef][Medline Link]35. Virappane P, Gale R, Hills R, et al. Mutation of the Wilms’ tumor 1 gene is a poor prognostic factor associated with chemotherapy resistance in normal karyotype acute myeloid leukemia: the United Kingdom Medical Research Council Adult Leukaemia Working Party. J Clin Oncol. 2008;26:5429–5435[Context Link][Full Text][CrossRef][Medline Link]36. Paschka P, Marcucci G, Ruppert AS, et al. Wilms’ tumor 1 gene mutations independently predict poor outcome in adults with cytogenetically normal acute myeloid leukemia: a cancer and leukemia group B study. J Clin Oncol. 2008;26:4595–4602[Context Link][Full Text][CrossRef][Medline Link]37. Nowakowska-Kopera A, Sacha T, Florek I, et al. Wilms’ tumor gene 1 expression analysis by real-time quantitative polymerase chain reaction for monitoring of minimal residual disease in acute leukemia. Leuk Lymphoma. 2009;50:1326–1332[Context Link][CrossRef][Medline Link]38. Lapillonne H, Renneville A, Auvrignon A, et al. High WT1 expression after induction therapy predicts high risk of relapse and death in pediatric acute myeloid leukemia. J Clin Oncol. 2006;24:1507–1515[Context Link][Full Text][CrossRef][Medline Link]39. Rubnitz JE, Inaba H, Dahl G, et al. Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol. 2010;11:543–552[Context Link][CrossRef][Medline Link]40. Candoni A, Tiribelli M, Toffoletti E, et al. Quantitative assessment of WT1 gene expression after allogeneic stem cell transplantation is a useful tool for monitoring minimal residual disease in acute myeloid leukemia. Eur J Haematol. 2009;82:61–68[Context Link][Full Text][CrossRef][Medline Link]41. Jacobsohn DA, Tse WT, Chaleff S, et al. High WT1 gene expression before haematopoietic stem cell transplant in children with acute myeloid leukaemia predicts poor event-free survival. Br J Haematol. 2009;146:669–674[Context Link][Full Text][CrossRef][Medline Link]42. Wang YL, Lee JW, Cesarman E, et al. Molecular monitoring of chronic myelogenous leukemia: identification of the most suitable internal control gene for real-time quantification of BCR-ABL transcripts. J Mol Diagn. 2006;8:231–239[Context Link][CrossRef][Medline Link]43. Lee JW, Chen Q, Knowles DM, et al. Beta-glucuronidase is an optimal normalization control gene for molecular monitoring of chronic myelogenous leukemia. J Mol Diagn. 2006;8:385–389[Context Link][CrossRef][Medline Link]44. Tamaki H, Mishima M, Kawakami M, et al. Monitoring minimal residual disease in leukemia using real-time quantitative polymerase chain reaction for Wilms tumor gene (WT1). Int J Hematol. 2003;78:349–356[Context Link][CrossRef][Medline Link]45. Kreuzer KA, Lass U, Landt O, et al. Highly sensitive and specific fluorescence reverse transcription-PCR assay for the pseudogene-free detection of beta-actin transcripts as quantitative reference. Clin Chem. 1999;45:297–300[Context Link][Full Text][CrossRef][Medline Link]46. Souliotis VL, Dimopoulos MA, Episkopou HG, et al. Preferential in vivo DNA repair of melphalan-induced damage in human genes is greatly affected by the local chromatin structure. DNA Repair (Amst). 2006;5:972–985[Context Link][CrossRef][Medline Link]47. Gubits RM, Burke RE, Casey-McIntosh G, et al. Immediate early gene induction after neonatal hypoxia-ischemia. Brain Res Mol Brain Res. 1993;18:228–238[Context Link][CrossRef][Medline Link]48. Suzuki T, Higgins PJ, Crawford DR. Control selection for RNA quantitation. Biotechniques. 2000;29:332–337[Context Link][CrossRef][Medline Link]49. Bustin SA. Absolute quantification of mRNA using real-time reverse transcription polymerase chain reaction assays. J Mol Endocrinol. 2000;25:169–193[Context Link][CrossRef][Medline Link]50. Sugiyama H. Wilms tumor gene (WT1) as a new marker for the detection of minimal residual disease in leukemia. Leuk Lymphoma. 1998;30:55–61[Context Link][CrossRef][Medline Link]WT1 gene expression; acute myeloid leukemia; minimal residual disease; RQ-PCR; control genes00019606-201212000-0000500001795_2010_115_1779_westers_immunophenotype_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1605_citationRF_FLOATING))|11065213||ovftdb|SL000017952010115177911065213citation_FROM_JRF_ID_d3518e1605_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2009-08-23974900019606-201212000-0000500001795_2010_115_1779_westers_immunophenotype_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1605_citationRF_FLOATING))|11065405||ovftdb|SL000017952010115177911065405citation_FROM_JRF_ID_d3518e1605_citationRF_FLOATING[Medline Link]2003878800019606-201212000-0000500001622_2010_22_656_grimwade_assessment_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING))|11065404||ovftdb|SL0000162220102265611065404citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING[Full Text]00001622-201011000-0001900019606-201212000-0000500001622_2010_22_656_grimwade_assessment_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING))|11065213||ovftdb|SL0000162220102265611065213citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING[CrossRef]10.1097%2FCCO.0b013e32833ed83100019606-201212000-0000500001622_2010_22_656_grimwade_assessment_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING))|11065405||ovftdb|SL0000162220102265611065405citation_FROM_JRF_ID_d3518e1641_citationRF_FLOATING[Medline Link]2080574600019606-201212000-0000500005364_2007_31_1205_scholl_nucleophosmin_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1673_citationRF_FLOATING))|11065213||ovftdb|SL00005364200731120511065213citation_FROM_JRF_ID_d3518e1673_citationRF_FLOATING[CrossRef]10.1016%2Fj.leukres.2006.12.01100019606-201212000-0000500005364_2007_31_1205_scholl_nucleophosmin_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1673_citationRF_FLOATING))|11065405||ovftdb|SL00005364200731120511065405citation_FROM_JRF_ID_d3518e1673_citationRF_FLOATING[Medline Link]1730636800019606-201212000-0000500001795_2009_114_2220_schnittger_information_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1708_citationRF_FLOATING))|11065213||ovftdb|SL000017952009114222011065213citation_FROM_JRF_ID_d3518e1708_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2009-03-21338900019606-201212000-0000500001795_2009_114_2220_schnittger_information_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1708_citationRF_FLOATING))|11065405||ovftdb|SL000017952009114222011065405citation_FROM_JRF_ID_d3518e1708_citationRF_FLOATING[Medline Link]1958737500019606-201212000-0000500005083_2009_27_3650_grimwade_promyelocytic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING))|11065404||ovftdb|SL00005083200927365011065404citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING[Full Text]00005083-200927220-0001400019606-201212000-0000500005083_2009_27_3650_grimwade_promyelocytic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING))|11065213||ovftdb|SL00005083200927365011065213citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2008.20.153300019606-201212000-0000500005083_2009_27_3650_grimwade_promyelocytic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING))|11065405||ovftdb|SL00005083200927365011065405citation_FROM_JRF_ID_d3518e1743_citationRF_FLOATING[Medline Link]1950616100019606-201212000-0000500005083_2010_28_3724_corbacioglu_prognostic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING))|11065404||ovftdb|SL00005083201028372411065404citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING[Full Text]00005083-201028230-0000900019606-201212000-0000500005083_2010_28_3724_corbacioglu_prognostic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING))|11065213||ovftdb|SL00005083201028372411065213citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2010.28.646800019606-201212000-0000500005083_2010_28_3724_corbacioglu_prognostic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING))|11065405||ovftdb|SL00005083201028372411065405citation_FROM_JRF_ID_d3518e1778_citationRF_FLOATING[Medline Link]2062512400019606-201212000-0000500001795_1994_84_3071_inoue_prognostic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1813_citationRF_FLOATING))|11065213||ovftdb|SL00001795199484307111065213citation_FROM_JRF_ID_d3518e1813_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V84.9.3071.307100019606-201212000-0000500001795_1994_84_3071_inoue_prognostic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1813_citationRF_FLOATING))|11065405||ovftdb|SL00001795199484307111065405citation_FROM_JRF_ID_d3518e1813_citationRF_FLOATING[Medline Link]794917900019606-201212000-0000500003989_2008_93_921_cilloni_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1852_citationRF_FLOATING))|11065213||ovftdb|SL0000398920089392111065213citation_FROM_JRF_ID_d3518e1852_citationRF_FLOATING[CrossRef]10.3324%2Fhaematol.1216500019606-201212000-0000500003989_2008_93_921_cilloni_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1852_citationRF_FLOATING))|11065405||ovftdb|SL0000398920089392111065405citation_FROM_JRF_ID_d3518e1852_citationRF_FLOATING[Medline Link]1844327300019606-201212000-0000500002328_2004_125_590_ostergaard_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING))|11065404||ovftdb|SL00002328200412559011065404citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING[Full Text]00002328-200406050-0000900019606-201212000-0000500002328_2004_125_590_ostergaard_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING))|11065213||ovftdb|SL00002328200412559011065213citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING[CrossRef]10.1111%2Fj.1365-2141.2004.04952.x00019606-201212000-0000500002328_2004_125_590_ostergaard_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING))|11065405||ovftdb|SL00002328200412559011065405citation_FROM_JRF_ID_d3518e1890_citationRF_FLOATING[Medline Link]1514737400019606-201212000-0000500003693_1997_25_312_baird_hemopoiesis_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1928_citationRF_FLOATING))|11065405||ovftdb|SL0000369319972531211065405citation_FROM_JRF_ID_d3518e1928_citationRF_FLOATING[Medline Link]913100600019606-201212000-0000500001795_2010_115_453_dohner_recommendations_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1283_citationRF_FLOATING))|11065213||ovftdb|SL00001795201011545311065213citation_FROM_JRF_ID_d3518e1283_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2009-07-23535800019606-201212000-0000500001795_2010_115_453_dohner_recommendations_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1283_citationRF_FLOATING))|11065405||ovftdb|SL00001795201011545311065405citation_FROM_JRF_ID_d3518e1283_citationRF_FLOATING[Medline Link]1988049700019606-201212000-0000500001795_1998_92_2322_grimwade_cytogenetics_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1958_citationRF_FLOATING))|11065213||ovftdb|SL00001795199892232211065213citation_FROM_JRF_ID_d3518e1958_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V92.7.232200019606-201212000-0000500001795_1998_92_2322_grimwade_cytogenetics_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1958_citationRF_FLOATING))|11065405||ovftdb|SL00001795199892232211065405citation_FROM_JRF_ID_d3518e1958_citationRF_FLOATING[Medline Link]974677000019606-201212000-0000500002272_2010_103_1255_sitaram_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1993_citationRF_FLOATING))|11065213||ovftdb|SL000022722010103125511065213citation_FROM_JRF_ID_d3518e1993_citationRF_FLOATING[CrossRef]10.1038%2Fsj.bjc.660587800019606-201212000-0000500002272_2010_103_1255_sitaram_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1993_citationRF_FLOATING))|11065405||ovftdb|SL000022722010103125511065405citation_FROM_JRF_ID_d3518e1993_citationRF_FLOATING[Medline Link]2084211200019606-201212000-0000500001795_2003_101_1698_ogawa_transplantation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2028_citationRF_FLOATING))|11065213||ovftdb|SL000017952003101169811065213citation_FROM_JRF_ID_d3518e2028_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2002-06-183100019606-201212000-0000500001795_2003_101_1698_ogawa_transplantation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2028_citationRF_FLOATING))|11065405||ovftdb|SL000017952003101169811065405citation_FROM_JRF_ID_d3518e2028_citationRF_FLOATING[Medline Link]1240691500019606-201212000-0000500005597_2009_23_1472_willasch_standardization_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING))|11065404||ovftdb|SL00005597200923147211065404citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING[Full Text]00005597-200908000-0001500019606-201212000-0000500005597_2009_23_1472_willasch_standardization_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING))|11065213||ovftdb|SL00005597200923147211065213citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING[CrossRef]10.1038%2Fleu.2009.5100019606-201212000-0000500005597_2009_23_1472_willasch_standardization_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING))|11065405||ovftdb|SL00005597200923147211065405citation_FROM_JRF_ID_d3518e2067_citationRF_FLOATING[Medline Link]1932220600019606-201212000-0000500002328_2001_114_313_kreuzer_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING))|11065404||ovftdb|SL00002328200111431311065404citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING[Full Text]00002328-200108020-0001000019606-201212000-0000500002328_2001_114_313_kreuzer_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING))|11065213||ovftdb|SL00002328200111431311065213citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING[CrossRef]10.1046%2Fj.1365-2141.2001.02912.x00019606-201212000-0000500002328_2001_114_313_kreuzer_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING))|11065405||ovftdb|SL00002328200111431311065405citation_FROM_JRF_ID_d3518e2108_citationRF_FLOATING[Medline Link]1152984900019606-201212000-0000500001795_1997_89_1405_inoue_overexpression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2146_citationRF_FLOATING))|11065213||ovftdb|SL00001795199789140511065213citation_FROM_JRF_ID_d3518e2146_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V89.4.140500019606-201212000-0000500001795_1997_89_1405_inoue_overexpression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2146_citationRF_FLOATING))|11065405||ovftdb|SL00001795199789140511065405citation_FROM_JRF_ID_d3518e2146_citationRF_FLOATING[Medline Link]902896400019606-201212000-0000500005597_2003_17_2474_beillard_reversetranscriptase_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING))|11065404||ovftdb|SL00005597200317247411065404citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING[Full Text]00005597-200312000-0001600019606-201212000-0000500005597_2003_17_2474_beillard_reversetranscriptase_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING))|11065213||ovftdb|SL00005597200317247411065213citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240313600019606-201212000-0000500005597_2003_17_2474_beillard_reversetranscriptase_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING))|11065405||ovftdb|SL00005597200317247411065405citation_FROM_JRF_ID_d3518e2184_citationRF_FLOATING[Medline Link]1456212400019606-201212000-0000500005597_2002_16_1381_trka_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2219_citationRF_FLOATING))|11065213||ovftdb|SL00005597200216138111065213citation_FROM_JRF_ID_d3518e2219_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240251200019606-201212000-0000500005597_2002_16_1381_trka_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2219_citationRF_FLOATING))|11065405||ovftdb|SL00005597200216138111065405citation_FROM_JRF_ID_d3518e2219_citationRF_FLOATING[Medline Link]1209426400019606-201212000-0000500001795_1997_90_1217_bergmann_associated_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2257_citationRF_FLOATING))|11065213||ovftdb|SL00001795199790121711065213citation_FROM_JRF_ID_d3518e2257_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V90.3.121700019606-201212000-0000500001795_1997_90_1217_bergmann_associated_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2257_citationRF_FLOATING))|11065405||ovftdb|SL00001795199790121711065405citation_FROM_JRF_ID_d3518e2257_citationRF_FLOATING[Medline Link]924255500019606-201212000-0000500005597_1997_11_639_schmid_significance_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2296_citationRF_FLOATING))|11065213||ovftdb|SL0000559719971163911065213citation_FROM_JRF_ID_d3518e2296_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240062000019606-201212000-0000500005597_1997_11_639_schmid_significance_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2296_citationRF_FLOATING))|11065405||ovftdb|SL0000559719971163911065405citation_FROM_JRF_ID_d3518e2296_citationRF_FLOATING[Medline Link]918028500019606-201212000-0000500001795_2009_113_3666_derolf_populationbased_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1318_citationRF_FLOATING))|11065213||ovftdb|SL000017952009113366611065213citation_FROM_JRF_ID_d3518e1318_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2008-09-17934100019606-201212000-0000500001795_2009_113_3666_derolf_populationbased_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1318_citationRF_FLOATING))|11065405||ovftdb|SL000017952009113366611065405citation_FROM_JRF_ID_d3518e1318_citationRF_FLOATING[Medline Link]1902030600019606-201212000-0000500001795_1996_88_2267_inoue_monitoring_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2334_citationRF_FLOATING))|11065213||ovftdb|SL00001795199688226711065213citation_FROM_JRF_ID_d3518e2334_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V88.6.2267.bloodjournal886226700019606-201212000-0000500001795_1996_88_2267_inoue_monitoring_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2334_citationRF_FLOATING))|11065405||ovftdb|SL00001795199688226711065405citation_FROM_JRF_ID_d3518e2334_citationRF_FLOATING[Medline Link]882294800019606-201212000-0000500005597_2002_16_2115_cilloni_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2372_citationRF_FLOATING))|11065213||ovftdb|SL00005597200216211511065213citation_FROM_JRF_ID_d3518e2372_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240267500019606-201212000-0000500005597_2002_16_2115_cilloni_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2372_citationRF_FLOATING))|11065405||ovftdb|SL00005597200216211511065405citation_FROM_JRF_ID_d3518e2372_citationRF_FLOATING[Medline Link]1235736500019606-201212000-0000500002808_2008_112_4_kern_monitoring_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING))|11065404||ovftdb|SL000028082008112411065404citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING[Full Text]01445386-200801010-0000200019606-201212000-0000500002808_2008_112_4_kern_monitoring_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING))|11065213||ovftdb|SL000028082008112411065213citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING[CrossRef]10.1002%2Fcncr.2312800019606-201212000-0000500002808_2008_112_4_kern_monitoring_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING))|11065405||ovftdb|SL000028082008112411065405citation_FROM_JRF_ID_d3518e2410_citationRF_FLOATING[Medline Link]1800081100019606-201212000-0000500001795_1998_91_2961_underwood_resistance_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2445_citationRF_FLOATING))|11065213||ovftdb|SL00001795199891296111065213citation_FROM_JRF_ID_d3518e2445_citationRF_FLOATING[CrossRef]10.1182%2Fblood.V91.8.2961.2961_2961_296800019606-201212000-0000500001795_1998_91_2961_underwood_resistance_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2445_citationRF_FLOATING))|11065405||ovftdb|SL00001795199891296111065405citation_FROM_JRF_ID_d3518e2445_citationRF_FLOATING[Medline Link]953160700019606-201212000-0000500005597_2007_21_550_summers_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING))|11065404||ovftdb|SL0000559720072155011065404citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING[Full Text]00005597-200703000-0002400019606-201212000-0000500005597_2007_21_550_summers_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING))|11065213||ovftdb|SL0000559720072155011065213citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240451400019606-201212000-0000500005597_2007_21_550_summers_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING))|11065405||ovftdb|SL0000559720072155011065405citation_FROM_JRF_ID_d3518e2475_citationRF_FLOATING[Medline Link]1720505500019606-201212000-0000500005083_2008_26_5429_virappane_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING))|11065404||ovftdb|SL00005083200826542911065404citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING[Full Text]00005083-200826330-0002000019606-201212000-0000500005083_2008_26_5429_virappane_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING))|11065213||ovftdb|SL00005083200826542911065213citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2008.16.033300019606-201212000-0000500005083_2008_26_5429_virappane_chemotherapy_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING))|11065405||ovftdb|SL00005083200826542911065405citation_FROM_JRF_ID_d3518e2511_citationRF_FLOATING[Medline Link]1859154600019606-201212000-0000500005083_2008_26_4595_paschka_cytogenetically_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING))|11065404||ovftdb|SL00005083200826459511065404citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING[Full Text]00005083-200826280-0001500019606-201212000-0000500005083_2008_26_4595_paschka_cytogenetically_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING))|11065213||ovftdb|SL00005083200826459511065213citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2007.15.205800019606-201212000-0000500005083_2008_26_4595_paschka_cytogenetically_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING))|11065405||ovftdb|SL00005083200826459511065405citation_FROM_JRF_ID_d3518e2546_citationRF_FLOATING[Medline Link]1855987400019606-201212000-0000500008498_2009_50_1326_nowakowska_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2581_citationRF_FLOATING))|11065213||ovftdb|SL00008498200950132611065213citation_FROM_JRF_ID_d3518e2581_citationRF_FLOATING[CrossRef]10.1080%2F1042819090305002100019606-201212000-0000500008498_2009_50_1326_nowakowska_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2581_citationRF_FLOATING))|11065405||ovftdb|SL00008498200950132611065405citation_FROM_JRF_ID_d3518e2581_citationRF_FLOATING[Medline Link]1981133300019606-201212000-0000500005083_2006_24_1507_lapillonne_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING))|11065404||ovftdb|SL00005083200624150711065404citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING[Full Text]00005083-200604010-0000500019606-201212000-0000500005083_2006_24_1507_lapillonne_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING))|11065213||ovftdb|SL00005083200624150711065213citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2005.03.530300019606-201212000-0000500005083_2006_24_1507_lapillonne_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING))|11065405||ovftdb|SL00005083200624150711065405citation_FROM_JRF_ID_d3518e2616_citationRF_FLOATING[Medline Link]1657500000019606-201212000-0000500130981_2010_11_543_rubnitz_multicentre_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2654_citationRF_FLOATING))|11065213||ovftdb|SL0013098120101154311065213citation_FROM_JRF_ID_d3518e2654_citationRF_FLOATING[CrossRef]10.1016%2FS1470-2045%2810%2970090-500019606-201212000-0000500130981_2010_11_543_rubnitz_multicentre_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2654_citationRF_FLOATING))|11065405||ovftdb|SL0013098120101154311065405citation_FROM_JRF_ID_d3518e2654_citationRF_FLOATING[Medline Link]2045145400019606-201212000-0000500005083_2009_27_5195_cilloni_stratification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING))|11065404||ovftdb|SL00005083200927519511065404citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING[Full Text]00005083-200927310-0001500019606-201212000-0000500005083_2009_27_5195_cilloni_stratification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING))|11065213||ovftdb|SL00005083200927519511065213citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING[CrossRef]10.1200%2FJCO.2009.22.486500019606-201212000-0000500005083_2009_27_5195_cilloni_stratification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING))|11065405||ovftdb|SL00005083200927519511065405citation_FROM_JRF_ID_d3518e1353_citationRF_FLOATING[Medline Link]1975233500019606-201212000-0000500003715_2009_82_61_candoni_transplantation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING))|11065404||ovftdb|SL000037152009826111065404citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING[Full Text]00003715-200901000-0001000019606-201212000-0000500003715_2009_82_61_candoni_transplantation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING))|11065213||ovftdb|SL000037152009826111065213citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING[CrossRef]10.1111%2Fj.1600-0609.2008.01158.x00019606-201212000-0000500003715_2009_82_61_candoni_transplantation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING))|11065405||ovftdb|SL000037152009826111065405citation_FROM_JRF_ID_d3518e2689_citationRF_FLOATING[Medline Link]1880105800019606-201212000-0000500002328_2009_146_669_jacobsohn_haematopoietic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING))|11065404||ovftdb|SL00002328200914666911065404citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING[Full Text]00002328-200909020-0001300019606-201212000-0000500002328_2009_146_669_jacobsohn_haematopoietic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING))|11065213||ovftdb|SL00002328200914666911065213citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING[CrossRef]10.1111%2Fj.1365-2141.2009.07770.x00019606-201212000-0000500002328_2009_146_669_jacobsohn_haematopoietic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING))|11065405||ovftdb|SL00002328200914666911065405citation_FROM_JRF_ID_d3518e2728_citationRF_FLOATING[Medline Link]1965088400019606-201212000-0000500129312_2006_8_231_wang_identification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2766_citationRF_FLOATING))|11065213||ovftdb|SL001293122006823111065213citation_FROM_JRF_ID_d3518e2766_citationRF_FLOATING[CrossRef]10.2353%2Fjmoldx.2006.04040400019606-201212000-0000500129312_2006_8_231_wang_identification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2766_citationRF_FLOATING))|11065405||ovftdb|SL001293122006823111065405citation_FROM_JRF_ID_d3518e2766_citationRF_FLOATING[Medline Link]1664521000019606-201212000-0000500129312_2006_8_385_lee_glucuronidase_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2801_citationRF_FLOATING))|11065213||ovftdb|SL001293122006838511065213citation_FROM_JRF_ID_d3518e2801_citationRF_FLOATING[CrossRef]10.2353%2Fjmoldx.2006.05015000019606-201212000-0000500129312_2006_8_385_lee_glucuronidase_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2801_citationRF_FLOATING))|11065405||ovftdb|SL001293122006838511065405citation_FROM_JRF_ID_d3518e2801_citationRF_FLOATING[Medline Link]1682551300019606-201212000-0000500001778_2003_78_349_tamaki_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2836_citationRF_FLOATING))|11065213||ovftdb|SL0000177820037834911065213citation_FROM_JRF_ID_d3518e2836_citationRF_FLOATING[CrossRef]10.1007%2FBF0298356100019606-201212000-0000500001778_2003_78_349_tamaki_quantitative_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2836_citationRF_FLOATING))|11065405||ovftdb|SL0000177820037834911065405citation_FROM_JRF_ID_d3518e2836_citationRF_FLOATING[Medline Link]1468649400019606-201212000-0000500003030_1999_45_297_kreuzer_transcription_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING))|11065404||ovftdb|SL0000303019994529711065404citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING[Full Text]00003030-199902000-0002500019606-201212000-0000500003030_1999_45_297_kreuzer_transcription_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING))|11065213||ovftdb|SL0000303019994529711065213citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING[CrossRef]10.1093%2Fclinchem%2F45.2.29700019606-201212000-0000500003030_1999_45_297_kreuzer_transcription_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING))|11065405||ovftdb|SL0000303019994529711065405citation_FROM_JRF_ID_d3518e2874_citationRF_FLOATING[Medline Link]993105900019606-201212000-0000500134429_2006_5_972_souliotis_preferential_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2909_citationRF_FLOATING))|11065213||ovftdb|SL001344292006597211065213citation_FROM_JRF_ID_d3518e2909_citationRF_FLOATING[CrossRef]10.1016%2Fj.dnarep.2006.05.00600019606-201212000-0000500134429_2006_5_972_souliotis_preferential_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2909_citationRF_FLOATING))|11065405||ovftdb|SL001344292006597211065405citation_FROM_JRF_ID_d3518e2909_citationRF_FLOATING[Medline Link]1678119900019606-201212000-0000500005740_1993_18_228_gubits_immediate_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2945_citationRF_FLOATING))|11065213||ovftdb|SL0000574019931822811065213citation_FROM_JRF_ID_d3518e2945_citationRF_FLOATING[CrossRef]10.1016%2F0169-328X%2893%2990194-T00019606-201212000-0000500005740_1993_18_228_gubits_immediate_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2945_citationRF_FLOATING))|11065405||ovftdb|SL0000574019931822811065405citation_FROM_JRF_ID_d3518e2945_citationRF_FLOATING[Medline Link]768448300019606-201212000-0000500002112_2000_29_332_suzuki_quantitation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2980_citationRF_FLOATING))|11065213||ovftdb|SL0000211220002933211065213citation_FROM_JRF_ID_d3518e2980_citationRF_FLOATING[CrossRef]10.2144%2F00292rv0200019606-201212000-0000500002112_2000_29_332_suzuki_quantitation_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e2980_citationRF_FLOATING))|11065405||ovftdb|SL0000211220002933211065405citation_FROM_JRF_ID_d3518e2980_citationRF_FLOATING[Medline Link]1094843400019606-201212000-0000500001934_2000_25_169_bustin_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e3012_citationRF_FLOATING))|11065213||ovftdb|SL0000193420002516911065213citation_FROM_JRF_ID_d3518e3012_citationRF_FLOATING[CrossRef]10.1677%2Fjme.0.025016900019606-201212000-0000500001934_2000_25_169_bustin_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e3012_citationRF_FLOATING))|11065405||ovftdb|SL0000193420002516911065405citation_FROM_JRF_ID_d3518e3012_citationRF_FLOATING[Medline Link]1101334500019606-201212000-0000500001795_2004_104_3078_kern_multiparameter_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1391_citationRF_FLOATING))|11065213||ovftdb|SL000017952004104307811065213citation_FROM_JRF_ID_d3518e1391_citationRF_FLOATING[CrossRef]10.1182%2Fblood-2004-03-103600019606-201212000-0000500001795_2004_104_3078_kern_multiparameter_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1391_citationRF_FLOATING))|11065405||ovftdb|SL000017952004104307811065405citation_FROM_JRF_ID_d3518e1391_citationRF_FLOATING[Medline Link]1528411400019606-201212000-0000500008498_1998_30_55_sugiyama_detection_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e3034_citationRF_FLOATING))|11065213||ovftdb|SL000084981998305511065213citation_FROM_JRF_ID_d3518e3034_citationRF_FLOATING[CrossRef]10.3109%2F1042819980905092900019606-201212000-0000500008498_1998_30_55_sugiyama_detection_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e3034_citationRF_FLOATING))|11065405||ovftdb|SL000084981998305511065405citation_FROM_JRF_ID_d3518e3034_citationRF_FLOATING[Medline Link]966967600019606-201212000-0000500005597_2005_19_1416_weisser_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING))|11065404||ovftdb|SL00005597200519141611065404citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING[Full Text]00005597-200508000-0002100019606-201212000-0000500005597_2005_19_1416_weisser_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING))|11065213||ovftdb|SL00005597200519141611065213citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING[CrossRef]10.1038%2Fsj.leu.240380900019606-201212000-0000500005597_2005_19_1416_weisser_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING))|11065405||ovftdb|SL00005597200519141611065405citation_FROM_JRF_ID_d3518e1427_citationRF_FLOATING[Medline Link]1592049300019606-201212000-0000500030512_2002_30_1170_li_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1465_citationRF_FLOATING))|11065213||ovftdb|SL00030512200230117011065213citation_FROM_JRF_ID_d3518e1465_citationRF_FLOATING[CrossRef]10.1016%2FS0301-472X%2802%2900892-500019606-201212000-0000500030512_2002_30_1170_li_quantification_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1465_citationRF_FLOATING))|11065405||ovftdb|SL00030512200230117011065405citation_FROM_JRF_ID_d3518e1465_citationRF_FLOATING[Medline Link]1238414800019606-201212000-0000500002328_2011_152_743_thorn_lymphoblastic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING))|11065404||ovftdb|SL00002328201115274311065404citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING[Full Text]00002328-201103010-0001000019606-201212000-0000500002328_2011_152_743_thorn_lymphoblastic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING))|11065213||ovftdb|SL00002328201115274311065213citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING[CrossRef]10.1111%2Fj.1365-2141.2010.08456.x00019606-201212000-0000500002328_2011_152_743_thorn_lymphoblastic_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING))|11065405||ovftdb|SL00002328201115274311065405citation_FROM_JRF_ID_d3518e1500_citationRF_FLOATING[Medline Link]2125097000019606-201212000-0000500128088_2010_23_379_kern_multiparameter_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1535_citationRF_FLOATING))|11065213||ovftdb|SL0012808820102337911065213citation_FROM_JRF_ID_d3518e1535_citationRF_FLOATING[CrossRef]10.1016%2Fj.beha.2010.06.00700019606-201212000-0000500128088_2010_23_379_kern_multiparameter_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1535_citationRF_FLOATING))|11065405||ovftdb|SL0012808820102337911065405citation_FROM_JRF_ID_d3518e1535_citationRF_FLOATING[Medline Link]2111203700019606-201212000-0000500002996_2000_42_247_oelschlagel_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1570_citationRF_FLOATING))|11065213||ovftdb|SL0000299620004224711065213citation_FROM_JRF_ID_d3518e1570_citationRF_FLOATING[CrossRef]10.1002%2F1097-0320%2820000815%2942%3A4%3C247%3A%3AAID-CYTO5%3E3.0.CO%3B2-V00019606-201212000-0000500002996_2000_42_247_oelschlagel_expression_|00019606-201212000-00005#xpointer(id(citation_FROM_JRF_ID_d3518e1570_citationRF_FLOATING))|11065405||ovftdb|SL0000299620004224711065405citation_FROM_JRF_ID_d3518e1570_citationRF_FLOATING[Medline Link]10934344Positive correlation between Wilms tumor gene 1 (WT1) mRNA expression levels normalized against those of β-actin (y-axis) and those of ABL1 (x-axis). Samples with low expression levels for both WT1/β-actin (≤0.1) and WT1/ABL1 (≤100) also showed a similar trend.WT1 Gene Expression Levels and Clinical Characteristics at Diagnosis in Patients With Acute Myeloid LeukemiaKaplan-Meier plot of overall survival (A) and freedom from relapse (B). Acute myeloid leukemia patients were divided into groups on the basis of a ≥1-log or a ≤1-log reduction in Wilms tumor gene 1 WT1 expression (relative to expression of the β-actin gene) in bone marrow at <1 month.Kaplan-Meier plot of the overall survival of acute myeloid leukemia patients with a reduction in Wilms tumor gene 1 (WT1) gene expression in peripheral blood of above or below 2 logs, between 1 and 6 months. A, WT1 gene expression normalized against β-actin gene expression. B, WT1 gene expression normalized against ABL1 gene expression.Kaplan-Meier plot of freedom from relapse of acute myeloid leukemia patients with a reduction in Wilms tumor gene 1(WT1) gene expression in peripheral blood of above or below 2 logs, between 1 and 6 months. A, WT1 gene expression normalized against β-actin gene expression. B, WT1 gene expression normalized against ABL1 gene expression.WT1 Gene Expression Before and After Hematopoietic Stem Cell Transplantation in Cases With Acute Myeloid LeukemiaReduction in <em xmlns:mrws="http://webservices.ovid.com/mrws/1.0">WT1</em> Gene Expression During Early Treatment Predicts the Outcome in Patients With Acute Myeloid LeukemiaAndersson Charlotta MD; Li, Xingru MD; Lorenz, Fryderyk MD; Golovleva, Irina MD, PhD; Wahlin, Anders MD, PhD; Li, Aihong MD, PhDOriginal ArticlesOriginal Articles421p 225-233
