TEL-AML1 POSITIVE CHILDHOOD ACUTE LYMPHOBLASTIC LEUKEMIA-SINGLE CENTRE EXPERIENCE
(Abstract release date: 05/19/16)
EHA Library. Kourti M. 06/09/16; 134520; PB1620
Dr. Maria Kourti
Contributions
Contributions
Abstract
Abstract: PB1620
Type: Publication Only
Background
Objective: The reciprocal translocation t(12;21)(p13;q22) is the most frequent chromosomal rearrangement in childhood B-cell precursor acute lymphoblastic leukaemia (ALL), which results in a chimeric transcription factor TEL-AML1 (ETV6-RUNX1) and is associated with favorable prognosis. Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry. Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%. Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted.
Aims
We performed a retrospective analysis of B-cell ALL patients who were treated in the last five years in our department in order to investigate the incidence, the clinical characteristics and cytogenetic features of TEL-AML1 positive patients.
Methods
Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry.
Results
Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%.
Conclusion
Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted
Session topic: E-poster
Keyword(s): Acute lymphoblastic leukemia, Childhood, TEL-AML1
Type: Publication Only
Background
Objective: The reciprocal translocation t(12;21)(p13;q22) is the most frequent chromosomal rearrangement in childhood B-cell precursor acute lymphoblastic leukaemia (ALL), which results in a chimeric transcription factor TEL-AML1 (ETV6-RUNX1) and is associated with favorable prognosis. Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry. Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%. Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted.
Aims
We performed a retrospective analysis of B-cell ALL patients who were treated in the last five years in our department in order to investigate the incidence, the clinical characteristics and cytogenetic features of TEL-AML1 positive patients.
Methods
Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry.
Results
Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%.
Conclusion
Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted
Session topic: E-poster
Keyword(s): Acute lymphoblastic leukemia, Childhood, TEL-AML1
Abstract: PB1620
Type: Publication Only
Background
Objective: The reciprocal translocation t(12;21)(p13;q22) is the most frequent chromosomal rearrangement in childhood B-cell precursor acute lymphoblastic leukaemia (ALL), which results in a chimeric transcription factor TEL-AML1 (ETV6-RUNX1) and is associated with favorable prognosis. Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry. Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%. Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted.
Aims
We performed a retrospective analysis of B-cell ALL patients who were treated in the last five years in our department in order to investigate the incidence, the clinical characteristics and cytogenetic features of TEL-AML1 positive patients.
Methods
Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry.
Results
Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%.
Conclusion
Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted
Session topic: E-poster
Keyword(s): Acute lymphoblastic leukemia, Childhood, TEL-AML1
Type: Publication Only
Background
Objective: The reciprocal translocation t(12;21)(p13;q22) is the most frequent chromosomal rearrangement in childhood B-cell precursor acute lymphoblastic leukaemia (ALL), which results in a chimeric transcription factor TEL-AML1 (ETV6-RUNX1) and is associated with favorable prognosis. Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry. Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%. Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted.
Aims
We performed a retrospective analysis of B-cell ALL patients who were treated in the last five years in our department in order to investigate the incidence, the clinical characteristics and cytogenetic features of TEL-AML1 positive patients.
Methods
Methods: Pretreatment bone marrow (BM) samples were successfully analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) for the molecular detection of the TEL/AML1 fusion gene. BM samples were also cultured and analyzed by standard cytogenetic methods. The immunophenotype was determined using a panel of monoclonal antibodies (MoAbs) with flow cytometry.
Results
Results: A total of 51 patients with ALL displayed G-banded karyotypes and were informative for molecular analysis and were included for analysis. All patients were treated according to ALLIC-BFM 2009 protocol. On the basis of EGIL classification, the immunophenotype analysis permitted the characterization of 32 cases (62.7%) as pre-B ALL, 10 (19.6 %) as common ALL and 9 (17.7%) as pro-B ALL. The TEL-AML1 fusion gene was identified in 11 patients of which 7 (63.6%) had pre-B, 3 (27.3%) pro-B ALL and 1 (90.1%) common ALL. The incidence of TEL-AML1 fusion gene was 21.6% (11/51 patients). The TEL-AML1 positive patients were studied with regard to their gender and it revealed that 7 were females and 4 males with median age of 4.16 (range:3.41-13.16 years). The median leucocyte count was 8.3x109/L (range 2.6-67x109/L) According to the presenting features, 91% of the TEL/AML1-positive cases were enrolled in the IR group and 9% in the SR. Moreover, all TEL/AML1-positive cases lacked evidence for BCR/ABL and MLL/AF4 fusion mRNAs. No structural chromosomal changes were noted in TEL-AML1 positive children. Hyperdiploidy of 47–48 chromosomes was encountered in 18.18% (2/11) of the children with TEL-AML1 rearrangement; however, none of TEL-AML1 positive patients had hyperdiploidy of more than 50 chromosomes. All cases were prednisone good responders and they were all very early good responders (minimal residual disease <10-3 at day 15. All patients are in continuous complete remission with event-free and overall survival of 100%.
Conclusion
Conclusions: The TEL-AML1 fusion gene is a common genetic anomaly in childhood ALL patients and our results are consistent with literature. Further investigation with a larger sample size and for a longer time is warranted
Session topic: E-poster
Keyword(s): Acute lymphoblastic leukemia, Childhood, TEL-AML1
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