Molecular classification improves risk assessment in adult BCR-ABL1-negative B-ALL
Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international UKALLXII/ECOG-ACRIN E2993 (#NCT00002514) trial accrued 1229 adolescent/adult patients with BCR-ABL1- B-ALL (aged 14 to 65 years). Although 93% of patients...
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| Veröffentlicht in: | Blood Jg. 138; H. 11; S. 948 |
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16.09.2021
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| Abstract | Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international UKALLXII/ECOG-ACRIN E2993 (#NCT00002514) trial accrued 1229 adolescent/adult patients with BCR-ABL1- B-ALL (aged 14 to 65 years). Although 93% of patients achieved remission, 41% relapsed at a median of 13 months (range, 28 days to 12 years). Five-year overall survival (OS) was 42% (95% confidence interval, 39, 44). Transcriptome sequencing, gene expression profiling, cytogenetics, and fusion polymerase chain reaction enabled genomic subtyping of 282 patient samples, of which 264 were eligible for trial, accounting for 64.5% of E2993 patients. Among patients with outcome data, 29.5% with favorable outcomes (5-year OS 65% to 80%) were deemed standard risk (DUX4-rearranged [9.2%], ETV6-RUNX1/-like [2.3%], TCF3-PBX1 [6.9%], PAX5 P80R [4.1%], high-hyperdiploid [6.9%]); 50.2% had high-risk genotypes with 5-year OS of 0% to 27% (Ph-like [21.2%], KMT2A-AFF1 [12%], low-hypodiploid/near-haploid [14.3%], BCL2/MYC-rearranged [2.8%]); 20.3% had intermediate-risk genotypes with 5-year OS of 33% to 45% (PAX5alt [12.4%], ZNF384/-like [5.1%], MEF2D-rearranged [2.8%]). IKZF1 alterations occurred in 86% of Ph-like, and TP53 mutations in patients who were low-hypodiploid (54%) and BCL2/MYC-rearranged (33%) but were not independently associated with outcome. Of patients considered high risk based on presenting age and white blood cell count, 40% harbored subtype-defining genetic alterations associated with standard- or intermediate-risk outcomes. We identified distinct immunophenotypic features for DUX4-rearranged, PAX5 P80R, ZNF384-R/-like, and Ph-like genotypes. These data in a large adult B-ALL cohort treated with a non-risk-adapted approach on a single trial show the prognostic importance of genomic analyses, which may translate into future therapeutic benefits. |
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| AbstractList | Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international UKALLXII/ECOG-ACRIN E2993 (#NCT00002514) trial accrued 1229 adolescent/adult patients with BCR-ABL1- B-ALL (aged 14 to 65 years). Although 93% of patients achieved remission, 41% relapsed at a median of 13 months (range, 28 days to 12 years). Five-year overall survival (OS) was 42% (95% confidence interval, 39, 44). Transcriptome sequencing, gene expression profiling, cytogenetics, and fusion polymerase chain reaction enabled genomic subtyping of 282 patient samples, of which 264 were eligible for trial, accounting for 64.5% of E2993 patients. Among patients with outcome data, 29.5% with favorable outcomes (5-year OS 65% to 80%) were deemed standard risk (DUX4-rearranged [9.2%], ETV6-RUNX1/-like [2.3%], TCF3-PBX1 [6.9%], PAX5 P80R [4.1%], high-hyperdiploid [6.9%]); 50.2% had high-risk genotypes with 5-year OS of 0% to 27% (Ph-like [21.2%], KMT2A-AFF1 [12%], low-hypodiploid/near-haploid [14.3%], BCL2/MYC-rearranged [2.8%]); 20.3% had intermediate-risk genotypes with 5-year OS of 33% to 45% (PAX5alt [12.4%], ZNF384/-like [5.1%], MEF2D-rearranged [2.8%]). IKZF1 alterations occurred in 86% of Ph-like, and TP53 mutations in patients who were low-hypodiploid (54%) and BCL2/MYC-rearranged (33%) but were not independently associated with outcome. Of patients considered high risk based on presenting age and white blood cell count, 40% harbored subtype-defining genetic alterations associated with standard- or intermediate-risk outcomes. We identified distinct immunophenotypic features for DUX4-rearranged, PAX5 P80R, ZNF384-R/-like, and Ph-like genotypes. These data in a large adult B-ALL cohort treated with a non-risk-adapted approach on a single trial show the prognostic importance of genomic analyses, which may translate into future therapeutic benefits.Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international UKALLXII/ECOG-ACRIN E2993 (#NCT00002514) trial accrued 1229 adolescent/adult patients with BCR-ABL1- B-ALL (aged 14 to 65 years). Although 93% of patients achieved remission, 41% relapsed at a median of 13 months (range, 28 days to 12 years). Five-year overall survival (OS) was 42% (95% confidence interval, 39, 44). Transcriptome sequencing, gene expression profiling, cytogenetics, and fusion polymerase chain reaction enabled genomic subtyping of 282 patient samples, of which 264 were eligible for trial, accounting for 64.5% of E2993 patients. Among patients with outcome data, 29.5% with favorable outcomes (5-year OS 65% to 80%) were deemed standard risk (DUX4-rearranged [9.2%], ETV6-RUNX1/-like [2.3%], TCF3-PBX1 [6.9%], PAX5 P80R [4.1%], high-hyperdiploid [6.9%]); 50.2% had high-risk genotypes with 5-year OS of 0% to 27% (Ph-like [21.2%], KMT2A-AFF1 [12%], low-hypodiploid/near-haploid [14.3%], BCL2/MYC-rearranged [2.8%]); 20.3% had intermediate-risk genotypes with 5-year OS of 33% to 45% (PAX5alt [12.4%], ZNF384/-like [5.1%], MEF2D-rearranged [2.8%]). IKZF1 alterations occurred in 86% of Ph-like, and TP53 mutations in patients who were low-hypodiploid (54%) and BCL2/MYC-rearranged (33%) but were not independently associated with outcome. Of patients considered high risk based on presenting age and white blood cell count, 40% harbored subtype-defining genetic alterations associated with standard- or intermediate-risk outcomes. We identified distinct immunophenotypic features for DUX4-rearranged, PAX5 P80R, ZNF384-R/-like, and Ph-like genotypes. These data in a large adult B-ALL cohort treated with a non-risk-adapted approach on a single trial show the prognostic importance of genomic analyses, which may translate into future therapeutic benefits. Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international UKALLXII/ECOG-ACRIN E2993 (#NCT00002514) trial accrued 1229 adolescent/adult patients with BCR-ABL1- B-ALL (aged 14 to 65 years). Although 93% of patients achieved remission, 41% relapsed at a median of 13 months (range, 28 days to 12 years). Five-year overall survival (OS) was 42% (95% confidence interval, 39, 44). Transcriptome sequencing, gene expression profiling, cytogenetics, and fusion polymerase chain reaction enabled genomic subtyping of 282 patient samples, of which 264 were eligible for trial, accounting for 64.5% of E2993 patients. Among patients with outcome data, 29.5% with favorable outcomes (5-year OS 65% to 80%) were deemed standard risk (DUX4-rearranged [9.2%], ETV6-RUNX1/-like [2.3%], TCF3-PBX1 [6.9%], PAX5 P80R [4.1%], high-hyperdiploid [6.9%]); 50.2% had high-risk genotypes with 5-year OS of 0% to 27% (Ph-like [21.2%], KMT2A-AFF1 [12%], low-hypodiploid/near-haploid [14.3%], BCL2/MYC-rearranged [2.8%]); 20.3% had intermediate-risk genotypes with 5-year OS of 33% to 45% (PAX5alt [12.4%], ZNF384/-like [5.1%], MEF2D-rearranged [2.8%]). IKZF1 alterations occurred in 86% of Ph-like, and TP53 mutations in patients who were low-hypodiploid (54%) and BCL2/MYC-rearranged (33%) but were not independently associated with outcome. Of patients considered high risk based on presenting age and white blood cell count, 40% harbored subtype-defining genetic alterations associated with standard- or intermediate-risk outcomes. We identified distinct immunophenotypic features for DUX4-rearranged, PAX5 P80R, ZNF384-R/-like, and Ph-like genotypes. These data in a large adult B-ALL cohort treated with a non-risk-adapted approach on a single trial show the prognostic importance of genomic analyses, which may translate into future therapeutic benefits. |
| Author | Roberts, Kathryn G Cheng, Cheng Buck, Georgina A N Willman, Cheryl L Pounds, Stanley Rowe, Jacob M Cheng, Zhongshan Alejos, David Patel, Bela Melnick, Ari Qu, Chunxu Pei, Deqing Harvey, Richard Foroni, Letizia Zhang, Yanming Shi, Lei Paietta, Elisabeth Wu, Gang Dewald, Gordon W Lazarus, Hillard M Levine, Ross L Fielding, Adele K Gu, Zhaohui Abdel-Wahab, Omar Wiernik, Peter H Goldstone, Anthony H Racevskis, Janis Barinka, Jan Tallman, Martin S Marks, David I Wang, Victoria Ketterling, Rhett P Moorman, Anthony V Litzow, Mark R Luger, Selina M Mullighan, Charles G |
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Children's Research Hospital, Memphis, TN – sequence: 7 givenname: Cheng surname: Cheng fullname: Cheng, Cheng organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN – sequence: 8 givenname: Ross L surname: Levine fullname: Levine, Ross L organization: Human Oncology and Pathogenesis Program-Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY – sequence: 9 givenname: Omar surname: Abdel-Wahab fullname: Abdel-Wahab, Omar organization: Human Oncology and Pathogenesis Program-Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY – sequence: 10 givenname: Zhongshan surname: Cheng fullname: Cheng, Zhongshan organization: Centre for Applied Bioinformatics, St Jude Children's Research Hospital, Memphis, TN – sequence: 11 givenname: Gang surname: Wu fullname: Wu, Gang organization: Centre for Applied Bioinformatics, St Jude Children's Research Hospital, Memphis, TN – sequence: 12 givenname: Chunxu surname: Qu fullname: Qu, Chunxu organization: Department of Pathology, St Jude Children's Research Hospital, Memphis, TN – sequence: 13 givenname: Lei surname: Shi fullname: Shi, Lei organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN – sequence: 14 givenname: Stanley surname: Pounds fullname: Pounds, Stanley organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN – sequence: 15 givenname: Cheryl L surname: Willman fullname: Willman, Cheryl L organization: University of New Mexico Comprehensive Cancer Center, Albuquerque, NM – sequence: 16 givenname: Richard orcidid: 0000-0002-4904-9767 surname: Harvey fullname: Harvey, Richard organization: University of New Mexico Comprehensive Cancer Center, Albuquerque, NM – sequence: 17 givenname: Janis surname: Racevskis fullname: Racevskis, Janis organization: Department of Oncology, Montefiore Medical Center, Bronx, NY – sequence: 18 givenname: Jan surname: Barinka fullname: Barinka, Jan organization: Department of Pathology, St Jude Children's Research Hospital, Memphis, TN – sequence: 19 givenname: Yanming surname: Zhang fullname: Zhang, Yanming organization: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY – sequence: 20 givenname: Gordon W surname: Dewald fullname: Dewald, Gordon W organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN – sequence: 21 givenname: Rhett P surname: Ketterling fullname: Ketterling, Rhett P organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN – sequence: 22 givenname: David surname: Alejos fullname: Alejos, David organization: Department of Oncology, Montefiore Medical Center, Bronx, NY – sequence: 23 givenname: Hillard M orcidid: 0000-0002-1159-5607 surname: Lazarus fullname: Lazarus, Hillard M organization: Department of Medicine, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, OH – sequence: 24 givenname: Selina M surname: Luger fullname: Luger, Selina M organization: Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA – sequence: 25 givenname: Letizia surname: Foroni fullname: Foroni, Letizia organization: Centre for Haematology, Department of Medicine, Imperial College London Hammersmith Hospital, London, United Kingdom – sequence: 26 givenname: Bela surname: Patel fullname: Patel, Bela organization: Centre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom – sequence: 27 givenname: Adele K orcidid: 0000-0002-4746-7789 surname: Fielding fullname: Fielding, Adele K organization: UCL Cancer Institute, London, United Kingdom – sequence: 28 givenname: Ari orcidid: 0000-0002-8074-2287 surname: Melnick fullname: Melnick, Ari organization: Division of Hematology and Medical Oncology, Department of Medicine, Weill Medical College of Cornell University, New York, NY – sequence: 29 givenname: David I surname: Marks fullname: Marks, David I organization: Bristol Haematology and Oncology Centre, Bristol, United Kingdom – sequence: 30 givenname: Anthony V surname: Moorman fullname: Moorman, Anthony V organization: Leukaemia Research Cytogenetics Group, Newcastle University Translational and Clinical Research Institute, Newcastle-upon-Tyne, United Kingdom – sequence: 31 givenname: Peter H surname: Wiernik fullname: Wiernik, Peter H organization: Cancer Research Foundation, Bronx, NY – sequence: 32 givenname: Jacob M surname: Rowe fullname: Rowe, Jacob M organization: Department of Hematology, Shaare Zedek Medical Center, Jerusalem, Israel – sequence: 33 givenname: Martin S surname: Tallman fullname: Tallman, Martin S organization: Leukemia Service, Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College, New York, NY – sequence: 34 givenname: Anthony H surname: Goldstone fullname: Goldstone, Anthony H organization: University College London Hospitals, London, United Kingdom; and – sequence: 35 givenname: Charles G orcidid: 0000-0002-1871-1850 surname: Mullighan fullname: Mullighan, Charles G organization: Department of Pathology, St Jude Children's Research Hospital, Memphis, TN – sequence: 36 givenname: Mark R orcidid: 0000-0002-9816-6302 surname: Litzow fullname: Litzow, Mark R organization: Division of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN |
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| Snippet | Genomic classification has improved risk assignment of pediatric, but not adult B-lineage acute lymphoblastic leukemia (B-ALL). The international... |
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| SubjectTerms | Adolescent Adult Female Fusion Proteins, bcr-abl - genetics Gene Rearrangement Humans Male Middle Aged Mutation Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - diagnosis Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - therapy Prognosis Proto-Oncogene Proteins c-abl - genetics Proto-Oncogene Proteins c-bcr - genetics Risk Assessment Transcriptome Young Adult |
| Title | Molecular classification improves risk assessment in adult BCR-ABL1-negative B-ALL |
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