Outcomes of children with BCR-ABL1–like acute lymphoblastic leukemia treated with risk-directed therapy based on the levels of minimal residual disease

BCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile similar to BCR-ABL1-positive ALL but lacks the BCR-ABL1 fusion protein. We examined the outcome of children with BCR-ABL1–like ALL treated wit...

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Vydané v:Journal of clinical oncology Ročník 32; číslo 27; s. 3012
Hlavní autori: Roberts, Kathryn G, Pei, Deqing, Campana, Dario, Payne-Turner, Debbie, Li, Yongjin, Cheng, Cheng, Sandlund, John T, Jeha, Sima, Easton, John, Becksfort, Jared, Zhang, Jinghui, Coustan-Smith, Elaine, Raimondi, Susana C, Leung, Wing H, Relling, Mary V, Evans, William E, Downing, James R, Mullighan, Charles G, Pui, Ching-Hon
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 20.09.2014
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Abstract BCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile similar to BCR-ABL1-positive ALL but lacks the BCR-ABL1 fusion protein. We examined the outcome of children with BCR-ABL1–like ALL treated with risk-directed therapy based on minimal residual disease (MRD) levels during remission induction. Among 422 patients with B-ALL enrolled onto the Total Therapy XV study between 2000 and 2007, 344 had adequate samples for gene expression profiling. Next-generation sequencing and/or analysis of genes known to be altered in B-ALL were performed in patients with BCR-ABL1–likeALL who had available material. Outcome was compared between patients with and those without BCR-ABL1–like ALL. Forty (11.6%) of the 344 patients had BCR-ABL1–like ALL. They were significantly more likely to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction than did other patients with B-ALL. Among 25 patients comprehensively studied for genetic abnormalities, 11 harbored a genomic rearrangement of CRLF2, six had fusion transcripts responsive to ABL tyrosine kinase inhibitors or JAK inhibitors, and seven had mutations involving the Ras signaling pathway. There were no significant differences in event-free survival (90.0% +/- 4.7% [SE] v. 88.4% +/- .9% at 5 years; P = .41or in overall survival (92.5% +/- 4.2% v. 95.1% +/- 1.3% at 5 years; P = .41) between patients with and without BCR-ABL1–like ALL. Patients who have BCR-ABL1–like ALL with poor initial treatment response can be salvaged with MRD-based risk-directed therapy and may benefit from identification of kinase-activating lesions for targeted therapies.
AbstractList BCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile similar to BCR-ABL1-positive ALL but lacks the BCR-ABL1 fusion protein. We examined the outcome of children with BCR-ABL1–like ALL treated with risk-directed therapy based on minimal residual disease (MRD) levels during remission induction. Among 422 patients with B-ALL enrolled onto the Total Therapy XV study between 2000 and 2007, 344 had adequate samples for gene expression profiling. Next-generation sequencing and/or analysis of genes known to be altered in B-ALL were performed in patients with BCR-ABL1–likeALL who had available material. Outcome was compared between patients with and those without BCR-ABL1–like ALL. Forty (11.6%) of the 344 patients had BCR-ABL1–like ALL. They were significantly more likely to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction than did other patients with B-ALL. Among 25 patients comprehensively studied for genetic abnormalities, 11 harbored a genomic rearrangement of CRLF2, six had fusion transcripts responsive to ABL tyrosine kinase inhibitors or JAK inhibitors, and seven had mutations involving the Ras signaling pathway. There were no significant differences in event-free survival (90.0% +/- 4.7% [SE] v. 88.4% +/- .9% at 5 years; P = .41or in overall survival (92.5% +/- 4.2% v. 95.1% +/- 1.3% at 5 years; P = .41) between patients with and without BCR-ABL1–like ALL. Patients who have BCR-ABL1–like ALL with poor initial treatment response can be salvaged with MRD-based risk-directed therapy and may benefit from identification of kinase-activating lesions for targeted therapies.
BCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile similar to BCR-ABL1-positive ALL but lacks the BCR-ABL1 fusion protein. We examined the outcome of children with BCR-ABL1–like ALL treated with risk-directed therapy based on minimal residual disease (MRD) levels during remission induction.PURPOSEBCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile similar to BCR-ABL1-positive ALL but lacks the BCR-ABL1 fusion protein. We examined the outcome of children with BCR-ABL1–like ALL treated with risk-directed therapy based on minimal residual disease (MRD) levels during remission induction.Among 422 patients with B-ALL enrolled onto the Total Therapy XV study between 2000 and 2007, 344 had adequate samples for gene expression profiling. Next-generation sequencing and/or analysis of genes known to be altered in B-ALL were performed in patients with BCR-ABL1–likeALL who had available material. Outcome was compared between patients with and those without BCR-ABL1–like ALL.PATIENTS AND METHODSAmong 422 patients with B-ALL enrolled onto the Total Therapy XV study between 2000 and 2007, 344 had adequate samples for gene expression profiling. Next-generation sequencing and/or analysis of genes known to be altered in B-ALL were performed in patients with BCR-ABL1–likeALL who had available material. Outcome was compared between patients with and those without BCR-ABL1–like ALL.Forty (11.6%) of the 344 patients had BCR-ABL1–like ALL. They were significantly more likely to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction than did other patients with B-ALL. Among 25 patients comprehensively studied for genetic abnormalities, 11 harbored a genomic rearrangement of CRLF2, six had fusion transcripts responsive to ABL tyrosine kinase inhibitors or JAK inhibitors, and seven had mutations involving the Ras signaling pathway. There were no significant differences in event-free survival (90.0% +/- 4.7% [SE] v. 88.4% +/- .9% at 5 years; P = .41or in overall survival (92.5% +/- 4.2% v. 95.1% +/- 1.3% at 5 years; P = .41) between patients with and without BCR-ABL1–like ALL.RESULTSForty (11.6%) of the 344 patients had BCR-ABL1–like ALL. They were significantly more likely to be male, have Down syndrome, and have higher MRD levels on day 19 and at the end of induction than did other patients with B-ALL. Among 25 patients comprehensively studied for genetic abnormalities, 11 harbored a genomic rearrangement of CRLF2, six had fusion transcripts responsive to ABL tyrosine kinase inhibitors or JAK inhibitors, and seven had mutations involving the Ras signaling pathway. There were no significant differences in event-free survival (90.0% +/- 4.7% [SE] v. 88.4% +/- .9% at 5 years; P = .41or in overall survival (92.5% +/- 4.2% v. 95.1% +/- 1.3% at 5 years; P = .41) between patients with and without BCR-ABL1–like ALL.Patients who have BCR-ABL1–like ALL with poor initial treatment response can be salvaged with MRD-based risk-directed therapy and may benefit from identification of kinase-activating lesions for targeted therapies.CONCLUSIONPatients who have BCR-ABL1–like ALL with poor initial treatment response can be salvaged with MRD-based risk-directed therapy and may benefit from identification of kinase-activating lesions for targeted therapies.
Author Roberts, Kathryn G
Raimondi, Susana C
Jeha, Sima
Cheng, Cheng
Downing, James R
Payne-Turner, Debbie
Relling, Mary V
Evans, William E
Pui, Ching-Hon
Li, Yongjin
Sandlund, John T
Easton, John
Pei, Deqing
Zhang, Jinghui
Coustan-Smith, Elaine
Leung, Wing H
Becksfort, Jared
Campana, Dario
Mullighan, Charles G
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25049327$$D View this record in MEDLINE/PubMed
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PublicationPlace_xml – name: United States
PublicationTitle Journal of clinical oncology
PublicationTitleAlternate J Clin Oncol
PublicationYear 2014
References 23334668 - Nat Genet. 2013 Mar;45(3):242-52
22237106 - Nature. 2012 Jan 12;481(7380):157-63
22955920 - Blood. 2012 Oct 25;120(17):3510-8
17344859 - Nature. 2007 Apr 12;446(7137):758-64
21863287 - Int J Hematol. 2011 Sep;94(3):255-60
19641190 - Blood. 2009 Sep 24;114(13):2688-98
19805687 - J Clin Oncol. 2009 Nov 1;27(31):5175-81
19838194 - Nat Genet. 2009 Nov;41(11):1243-6
21680795 - Blood. 2011 Sep 15;118(11):3080-7
9718381 - N Engl J Med. 1998 Aug 27;339(9):605-15
22368272 - Blood. 2012 Apr 12;119(15):3512-22
17234643 - Bioinformatics. 2007 Mar 15;23(6):657-63
22897847 - Cancer Cell. 2012 Aug 14;22(2):153-66
22436535 - Blood Rev. 2012 May;26(3):123-35
19129520 - N Engl J Med. 2009 Jan 29;360(5):470-80
12011421 - Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72
24186319 - Haematologica. 2013 Nov;98(11):e146-8
23212523 - Blood. 2013 Jan 17;121(3):485-8
11023499 - Blood. 2000 Oct 15;96(8):2691-6
20699438 - Blood. 2010 Dec 2;116(23):4874-84
23953334 - Semin Hematol. 2013 Jul;50(3):185-96
22898679 - Lancet Oncol. 2012 Sep;13(9):936-45
22685175 - Blood. 2012 Jul 26;120(4):833-42
19138562 - Lancet Oncol. 2009 Feb;10(2):125-34
19553647 - N Engl J Med. 2009 Jun 25;360(26):2730-41
24013638 - Nat Genet. 2013 Oct;45(10):1226-31
19470474 - Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9414-8
23835704 - J Clin Oncol. 2013 Sep 1;31(25):e413-6
24141364 - Nat Genet. 2013 Dec;45(12):1494-8
23974192 - Blood. 2013 Oct 10;122(15):2622-9
15029212 - Leukemia. 2004 May;18(5):934-8
20139093 - Blood. 2010 Jul 1;115(26):5312-21
19052058 - Bioinformatics. 2009 Feb 1;25(3):315-21
References_xml – reference: 9718381 - N Engl J Med. 1998 Aug 27;339(9):605-15
– reference: 22897847 - Cancer Cell. 2012 Aug 14;22(2):153-66
– reference: 24186319 - Haematologica. 2013 Nov;98(11):e146-8
– reference: 19641190 - Blood. 2009 Sep 24;114(13):2688-98
– reference: 11023499 - Blood. 2000 Oct 15;96(8):2691-6
– reference: 20139093 - Blood. 2010 Jul 1;115(26):5312-21
– reference: 19129520 - N Engl J Med. 2009 Jan 29;360(5):470-80
– reference: 22685175 - Blood. 2012 Jul 26;120(4):833-42
– reference: 15029212 - Leukemia. 2004 May;18(5):934-8
– reference: 19553647 - N Engl J Med. 2009 Jun 25;360(26):2730-41
– reference: 17234643 - Bioinformatics. 2007 Mar 15;23(6):657-63
– reference: 17344859 - Nature. 2007 Apr 12;446(7137):758-64
– reference: 19470474 - Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9414-8
– reference: 19838194 - Nat Genet. 2009 Nov;41(11):1243-6
– reference: 22955920 - Blood. 2012 Oct 25;120(17):3510-8
– reference: 23334668 - Nat Genet. 2013 Mar;45(3):242-52
– reference: 23953334 - Semin Hematol. 2013 Jul;50(3):185-96
– reference: 23835704 - J Clin Oncol. 2013 Sep 1;31(25):e413-6
– reference: 20699438 - Blood. 2010 Dec 2;116(23):4874-84
– reference: 19805687 - J Clin Oncol. 2009 Nov 1;27(31):5175-81
– reference: 21680795 - Blood. 2011 Sep 15;118(11):3080-7
– reference: 22436535 - Blood Rev. 2012 May;26(3):123-35
– reference: 24141364 - Nat Genet. 2013 Dec;45(12):1494-8
– reference: 24013638 - Nat Genet. 2013 Oct;45(10):1226-31
– reference: 22237106 - Nature. 2012 Jan 12;481(7380):157-63
– reference: 12011421 - Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72
– reference: 19138562 - Lancet Oncol. 2009 Feb;10(2):125-34
– reference: 22368272 - Blood. 2012 Apr 12;119(15):3512-22
– reference: 23974192 - Blood. 2013 Oct 10;122(15):2622-9
– reference: 19052058 - Bioinformatics. 2009 Feb 1;25(3):315-21
– reference: 22898679 - Lancet Oncol. 2012 Sep;13(9):936-45
– reference: 23212523 - Blood. 2013 Jan 17;121(3):485-8
– reference: 21863287 - Int J Hematol. 2011 Sep;94(3):255-60
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Snippet BCR-ABL1–like acute lymphoblastic leukemia (ALL) is a recently identified B-cell ALL (B-ALL)subtype with poor outcome that exhibits a gene expression profile...
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StartPage 3012
SubjectTerms Adolescent
Antineoplastic Agents - pharmacology
Antineoplastic Agents - therapeutic use
Child
Child, Preschool
Disease-Free Survival
Female
Fusion Proteins, bcr-abl - drug effects
Fusion Proteins, bcr-abl - genetics
Gene Expression Profiling
Humans
Infant
Kaplan-Meier Estimate
Male
Molecular Targeted Therapy - methods
Neoplasm, Residual - drug therapy
Neoplasm, Residual - genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma - pathology
Risk Assessment
Risk Factors
Salvage Therapy - methods
Title Outcomes of children with BCR-ABL1–like acute lymphoblastic leukemia treated with risk-directed therapy based on the levels of minimal residual disease
URI https://www.ncbi.nlm.nih.gov/pubmed/25049327
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Volume 32
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