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Article ; Online: CDX2 and IDH1/2: new potential players in ALL.

Roberts, Kathryn G

2022 Volume 139, Issue 12, Page(s) 1778–1779

MeSH term(s)	Homeodomain Proteins
Chemical Substances	Homeodomain Proteins
Language	English
Publishing date	2022-03-24
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021014429
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Article ; Online: Genetics and prognosis of ALL in children vs adults.

Roberts, Kathryn G

Hematology. American Society of Hematology. Education Program

2018 Volume 2018, Issue 1, Page(s) 137–145

Abstract: Acute lymphoblastic leukemia (ALL) is characterized by genetic alterations that block differentiation, promote proliferation of lymphoid precursor cells, and are important for risk stratification. Although ALL is less common in adolescents and young ... ...

Abstract	Acute lymphoblastic leukemia (ALL) is characterized by genetic alterations that block differentiation, promote proliferation of lymphoid precursor cells, and are important for risk stratification. Although ALL is less common in adolescents and young adults (AYAs) and adults than children, survival rates are inferior, and long-term prognosis for adults is poor. Thus, ALL remains a challenging disease to treat in the AYA and adult populations. A major contributing factor that influences prognosis in this population is the reduced prevalence of genetic subtypes associated with favorable outcome and a concomitant increase in subtypes associated with poor outcome. Recent advances in genomic profiling across the age spectrum continue to enhance our knowledge of the differences in disease biology between children and adults and are providing important insights into novel therapeutic targets. Philadelphia chromosome-like (Ph-like) ALL is one such subtype characterized by alterations that deregulate cytokine receptor or tyrosine kinase signaling and are amenable to inhibition with approved tyrosine kinase inhibitors. One of the greatest challenges now remaining is determining how to implement this breadth of genomic information into rapid and accurate diagnostic testing to facilitate the development of novel clinical trials that improve the outcome of AYAs and adults with ALL.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/diagnosis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Prognosis
Language	English
Publishing date	2018-11-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2084287-9
ISSN	1520-4383 ; 1520-4391
ISSN (online)	1520-4383
ISSN	1520-4391
DOI	10.1182/asheducation-2018.1.137
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Article ; Online: TKI resistance in Ph-like ALL.

Roberts, Kathryn G

Blood

2018 Volume 131, Issue 20, Page(s) 2181–2182

MeSH term(s)	Humans ; Mutation/drug effects ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Protein Kinase Inhibitors ; Receptor, Platelet-Derived Growth Factor beta/genetics
Chemical Substances	Protein Kinase Inhibitors ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.10.1)
Language	English
Publishing date	2018-05-16
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2018-03-833665
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Article ; Online: Why and how to treat Ph-like ALL?

Roberts, Kathryn G

Best practice & research. Clinical haematology

2018 Volume 31, Issue 4, Page(s) 351–356

Abstract: Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL), or BCR-ABL1-like ALL, is a high-risk subtype of B-cell precursor ALL characterized by a gene expression profile similar to Ph-positive ALL, a high frequency of IKZF1 alterations, ... ...

Abstract	Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL), or BCR-ABL1-like ALL, is a high-risk subtype of B-cell precursor ALL characterized by a gene expression profile similar to Ph-positive ALL, a high frequency of IKZF1 alterations, and poor outcome. The prevalence of Ph-like ALL is common among all ages, ranging from 10% to 15% in children to over 25% in young adults. Patients with Ph-like ALL harbor a diverse range of genetic alterations that activate cytokine receptor and kinase signaling and can be targeted with tyrosine kinase inhibitors. The majority of Ph-like ALL alterations are divided into two main groups based on activation of ABL-class or JAK-STAT alterations. Accordingly, preclinical studies and anecdotal reports suggest patients harboring ABL-class fusions are candidates for ABL1-inhibitors, whilst alterations activating the JAK-STAT pathway may be amenable to treatment with JAK inhibitors. Diagnostic screening approaches and precision medicine trials are now being developed and implemented to test the efficacy of targeted therapy with a backbone of chemotherapy, similar to the treatment of Ph-positive ALL.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/genetics ; Fusion Proteins, bcr-abl/metabolism ; Humans ; Infant ; Male ; Mutation ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	BCR-ABL1 fusion protein, human ; Protein Kinase Inhibitors ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2018-09-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2048027-1
ISSN	1532-1924 ; 1521-6926
ISSN (online)	1532-1924
ISSN	1521-6926
DOI	10.1016/j.beha.2018.09.003
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Article ; Online: Genetic Alterations and Therapeutic Targeting of Philadelphia-Like Acute Lymphoblastic Leukemia.

Iacobucci, Ilaria / Roberts, Kathryn G

Genes

2021 Volume 12, Issue 5

Abstract: Philadelphia-like (Ph-like) acute lymphoblastic leukemia (ALL) is a subgroup of B-cell precursor ALL which by gene expression analysis clusters with Philadelphia-positive ALL although lacking the pathognomonic BCR-ABL1 oncoprotein. Its prevalence ... ...

Abstract	Philadelphia-like (Ph-like) acute lymphoblastic leukemia (ALL) is a subgroup of B-cell precursor ALL which by gene expression analysis clusters with Philadelphia-positive ALL although lacking the pathognomonic BCR-ABL1 oncoprotein. Its prevalence increases with age and similar to
MeSH term(s)	Genetic Heterogeneity ; Humans ; Immunotherapy/methods ; Janus Kinases/genetics ; Janus Kinases/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins c-abl/genetics ; Proto-Oncogene Proteins c-abl/metabolism
Chemical Substances	Protein Kinase Inhibitors ; ABL1 protein, human (EC 2.7.10.2) ; Janus Kinases (EC 2.7.10.2) ; Proto-Oncogene Proteins c-abl (EC 2.7.10.2)
Language	English
Publishing date	2021-05-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12050687
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Article: Genetic Alterations and Therapeutic Targeting of Philadelphia-Like Acute Lymphoblastic Leukemia

Iacobucci, Ilaria / Roberts, Kathryn G

Genes. 2021 May 01, v. 12, no. 5

2021

Abstract	Philadelphia-like (Ph-like) acute lymphoblastic leukemia (ALL) is a subgroup of B-cell precursor ALL which by gene expression analysis clusters with Philadelphia-positive ALL although lacking the pathognomonic BCR-ABL1 oncoprotein. Its prevalence increases with age and similar to BCR-ABL1-positive ALL, Ph-like ALL is characterized by IKZF1 or other B-lymphoid transcription factor gene deletions and by poor outcome to conventional therapeutic approaches. Genetic alterations are highly heterogenous across patients and include gene fusions, sequence mutations, DNA copy number changes and cryptic rearrangements. These lesions drive constitutively active cytokine receptor and kinase signaling pathways which deregulate ABL1 or JAK signaling and more rarely other kinase-driven pathways. The presence of activated kinase alterations and cytokine receptors has led to the incorporation of targeted therapy to the chemotherapy backbone which has improved treatment outcome for this high-risk subtype. More recently, retrospective studies have shown the efficacy of immunotherapies including both antibody drug-conjugates and chimeric antigen receptor T cell therapy and as they are not dependent on a specific genetic alteration, it is likely their use will increase in prospective clinical trials. This review summarizes the genomic landscape, clinical features, diagnostic assays, and novel therapeutic approaches for patients with Ph-like ALL.
Keywords	B-lymphocytes ; DNA ; T-lymphocytes ; antibodies ; antigens ; cytokine receptors ; cytokines ; drug therapy ; gene expression ; genes ; lymphocytic leukemia ; oncogene proteins ; transcription factors
Language	English
Dates of publication	2021-0501
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12050687
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The biology of Philadelphia chromosome-like ALL.

Roberts, Kathryn G

Best practice & research. Clinical haematology

2017 Volume 30, Issue 3, Page(s) 212–221

Abstract: Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a recently described subtype of B-cell precursor ALL with a gene expression profile similar to Ph-positive ALL and a high frequency of IKZF1 alterations. The prevalence of Ph-like ...

Abstract	Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a recently described subtype of B-cell precursor ALL with a gene expression profile similar to Ph-positive ALL and a high frequency of IKZF1 alterations. The prevalence of Ph-like ALL increases with age, ranging from 10-15% of children to over 25% of young adults with ALL. It occurs more frequently in males and is associated with adverse clinical features including elevated minimal residual disease levels and poor survival in both children and adults. The genomic landscape of Ph-like ALL is characterized by a diverse range of genetic alterations that dysregulate cytokine receptor and kinase signaling pathways, including rearrangement of CRLF2 and other tyrosine kinases (predominantly ABL-class and Janus kinases). Compelling preclinical data suggest patients harboring ABL-class rearrangements are candidates for ABL1-inhibitors, whilst alterations activating the JAK-STAT pathway may be amenable to treatment with JAK inhibitors. The success of combinatorial treatment of tyrosine kinase inhibitors with chemotherapy in Ph-positive ALL provides a framework for testing this approach in Ph-like ALL. Ongoing prospective studies will determine if incorporation of targeted therapy with intensive chemotherapy regimens will improve the outcome of patients with Ph-like ALL.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Gene Expression Regulation, Leukemic ; Hematopoietic Stem Cell Transplantation ; Humans ; Ikaros Transcription Factor/antagonists & inhibitors ; Ikaros Transcription Factor/genetics ; Ikaros Transcription Factor/metabolism ; Janus Kinases/antagonists & inhibitors ; Janus Kinases/genetics ; Janus Kinases/metabolism ; Molecular Targeted Therapy ; Mutation ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/mortality ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Protein Kinase Inhibitors/therapeutic use ; Receptors, Cytokine/antagonists & inhibitors ; Receptors, Cytokine/genetics ; Receptors, Cytokine/metabolism ; STAT Transcription Factors/antagonists & inhibitors ; STAT Transcription Factors/genetics ; STAT Transcription Factors/metabolism ; Signal Transduction ; Survival Analysis ; Transplantation, Homologous
Chemical Substances	Antineoplastic Agents ; CRLF2 protein, human ; IKZF1 protein, human ; Protein Kinase Inhibitors ; Receptors, Cytokine ; STAT Transcription Factors ; Ikaros Transcription Factor (148971-36-2) ; Janus Kinases (EC 2.7.10.2)
Language	English
Publishing date	2017-07-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2048027-1
ISSN	1532-1924 ; 1521-6926
ISSN (online)	1532-1924
ISSN	1521-6926
DOI	10.1016/j.beha.2017.07.003
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Article ; Online: The Biology of B-Progenitor Acute Lymphoblastic Leukemia.

Roberts, Kathryn G / Mullighan, Charles G

Cold Spring Harbor perspectives in medicine

2020 Volume 10, Issue 7

Abstract: Genomic analyses have revolutionized our understanding of the biology of B-progenitor acute lymphoblastic leukemia (ALL). Studies of thousands of cases across the age spectrum have revised the taxonomy of B-ALL by identifying multiple new subgroups with ... ...

Abstract	Genomic analyses have revolutionized our understanding of the biology of B-progenitor acute lymphoblastic leukemia (ALL). Studies of thousands of cases across the age spectrum have revised the taxonomy of B-ALL by identifying multiple new subgroups with diverse sequence and structural initiating events that vary substantially by age at diagnosis and prognostic significance. There is a growing appreciation of the role of inherited genetic variation in predisposition to ALL and drug responsiveness and of the nature of genetic variegation and clonal evolution that may be targeted for improved diagnostic, risk stratification, disease monitoring, and therapeutic intervention. This review provides an overview of the current state of knowledge of the genetic basis of B-ALL, with an emphasis on recent discoveries that have changed our approach to diagnosis and monitoring.
MeSH term(s)	Child ; Female ; Genetic Predisposition to Disease ; Humans ; Male ; Molecular Targeted Therapy/methods ; Neoplasm Recurrence, Local ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Sequence Analysis, RNA ; Tumor Microenvironment/genetics
Language	English
Publishing date	2020-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a034835
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Article ; Online: Genomics in acute lymphoblastic leukaemia: insights and treatment implications.

Roberts, Kathryn G / Mullighan, Charles G

Nature reviews. Clinical oncology

2015 Volume 12, Issue 6, Page(s) 344–357

Abstract: Acute lymphoblastic leukaemia (ALL) is the commonest childhood cancer and an important cause of morbidity from haematological malignancies in adults. In the past several years, we have witnessed major advances in the understanding of the genetic basis of ...

Abstract	Acute lymphoblastic leukaemia (ALL) is the commonest childhood cancer and an important cause of morbidity from haematological malignancies in adults. In the past several years, we have witnessed major advances in the understanding of the genetic basis of ALL. Genome-wide profiling studies, including microarray analysis and genome sequencing, have helped identify multiple key cellular pathways that are frequently mutated in ALL such as lymphoid development, tumour suppression, cytokine receptors, kinase and Ras signalling, and chromatin remodeling. These studies have characterized new subtypes of ALL, notably Philadelphia chromosome-like ALL, which is a high-risk subtype characterized by a diverse range of alterations that activate cytokine receptors or tyrosine kinases amenable to inhibition with approved tyrosine kinase inhibitors. Genomic profiling has also enabled the identification of inherited genetic variants of ALL that influence the risk of leukaemia development, and characterization of the relationship between genetic variants, clonal heterogeneity and the risk of relapse. Many of these findings are of direct clinical relevance and ongoing studies implementing clinical sequencing in leukaemia diagnosis and management have great potential to improve the outcome of patients with high-risk ALL.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Chromosomes, Human, Pair 21/genetics ; DNA, Neoplasm/analysis ; Diploidy ; Epigenesis, Genetic/genetics ; Gene Amplification/genetics ; Gene Expression Profiling/methods ; Gene Rearrangement/genetics ; Genes, Neoplasm/genetics ; Genetic Variation/genetics ; Genomics ; Humans ; Infant ; Janus Kinases/genetics ; Mutation/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Receptors, Cytokine/genetics ; Recurrence ; Sequence Analysis, DNA/methods ; Trans-Activators/genetics ; Transcriptional Regulator ERG ; Young Adult
Chemical Substances	CRLF2 protein, human ; DNA, Neoplasm ; ERG protein, human ; Receptors, Cytokine ; Trans-Activators ; Transcriptional Regulator ERG ; Janus Kinases (EC 2.7.10.2)
Language	English
Publishing date	2015-03-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2015.38
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Article ; Online: Association of leukemic molecular profile with efficacy of inotuzumab ozogamicin in adults with relapsed/refractory ALL.

Blood advances

2024

Abstract: The phase 3 INO-VATE trial demonstrated higher rates of remission, measurable residual disease negativity, and improved overall survival for patients with relapsed/refractory (R/R) acute lymphoblastic leukemia (ALL) who received inotuzumab ozogamicin ( ... ...

Abstract	The phase 3 INO-VATE trial demonstrated higher rates of remission, measurable residual disease negativity, and improved overall survival for patients with relapsed/refractory (R/R) acute lymphoblastic leukemia (ALL) who received inotuzumab ozogamicin (InO) vs standard of care chemotherapy (SC). Here we examined associations between genomic alterations and the efficacy of InO. Of 326 randomized patients, 91 (InO, n=43; SC, n=48) had samples evaluable for genomic analysis. The spectrum of gene fusions and other genomic alterations observed was comparable with prior studies of adult ALL. Responses to InO were observed in all leukemic subtypes, genomic alterations, and risk groups. Significantly higher rates of complete remission (CR)/CR with incomplete count recovery rates were observed with InO vs SC in patients with BCR::ABL1-like ALL (85.7% [6/7] vs 0% [0/5] P=0.0076), with TP53 alterations (100% [5/5] vs 12.5% [1/8], P=0.0047), and in the high-risk BCR::ABL1- (BCR::ABL1-like, low hypodiploid, KMT2A-rearranged) group (83.3% [10/12] vs 10.5% [2/19]; P<0.0001). This retrospective, exploratory analysis of the INO-VATE trial demonstrated potential for benefit with InO for patients with R/R ALL across leukemic subtypes, including BCR::ABL1-like ALL, and for those bearing diverse genomic alterations. Further confirmation of the efficacy of InO in patients with R/R ALL exhibiting the BCR::ABL1-like subtype or harboring TP53 alterations is warranted. This trial was registered at www.clinicaltrials.gov as no. NCT01564784.
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023012430
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