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Article ; Online: Podcast on Emerging Treatment Options for Pediatric Patients with ALK-Positive Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic Tumors.

Lowe, Eric / Mossé, Yael P

2024

Abstract: Anaplastic large cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT) are rare cancers observed predominantly in children and young adults. ALCL accounts for 10-15% of all pediatric non-Hodgkin lymphomas and is commonly diagnosed at an ... ...

Abstract	Anaplastic large cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT) are rare cancers observed predominantly in children and young adults. ALCL accounts for 10-15% of all pediatric non-Hodgkin lymphomas and is commonly diagnosed at an advanced stage of disease. In children, 84-91% of cases of ALCL harbor an anaplastic lymphoma kinase (ALK) gene translocation. IMT is a rare mesenchymal neoplasm that also tends to occur in children and adolescents. Approximately 50-70% of IMT cases involve rearrangements in the ALK gene. A combination of chemotherapeutic drugs is typically used for children with ALK-positive ALCL, and the only known curative therapy for ALK-positive IMT is complete surgical resection. Crizotinib, a first-generation ALK inhibitor, was approved in the USA in 2021 for pediatric patients and young adults with relapsed or refractory ALK-positive ALCL; however, its safety and efficacy have not been established in older adults. In 2022, crizotinib was approved for adult and pediatric patients with unresectable, recurrent, or refractory ALK-positive IMT. This podcast provides an overview of ALK-positive ALCL and IMT. We discuss the current treatment landscape, the role of ALK tyrosine kinase inhibitors, and areas of future research.
Language	English
Publishing date	2024-04-27
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2848647-X
ISSN	2366-1089 ; 2366-1070
ISSN (online)	2366-1089
ISSN	2366-1070
DOI	10.1007/s40487-024-00275-6
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Article: Anaplastic Lymphoma Kinase as a Cancer Target in Pediatric Malignancies.

Mossé, Yael P

Clinical cancer research : an official journal of the American Association for Cancer Research

2016 Volume 22, Issue 3, Page(s) 546–552

Abstract: In this era of more rational therapies, substantial efforts are being made to identify optimal targets. The discovery of translocations involving the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase in a subset of non-small cell lung cancers has ...

Abstract	In this era of more rational therapies, substantial efforts are being made to identify optimal targets. The discovery of translocations involving the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase in a subset of non-small cell lung cancers has become a paradigm for precision medicine. Notably, ALK was initially discovered as the fusion gene in anaplastic large cell non-Hodgkin lymphoma, a disease predominantly of childhood. The discovery of activating kinase domain mutations of the full-length ALK receptor as the major cause of hereditary neuroblastoma, and that somatically acquired mutations and amplification events often drive the malignant process in a subset of sporadic tumors, has established ALK as a tractable molecular target across histologically diverse tumors in which ALK is a critical mediator of oncogenesis. We are now uncovering the reexpression of this developmentally regulated protein in a broader subset of pediatric cancers, providing therapeutic targeting opportunities for diseases with shared molecular etiology. This review focuses on the role of ALK in pediatric malignancies, alongside the prospects and challenges associated with the development of effective ALK-inhibition strategies.
MeSH term(s)	Adolescent ; Age Factors ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Child ; Child, Preschool ; Humans ; Immunotherapy ; Infant ; Infant, Newborn ; Molecular Targeted Therapy ; Mutation ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Protein Transport ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; anaplastic lymphoma kinase (EC 2.7.10.1)
Language	English
Publishing date	2016-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-14-1100
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Article ; Online: Thrown for a Loop: Awakening BORIS to Evade ALK Inhibition Therapy.

Berko, Esther R / Mossé, Yael P

Cancer cell

2019 Volume 36, Issue 4, Page(s) 345–347

Abstract: Mechanisms of acquired resistance to ALK inhibition therapy in neuroblastoma have not yet been elucidated. In a recent issue of Nature, Debruyne et al. demonstrate that resistant MYCN-amplified ALK-mutated neuroblastoma cells overexpress BORIS, resulting ...

Abstract	Mechanisms of acquired resistance to ALK inhibition therapy in neuroblastoma have not yet been elucidated. In a recent issue of Nature, Debruyne et al. demonstrate that resistant MYCN-amplified ALK-mutated neuroblastoma cells overexpress BORIS, resulting in wide-ranging changes in chromatin interaction and transcriptional reprogramming.
MeSH term(s)	AAA Domain ; Anaplastic Lymphoma Kinase ; Cell Line, Tumor ; Chromatin ; Humans ; N-Myc Proto-Oncogene Protein/genetics ; Neuroblastoma
Chemical Substances	Chromatin ; N-Myc Proto-Oncogene Protein ; Anaplastic Lymphoma Kinase (EC 2.7.10.1)
Language	English
Publishing date	2019-10-15
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2019.09.009
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Lorlatinib use in an infant with thalamic ALK-positive histiocytosis.

Eldem, Irem / Picarsic, Jennifer / Kumar, Ashish / Mossé, Yaël P / Roberts, Kaleigh Filisa / Armstrong, Amy E / Sisk, Bryan A

Pediatric blood & cancer

2023 , Page(s) e30378

Language	English
Publishing date	2023-04-19
Publishing country	United States
Document type	Letter
ZDB-ID	2131448-2
ISSN	1545-5017 ; 1545-5009
ISSN (online)	1545-5017
ISSN	1545-5009
DOI	10.1002/pbc.30378
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Article ; Online: Targeting ALK in neuroblastoma--preclinical and clinical advancements.

Carpenter, Erica L / Mossé, Yael P

Nature reviews. Clinical oncology

2012 Volume 9, Issue 7, Page(s) 391–399

Abstract: Despite improvements in cancer therapies in the past 50 years, neuroblastoma remains a devastating clinical problem and a leading cause of childhood cancer deaths. Advances in treatments for children with high-risk ... ...

Abstract	Despite improvements in cancer therapies in the past 50 years, neuroblastoma remains a devastating clinical problem and a leading cause of childhood cancer deaths. Advances in treatments for children with high-risk neuroblastoma have, until recently, involved addition of cytotoxic therapy to dose-intensive regimens. In this era of targeted therapies, substantial efforts have been made to identify optimal targets for different types of cancer. The discovery of hereditary and somatic activating mutations in the oncogene ALK has now placed neuroblastoma among other cancers, such as melanoma and non-small-cell lung cancer (NSCLC), which benefit from therapies with oncogene-specific small-molecule tyrosine kinase inhibitors. Crizotinib, a small-molecule inhibitor of ALK, has transformed the landscape for the treatment of NSCLC harbouring ALK translocations and has demonstrated activity in preclinical models of ALK-driven neuroblastomas. However, inhibition of mutated ALK is complex when compared with translocated ALK and remains a therapeutic challenge. This Review discusses the biology of ALK in the development of neuroblastoma, preclinical and clinical progress with the use of ALK inhibitors and immunotherapy, challenges associated with resistance to such therapies and the steps being taken to overcome some of these hurdles.
MeSH term(s)	Anaplastic Lymphoma Kinase ; Animals ; Humans ; Neuroblastoma/drug therapy ; Neuroblastoma/enzymology ; Protein Kinase Inhibitors/therapeutic use ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/metabolism
Chemical Substances	Protein Kinase Inhibitors ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2012-05-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2012.72
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 103: Show issues

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Article ; Online: Percutaneous biopsy for the diagnosis, risk stratification, and molecular profiling of neuroblastoma: A single-center retrospective study.

Schoeman, Sean / Bagatell, Rochelle / Cahill, Anne Marie / Maris, John / Mattei, Peter / Mosse, Yael / Pogoriler, Jennifer / Srinivasan, Abhay / Acord, Michael

Pediatric blood & cancer

2024 Volume 71, Issue 4, Page(s) e30887

Abstract: Purpose: To determine whether percutaneous core needle biopsy (PCNB) is adequate for the diagnosis and full molecular characterization of newly diagnosed neuroblastoma.: Materials and methods: Patients with newly diagnosed neuroblastoma who underwent ...

Abstract	Purpose: To determine whether percutaneous core needle biopsy (PCNB) is adequate for the diagnosis and full molecular characterization of newly diagnosed neuroblastoma. Materials and methods: Patients with newly diagnosed neuroblastoma who underwent PCNB in interventional radiology at a single center over a 5-year period were included. Pre-procedure imaging and procedure details were reviewed. Rates of diagnostic success and sufficiency for International Neuroblastoma Pathology Classification (INPC), risk stratification, and evaluation of genomic markers utilized in the Children's Oncology Group risk stratification, and status of the anaplastic lymphoma kinase (ALK) gene were assessed. Results: Thirty-five patients (13 females, median age 2.4 years [interquartile range, IQR: 0.9-4.4] and median weight 12.4 kg [IQR: 9.6-18]) were included. Most had International Neuroblastoma Risk Group Stage M disease (n = 22, 63%). Median longest axis of tumor target was 8.8 cm [IQR: 6.1-12]. A 16-gauge biopsy instrument was most often used (n = 20, 57%), with a median of 20 cores [IQR: 13-23] obtained. Twenty-five specimens were assessed for adequacy, and 14 procedures utilized contrast-enhanced ultrasound guidance. There were two post-procedure bleeds (5.7%). Thirty-four of 35 procedures (97%) were sufficient for histopathologic diagnosis and risk stratification, 94% (n = 32) were sufficient for INPC, and 85% (n = 29) were sufficient for complete molecular characterization, including ALK testing. Biologic information was otherwise obtained from bone marrow (4/34, 12%) or surgery (1/34, 2.9%). The number of cores did not differ between patients with sufficient versus insufficient biopsies. Conclusion: In this study, obtaining multiple cores with PCNB resulted in a high rate of diagnosis and successful molecular profiling for neuroblastoma.
MeSH term(s)	Child ; Female ; Humans ; Child, Preschool ; Retrospective Studies ; Biopsy/methods ; Biopsy, Large-Core Needle ; Neuroblastoma/diagnosis ; Neuroblastoma/genetics ; Neuroblastoma/pathology ; Risk Assessment ; Receptor Protein-Tyrosine Kinases ; Image-Guided Biopsy ; Nitrobenzenes
Chemical Substances	quintozene (Q37G40S4S8) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Nitrobenzenes
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2131448-2
ISSN	1545-5017 ; 1545-5009
ISSN (online)	1545-5017
ISSN	1545-5009
DOI	10.1002/pbc.30887
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Article ; Online: Evaluation of the DLL3-targeting antibody-drug conjugate rovalpituzumab tesirine in preclinical models of neuroblastoma.

Krytska, Kateryna / Casey, Colleen E / Pogoriler, Jennifer / Martinez, Daniel / Rathi, Komal S / Farrel, Alvin / Berko, Esther R / Tsang, Matthew / Sano, Renata R / Kendsersky, Nathan / Erickson, Stephen W / Teicher, Beverly A / Isse, Kumiko / Saunders, Laura / Smith, Malcolm A / Maris, John M / Mossé, Yael P

Cancer research communications

2022 Volume 2, Issue 7, Page(s) 616–623

Abstract: Neuroblastomas have neuroendocrine features and often show similar gene expression patterns to small cell lung cancer including high expression of delta-like ligand 3 ( ...

Abstract	Neuroblastomas have neuroendocrine features and often show similar gene expression patterns to small cell lung cancer including high expression of delta-like ligand 3 (
MeSH term(s)	Humans ; Child ; Small Cell Lung Carcinoma/drug therapy ; Lung Neoplasms/drug therapy ; Ligands ; Immunoconjugates/pharmacology ; Neuroblastoma/drug therapy ; Membrane Proteins/genetics ; Intracellular Signaling Peptides and Proteins
Chemical Substances	rovalpituzumab tesirine ; Ligands ; Immunoconjugates ; DLL3 protein, human ; Membrane Proteins ; Intracellular Signaling Peptides and Proteins
Language	English
Publishing date	2022-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.crc-22-0137
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Article ; Online: Circulating tumor DNA reveals mechanisms of lorlatinib resistance in patients with relapsed/refractory ALK-driven neuroblastoma.

Nature communications

2023 Volume 14, Issue 1, Page(s) 2601

Abstract: Activating point mutations in Anaplastic Lymphoma Kinase (ALK) have positioned ALK as the only mutated oncogene tractable for targeted therapy in neuroblastoma. Cells with these mutations respond to lorlatinib in pre-clinical studies, providing the ... ...

Abstract	Activating point mutations in Anaplastic Lymphoma Kinase (ALK) have positioned ALK as the only mutated oncogene tractable for targeted therapy in neuroblastoma. Cells with these mutations respond to lorlatinib in pre-clinical studies, providing the rationale for a first-in-child Phase 1 trial (NCT03107988) in patients with ALK-driven neuroblastoma. To track evolutionary dynamics and heterogeneity of tumors, and to detect early emergence of lorlatinib resistance, we collected serial circulating tumor DNA samples from patients enrolled on this trial. Here we report the discovery of off-target resistance mutations in 11 patients (27%), predominantly in the RAS-MAPK pathway. We also identify newly acquired secondary compound ALK mutations in 6 (15%) patients, all acquired at disease progression. Functional cellular and biochemical assays and computational studies elucidate lorlatinib resistance mechanisms. Our results establish the clinical utility of serial circulating tumor DNA sampling to track response and progression and to discover acquired resistance mechanisms that can be leveraged to develop therapeutic strategies to overcome lorlatinib resistance.
MeSH term(s)	Humans ; Aminopyridines/therapeutic use ; Anaplastic Lymphoma Kinase/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Circulating Tumor DNA/genetics ; Drug Resistance, Neoplasm/genetics ; Lactams, Macrocyclic/therapeutic use ; Lung Neoplasms/genetics ; Mutation ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Aminopyridines ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Circulating Tumor DNA ; Lactams, Macrocyclic ; lorlatinib (OSP71S83EU) ; Protein Kinase Inhibitors
Language	English
Publishing date	2023-05-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38195-0
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Article ; Online: Computational studies of anaplastic lymphoma kinase mutations reveal common mechanisms of oncogenic activation.

Patil, Keshav / Jordan, Earl Joseph / Park, Jin H / Suresh, Krishna / Smith, Courtney M / Lemmon, Abigail A / Mossé, Yaël P / Lemmon, Mark A / Radhakrishnan, Ravi

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 10

Abstract: Kinases play important roles in diverse cellular processes, including signaling, differentiation, proliferation, and metabolism. They are frequently mutated in cancer and are the targets of a large number of specific inhibitors. Surveys of cancer genome ... ...

Abstract	Kinases play important roles in diverse cellular processes, including signaling, differentiation, proliferation, and metabolism. They are frequently mutated in cancer and are the targets of a large number of specific inhibitors. Surveys of cancer genome atlases reveal that kinase domains, which consist of 300 amino acids, can harbor numerous (150 to 200) single-point mutations across different patients in the same disease. This preponderance of mutations-some activating, some silent-in a known target protein make clinical decisions for enrolling patients in drug trials challenging since the relevance of the target and its drug sensitivity often depend on the mutational status in a given patient. We show through computational studies using molecular dynamics (MD) as well as enhanced sampling simulations that the experimentally determined activation status of a mutated kinase can be predicted effectively by identifying a hydrogen bonding fingerprint in the activation loop and the αC-helix regions, despite the fact that mutations in cancer patients occur throughout the kinase domain. In our study, we find that the predictive power of MD is superior to a purely data-driven machine learning model involving biochemical features that we implemented, even though MD utilized far fewer features (in fact, just one) in an unsupervised setting. Moreover, the MD results provide key insights into convergent mechanisms of activation, primarily involving differential stabilization of a hydrogen bond network that engages residues of the activation loop and αC-helix in the active-like conformation (in >70% of the mutations studied, regardless of the location of the mutation).
MeSH term(s)	Anaplastic Lymphoma Kinase/chemistry ; Anaplastic Lymphoma Kinase/deficiency ; Enzyme Activation/genetics ; Humans ; Machine Learning ; Molecular Dynamics Simulation ; Mutation ; Protein Conformation, alpha-Helical
Chemical Substances	ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1)
Language	English
Publishing date	2021-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2019132118
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Article ; Online: Activity of Crizotinib in Patients with ALK-Aberrant Relapsed/Refractory Neuroblastoma: A Children's Oncology Group Study (ADVL0912).

Foster, Jennifer H / Voss, Stephan D / Hall, David C / Minard, Charles G / Balis, Frank M / Wilner, Keith / Berg, Stacey L / Fox, Elizabeth / Adamson, Peter C / Blaney, Susan M / Weigel, Brenda J / Mossé, Yael P

Clinical cancer research : an official journal of the American Association for Cancer Research

2021 Volume 27, Issue 13, Page(s) 3543–3548

Abstract: Purpose: Anaplastic lymphoma kinase (ALK) aberrations are a promising target for patients with neuroblastoma. We assessed the activity of first-generation ALK inhibitor crizotinib in patients with no known curative treatments and whose tumors harbored ... ...

Abstract	Purpose: Anaplastic lymphoma kinase (ALK) aberrations are a promising target for patients with neuroblastoma. We assessed the activity of first-generation ALK inhibitor crizotinib in patients with no known curative treatments and whose tumors harbored an activating ALK alteration. Patients and methods: Twenty patients with relapsed/refractory ALK-positive neuroblastoma received crizotinib at the recommended phase II dose of 280 mg/m Results: The objective response rate for patients with neuroblastoma was 15% [95% confidence interval (CI): 3.3%-34.3%]: two with partial responses and 1 with a complete response. All three patients had a somatic ALK Arg1275Gln mutation, the most common ALK hotspot mutation observed in neuroblastoma and the only mutation predicted to be sensitive to ALK inhibition with crizotinib. Two patients had prolonged stable disease (10 and 13 cycles, respectively); both harbored an ALK Arg1275Gln mutation. Three patients with ALK Phe1174Leu mutations progressed during cycle 1 of therapy, and one patient with an ALK Phe1174Val received three cycles before disease progression. The two patients with ALK amplification had no response. The most common adverse event was a decrease in neutrophil count. Conclusions: Despite limited activity seen in this trial, we conclude that this is more likely due to an inability to reach the higher concentrations of crizotinib needed to overcome the competing ATP affinity.
MeSH term(s)	Anaplastic Lymphoma Kinase/genetics ; Child ; Crizotinib/therapeutic use ; Humans ; Lung Neoplasms/drug therapy ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/genetics ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Protein Kinase Inhibitors/adverse effects
Chemical Substances	Protein Kinase Inhibitors ; Crizotinib (53AH36668S) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1)
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-20-4224
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