Evidence map›Paper›PMID 30803032›Full record

ReviewAPMIS : acta pathologica, microbiologica, et immunologica Scandinavica2019

Targeting anaplastic lymphoma kinase in neuroblastoma.

Ganesh Umapathy, Patricia Mendoza-Garcia, Bengt Hallberg, Ruth H Palmer

Abstract readReview
In one paragraph

Review in APMIS : acta pathologica, microbiologica, et immunologica Scandinavica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  11. ALK signaling primes the DNA damage response sensitizing ALK-driven neuroblastoma to therapeutic ATR inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  12. Review
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  17. Multiple approaches to repurposing drugs for neuroblastoma.Bioorganic & medicinal chemistry · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Ganesh UmapathyDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Patricia Mendoza-GarciaDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Bengt HallbergDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Ruth H PalmerDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Funding

Göran Gustafsson Foundation RHP2016Swedish Cancer Society BH CAN18/718Swedish Cancer Society RHP CAN18/729Swedish Childhood Cancer Foundation 2014-150Swedish Childhood Cancer Foundation BH 2015-80Swedish Childhood Cancer Foundation GU 2018-0056Swedish Childhood Cancer Foundation RHP 2015-96Swedish Foundation for Strategic Research RB13-0204Swedish Research Council BH 521-2012-2831Swedish Research Council RHP 2015-04466
6 · The paper itself

Abstract

Over the last decade, anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase (RTK), has been identified as a fusion partner in a diverse variety of translocation events resulting in oncogenic signaling in many different cancer types. In tumors where the full-length ALK RTK itself is mutated, such as neuroblastoma, the picture regarding the role of ALK as an oncogenic driver is less clear. Neuroblastoma is a complex and heterogeneous tumor that arises from the neural crest derived peripheral nervous system. Although high-risk neuroblastoma is rare, it often relapses and becomes refractory to treatment. Thus, neuroblastoma accounts for 10-15% of all childhood cancer deaths. Since most cases are in children under the age of 2, understanding the role and regulation of ALK during neural crest development is an important goal in addressing neuroblastoma tumorigenesis. An impressive array of tyrosine kinase inhibitors (TKIs) that act to inhibit ALK have been FDA approved for use in ALK-driven cancers. ALK TKIs bind differently within the ATP-binding pocket of the ALK kinase domain and have been associated with different resistance mutations within ALK itself that arise in response to therapeutic use, particularly in ALK-fusion positive non-small cell lung cancer (NSCLC). This patient population has highlighted the importance of considering the relevant ALK TKI to be used for a given ALK mutant variant. In this review, we discuss ALK in neuroblastoma, as well as the use of ALK TKIs and other strategies to inhibit tumor growth. Current efforts combining novel approaches and increasing our understanding of the oncogenic role of ALK in neuroblastoma are aimed at improving the efficacy of ALK TKIs as precision medicine options in the clinic.

Indexed as

Anaplastic Lymphoma KinaseBrain NeoplasmsGene FusionHumansMolecular Targeted TherapyNeuroblastomaPoint MutationProtein Kinase InhibitorsAnaplastic Lymphoma KinaseProtein Kinase InhibitorsALKALALK-positive tumoursAnaplastic lymphoma kinaseneuroblastomanon-small cell lung cancersignal transductionTKIs

Identifiers

PMID30803032
PMCPMC6850425

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.