Evidence map›Paper›PMID 29907598›Full record

ArticleCold Spring Harbor molecular case studies2018

Clinical response of the novel activating ALK-I1171T mutation in neuroblastoma to the ALK inhibitor ceritinib.

Jikui Guan, Susanne Fransson, Joachim Tetteh Siaw, Diana Treis, Jimmy Van den Eynden, Damini Chand, Ganesh Umapathy, Kristina Ruuth, Petter Svenberg, Sandra Wessman and 11 more

Open access · diamondAbstract readCase Reports
In one paragraph

Article in Cold Spring Harbor molecular case studies, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–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

35 citing papers in PubMed, 48 citations in OpenAlex.

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  6. 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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  16. Frequency and Prognostic Impact ofJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021
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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

21 authors at 4 institutions in 2 countries.

Jikui GuanDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0003-1723-0307
Susanne FranssonDepartment of Pathology and Genetics, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0002-9713-3074
Joachim Tetteh SiawDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0002-1286-4485
Diana TreisChildhood Cancer Research Unit, Department of Women's and Children's Health, and Pediatric Oncology Program Karolinska University Hospital, Stockholm 17176, Sweden.
Jimmy Van den EyndenDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0003-0002-5614
Damini ChandDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
Ganesh UmapathyDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
Kristina RuuthInstitute of Molecular Biology, Umeå University, Umeå 90187, Sweden.
Petter SvenbergChildhood Cancer Research Unit, Department of Women's and Children's Health, and Pediatric Oncology Program Karolinska University Hospital, Stockholm 17176, Sweden.
Sandra WessmanDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm 17176, Sweden.
Alia ShamikhDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm 17176, Sweden.
Hans JacobssonDepartment of Radiology, Karolinska University Hospital, Stockholm 17176, Sweden.
Lena GordonDepartment of Pediatric Radiology, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm 17176, Sweden.
Jakob StenmanDepartment of Pediatric Surgery, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm 17176, Sweden.
Pär-Johan SvenssonDepartment of Pediatric Surgery, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm 17176, Sweden.
Magnus HanssonDepartment of Pediatrics and Pathology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
Erik LarssonDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.
Tommy MartinssonDepartment of Pathology and Genetics, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0002-9403-3123
Ruth H PalmerDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0002-2735-8470
Per KognerDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm 17176, Sweden.ORCID 0000-0002-2202-9694
Bengt HallbergDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden.ORCID 0000-0003-2032-2616
University of Gothenburg · SEKarolinska University Hospital · SEUmeå University · SEZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors with anaplastic lymphoma kinase (ALK) fusion rearrangements, including non-small-cell lung cancer and anaplastic large cell lymphoma, are highly sensitive to ALK tyrosine kinase inhibitors (TKIs), underscoring the notion that such cancers are addicted to ALK activity. Although mutations in ALK are heavily implicated in childhood neuroblastoma, response to the ALK TKI crizotinib has been disappointing. Embryonal tumors in patients with DNA repair defects such as Fanconi anemia (FA) often have a poor prognosis, because of lack of therapeutic options. Here we report a child with underlying FA and ALK mutant high-risk neuroblastoma responding strongly to precision therapy with the ALK TKI ceritinib. Conventional chemotherapy treatment caused severe, life-threatening toxicity. Genomic analysis of the initial biopsy identified germline

Indexed as

3T3 CellsAdolescentAnaplastic Lymphoma KinaseAnimalsBrain NeoplasmsFanconi AnemiaFanconi Anemia Complementation Group A ProteinHumansMaleMiceMutation, MissenseNeuroblastomaPC12 CellsProtein Kinase InhibitorsPyrimidinesRatsALK protein, humanAnaplastic Lymphoma KinaseceritinibFANCA protein, humanFanconi Anemia Complementation Group A ProteinProtein Kinase InhibitorsPyrimidinesSulfonesabnormality of the enteric gangliaanaplastic large-cell lymphomaneuroblastoma

Identifiers

PMID29907598
PMCPMC6071567
OpenAlexW2808103253

What OpenQuestion holds

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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.