Evidence map›Paper›PMID 27036514›Full record

ArticleJournal of hematology & oncology2016

Functional and genetic screening of acute myeloid leukemia associated with mediastinal germ cell tumor identifies MEK inhibitor as an active clinical agent.

Jessica T Leonard, Philipp W Raess, Jennifer Dunlap, Brandon Hayes-Lattin, Jeffrey W Tyner, Elie Traer

Open access · goldAbstract readCase Reports
In one paragraph

Article in Journal of hematology & oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  5. Novel treatments in optic pathway gliomas.Frontiers in ophthalmology · 2022
    Review
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  15. Current Development Status of MEK Inhibitors.Molecules (Basel, Switzerland) · 2017
    Review
  16. Article
  17. Article
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

6 authors at 1 institution in 1 country.

Jessica T LeonardDivision of Hematology and Oncology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Philipp W RaessDepartment of Pathology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Jennifer DunlapDepartment of Pathology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Brandon Hayes-LattinCenter for Hematologic Malignancies, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Jeffrey W TynerDepartment of Cell, Developmental, and Cancer Biology, Portland, OR, USA.
Elie TraerCenter for Hematologic Malignancies, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA. traere@ohsu.edu.ORCID http://orcid.org/0000-0001-8844-2345
Oregon Health & Science University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHematologic malignancies arising in the setting of established germ cell tumors have been previously described and have a dismal prognosis. Identification of targetable mutations and pathway dysregulation through massively parallel sequencing and functional assays provides new approaches to disease management. CASE PRESENTATION: Herein, we report the case of a 23-year-old male who was diagnosed with a mediastinal germ cell tumor and subsequent acute myeloid leukemia. A shared clonal origin was demonstrated through identification of identical NRAS and TP53 somatic mutations in both malignancies. The patient's leukemia was refractory to standard therapies with short interval relapse. Functional assays demonstrated the patient's blasts to be sensitive to the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib, correlating with the activating NRAS mutation. The patient experienced a sustained partial remission while on trametinib therapy but ultimately suffered relapse of the germ cell tumor. The leukemic clone remained stable and sensitive to trametinib at that time.

conclusionsThis case highlights the potential power of combining genetic sequencing and in vitro functional assays with targeted therapies in the treatment of rare diseases.

Indexed as

Acute DiseaseGTP PhosphohydrolasesHigh-Throughput Nucleotide SequencingHumansLeukemia, MyeloidMaleMAP Kinase Kinase 1MAP Kinase Kinase 2Mediastinal NeoplasmsMembrane ProteinsNeoplasm Recurrence, LocalNeoplasms, Germ Cell and EmbryonalPoint MutationProtein Kinase InhibitorsPyridonesPyrimidinonesGTP PhosphohydrolasesMAP Kinase Kinase 1MAP Kinase Kinase 2Membrane ProteinsNRAS protein, humanProtein Kinase InhibitorsPyridonesPyrimidinonestrametinibTumor Suppressor Protein p53Acute myeloid leukemiaGerm cell neoplasmHigh-throughput nucleotide sequencingNRASTrametinib

Identifiers

PMID27036514
PMCPMC4815159
OpenAlexW2320554446

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.