Evidence map›Paper›PMID 30333516›Full record

ReviewNature reviews. Clinical oncology2018

NTRK fusion-positive cancers and TRK inhibitor therapy.

Emiliano Cocco, Maurizio Scaltriti, Alexander Drilon

Abstract readReview
In one paragraph

Review in Nature reviews. Clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 761 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
761citing papers in PubMed, 5 pooled it
100.1field-weighted citation impact, top 1% 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

761 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,423 citations in OpenAlex.

  1. SEOM-GECOD clinical guideline for cancer of unknown primary (update 2025).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Guideline
  2. Pooled it
  3. Future oncology (London, England) · 2025
    Pooled it
  4. Guideline
  5. A Systematic Review with a Demonstrative Case of KIT and DOG-1 Expressing Gastrointestinal Stromal Tumors Harboring ETV6-NTRK3 Fusions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Pooled it
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Article
  11. Article
  12. Review
  13. Multidisciplinary consensus recommendations for the management of IDH-mutant grade 2 gliomas in Spain: a Delphi study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  14. Article
  15. Article
  16. Annals of medicine and surgery (2012) · 2026
    Article
  17. Article
  18. Article
  19. Article
  20. Article

701 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Emiliano CoccoHuman Oncology & Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Maurizio ScaltritiHuman Oncology & Pathogenesis Program (HOPP), Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Alexander DrilonDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA. drilona@mskcc.org.ORCID http://orcid.org/0000-0001-6806-9061
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Understanding tumor addiction to TRK fusions and sensitivity to TRK inhibitionR01CA226864 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI DRILON, ALEXANDER, VENTURA, ANDREA · 2018 to 2021
$2.5M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA226864
6 · The paper itself

Abstract

NTRK gene fusions involving either NTRK1, NTRK2 or NTRK3 (encoding the neurotrophin receptors TRKA, TRKB and TRKC, respectively) are oncogenic drivers of various adult and paediatric tumour types. These fusions can be detected in the clinic using a variety of methods, including tumour DNA and RNA sequencing and plasma cell-free DNA profiling. The treatment of patients with NTRK fusion-positive cancers with a first-generation TRK inhibitor, such as larotrectinib or entrectinib, is associated with high response rates (>75%), regardless of tumour histology. First-generation TRK inhibitors are well tolerated by most patients, with toxicity profiles characterized by occasional off-tumour, on-target adverse events (attributable to TRK inhibition in non-malignant tissues). Despite durable disease control in many patients, advanced-stage NTRK fusion-positive cancers eventually become refractory to TRK inhibition; resistance can be mediated by the acquisition of NTRK kinase domain mutations. Fortunately, certain resistance mutations can be overcome by second-generation TRK inhibitors, including LOXO-195 and TPX-0005 that are being explored in clinical trials. In this Review, we discuss the biology of NTRK fusions, strategies to target these drivers in the treatment-naive and acquired-resistance disease settings, and the unique safety profile of TRK inhibitors.

Indexed as

Aza CompoundsChildCirculating Tumor DNAHumansMembrane GlycoproteinsNeoplasmsOncogene Proteins, FusionPediatricsProtein Kinase InhibitorsPyrazolesPyrimidinesReceptor, trkAReceptor, trkBReceptor, trkCSequence Analysis, RNAAza CompoundsCirculating Tumor DNAlarotrectinibMembrane GlycoproteinsOncogene Proteins, FusionProtein Kinase InhibitorsPyrazolesPyrimidinesReceptor, trkAReceptor, trkBReceptor, trkCselitrectinibtropomyosin-related kinase-B, human

Identifiers

PMID30333516
PMCPMC6419506
OpenAlexW2896424462

What OpenQuestion holds

Textmetadata
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Read underepoch 390

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.