Evidence map›Paper›PMID 37773318›Full record

ReviewNPJ precision oncology2023

ALK fusions in the pan-cancer setting: another tumor-agnostic target?

Aditya Shreenivas, Filip Janku, Mohamed A Gouda, Hui-Zi Chen, Ben George, Shumei Kato, Razelle Kurzrock

Open access · goldAbstract readReview
In one paragraph

Review in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
19.8field-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

73 citing papers in PubMed, 86 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. ALK Knock-In Reporter Reveals APE1 as a Negative Regulator ofInternational journal of molecular sciences · 2026
    Article
  13. Article
  14. Molecular origin, discovery, validation and application of neoantigens.Asian journal of pharmaceutical sciences · 2026
    Review
  15. ALK Inhibitor Response in NovelJTO clinical and research reports · 2026
    Article
  16. Article
  17. Observational
  18. Article
  19. Article
  20. Article

13 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

7 authors at 4 institutions in 1 country.

Aditya ShreenivasMedical College of Wisconsin (MCW) Cancer Center, Milwaukee, WI, USA. ashreenivas@mcw.edu.ORCID http://orcid.org/0000-0002-8523-1523
Filip JankuMonte Rosa Therapeutics, Boston, MA, USA.ORCID http://orcid.org/0000-0002-8123-4065
Mohamed A GoudaDepartment of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0003-4829-6739
Hui-Zi ChenMedical College of Wisconsin (MCW) Cancer Center, Milwaukee, WI, USA.
Ben GeorgeMedical College of Wisconsin (MCW) Cancer Center, Milwaukee, WI, USA.
Shumei KatoCenter for Personalized Cancer Therapy and Division of Hematology and Oncology, Department of Medicine, UC San Diego Moores Cancer Center, La Jolla, CA, USA.
Razelle KurzrockMedical College of Wisconsin (MCW) Cancer Center, Milwaukee, WI, USA. rkurzrock@mcw.edu.
Medical College of Wisconsin · USThe University of Texas MD Anderson Cancer Center · USUniversity of California San Diego · USUniversity of Nebraska at Omaha · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic lymphoma kinase (ALK) alterations (activating mutations, amplifications, and fusions/rearrangements) occur in ~3.3% of cancers. ALK fusions/rearrangements are discerned in >50% of inflammatory myofibroblastic tumors (IMTs) and anaplastic large cell lymphomas (ALCLs), but only in ~0.2% of other cancers outside of non-small cell lung cancer (NSCLC), a rate that may be below the viability threshold of even large-scale treatment trials. Five ALK inhibitors -alectinib, brigatinib, ceritinb, crizotinib, and lorlatinib-are FDA approved for ALK-aberrant NSCLCs, and crizotinib is also approved for ALK-aberrant IMTs and ALCL, including in children. Herein, we review the pharmacologic tractability of ALK alterations, focusing beyond NSCLC. Importantly, the hallmark of approved indications is the presence of ALK fusions/rearrangements, and response rates of ~50-85%. Moreover, there are numerous reports of ALK inhibitor activity in multiple solid and hematologic tumors (e.g., histiocytosis, leiomyosarcoma, lymphoma, myeloma, and colorectal, neuroendocrine, ovarian, pancreatic, renal, and thyroid cancer) bearing ALK fusions/rearrangements. Many reports used crizotinib or alectinib, but each of the approved ALK inhibitors have shown activity. ALK inhibitor activity is also seen in neuroblastoma, which bear ALK mutations (rather than fusions/rearrangements), but response rates are lower (~10-20%). Current data suggests that ALK inhibitors have tissue-agnostic activity in neoplasms bearing ALK fusions/rearrangements.

Identifiers

PMID37773318
PMCPMC10542332
OpenAlexW4387172152

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.