Evidence map›Paper›PMID 25979929›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Therapeutic targeting of anaplastic lymphoma kinase in lung cancer: a paradigm for precision cancer medicine.

Ryohei Katayama, Christine M Lovly, Alice T Shaw

Open access · greenAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
25.5field-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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Targeting Lung Cancer Metabolism: Therapeutic Opportunities and Challenges.Advances in experimental medicine and biology · 2026
    Review
  9. Article
  10. Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Small-molecule inhibition of MAP2K4 is synergistic with RAS inhibitors inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article

85 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.

Ryohei KatayamaCancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan. ryohei.katayama@jfcr.or.jp.
Christine M LovlyDepartment of Medicine, Vanderbilt University, Nashville, Tennessee.
Alice T ShawMassachusetts General Hospital Cancer Center, Boston, Massachusetts. Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Massachusetts General Hospital · US

Funding

The Role of Focal Oncogene Amplifications in Lung CancerP01CA129243 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Marc Ladanyi · 2007 to 2026
$31.2M
Overcoming Resistance Mechanisms to Anaplastic Lymphoma Kinase InhibitorsR01CA164273 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron N Hata, Jessica Jiyeong Lin · 2012 to 2026
$5.5M
Overcoming acquired resistance to EGFR inhibitors in lung cancerR01CA121210 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LOVLY, CHRISTINE M. · 2007 to 2016
$2.9M
NCI NIH HHS P01 CA129243NCI NIH HHS P01CA129243NCI NIH HHS R01 CA121210NCI NIH HHS R01CA121210NCI NIH HHS R01 CA164273NCI NIH HHS R01CA164273
6 · The paper itself

Abstract

The anaplastic lymphoma kinase (ALK) receptor tyrosine kinase was initially discovered as a component of the fusion protein nucleophosmin (NPM)-ALK in anaplastic large-cell lymphoma (ALCL). Genomic alterations in ALK, including rearrangements, point mutations, and genomic amplification, have now been identified in several malignancies, including lymphoma, non-small cell lung cancer (NSCLC), neuroblastoma, inflammatory myofibroblastic tumor, and others. Importantly, ALK serves as a validated therapeutic target in these diseases. Several ALK tyrosine kinase inhibitors (TKI), including crizotinib, ceritinib, and alectinib, have been developed, and some of them have already been approved for clinical use. These ALK inhibitors have all shown remarkable clinical outcomes in ALK-rearranged NSCLC. Unfortunately, as is the case for other kinase inhibitors in clinical use, sensitive tumors inevitably relapse due to acquired resistance. This review focuses on the discovery, function, and therapeutic targeting of ALK, with a particular focus on ALK-rearranged NSCLC.

Indexed as

Anaplastic Lymphoma KinaseAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmHumansLung NeoplasmsMolecular Targeted TherapyMutationOncogene Proteins, FusionPrecision MedicineProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesALK protein, humanAnaplastic Lymphoma KinaseAntineoplastic AgentsOncogene Proteins, FusionProtein Kinase InhibitorsReceptor Protein-Tyrosine Kinases

Identifiers

PMID25979929
PMCPMC4435823
OpenAlexW2107211259

What OpenQuestion holds

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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.