Evidence map›Paper›PMID 26872010›Full record

ArticleThe American journal of surgical pathology2016

Primary and Metastatic Cutaneous Melanomas Express ALK Through Alternative Transcriptional Initiation.

Klaus J Busam, Ricardo E Vilain, Trina Lum, Jonathan A Busam, Travis J Hollmann, Robyn P M Saw, Daniel C Coit, Richard A Scolyer, Thomas Wiesner

Open access · greenAbstract read
In one paragraph

Article in The American journal of surgical pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  12. Article
  13. Primary and Metastatic Melanoma With NTRK Fusions.The American journal of surgical pathology · 2018
    Article
  14. Review
  15. Alk and Ltk ligands are essential for iridophore development in zebrafish mediated by the receptor tyrosine kinase Ltk.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Review
  17. Article
  18. A review of kinase fusions in melanocytic tumors.Laboratory investigation; a journal of technical methods and pathology · 2017
    Review
  19. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Klaus J BusamDepartments of *Pathology ¶Surgery #Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY †Department of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown ‡Melanoma Institute of Australia, North Sydney §Sydney Medical School, The University of Sydney, Sydney, NSW, Australia ∥Dartmouth College, Hanover, NH.
Ricardo E Vilain
Trina Lum
Jonathan A Busam
Travis J Hollmann
Robyn P M Saw
Daniel C Coit
Richard A Scolyer
Thomas Wiesner
Royal Prince Alfred Hospital · AUDartmouth College · USMelanoma Institute Australia · AUMemorial Sloan Kettering Cancer Center · USUniversity of Sydney · AU

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

A number of common driver mutations have been identified in melanoma, but other genetic or epigenetic aberrations are also likely to play a role in the pathogenesis of melanoma and present potential therapeutic targets. Translocations of the anaplastic lymphoma kinase (ALK), for example, have been reported in spitzoid melanocytic neoplasms leading to kinase-fusion proteins that result in immunohistochemically detectable ALK expression. In this study, we sought to determine whether ALK was also expressed in nonspitzoid primary and metastatic cutaneous melanomas. ALK immunohistochemistry was performed on 603 melanomas (303 primary and 300 metastatic tumors) from 600 patients. ALK immunohistochemistry expression was identified in 7 primary and 9 metastatic tumors. In 5 of 7 primary tumors and in 6 of 9 metastatic lesions, the majority of tumor cells were immunoreactive for ALK. In the other 2 primary and 3 metastatic lesions, positive staining was identified in less than half of the tumor cells. ALK positivity was found in the presence or absence of BRAF or NRAS mutations. In contrast to prior observations with ALK-positive Spitz tumors, none of the ALK-positive melanomas harbored a translocation. Instead, the ALK-positive melanomas predominantly expressed the recently described ALK isoform, ALK, which lacks the extracellular and transmembrane domains of wild-type ALK, consists primarily of the intracellular tyrosine kinase domain, and originates from an alternative transcriptional initiation site within the ALK gene. The findings are clinically relevant as patients with metastatic melanoma who have ALK expression may potentially benefit from treatment with ALK kinase inhibitors.

Indexed as

AdultAgedAnaplastic Lymphoma KinaseBiomarkers, TumorCutaneous Malignant MelanomaFemaleHumansImmunohistochemistryIsoenzymesMaleMelanomaMiddle AgedReceptor Protein-Tyrosine KinasesSkin NeoplasmsTranscriptional ActivationALK protein, humanAnaplastic Lymphoma KinaseBiomarkers, TumorIsoenzymesReceptor Protein-Tyrosine Kinases

Identifiers

PMID26872010
PMCPMC5037961
OpenAlexW2323769476

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.