Evidence map›Paper›PMID 24163262›Full record

ArticleOncotarget2013

Identification of anaplastic lymphoma kinase as a potential therapeutic target in Basal Cell Carcinoma.

Hanna Ning, Hiroshi Mitsui, Claire Q F Wang, Mayte Suárez-Fariñas, Juana Gonzalez, Kejal R Shah, Jie Chen, Israel Coats, Diane Felsen, John A Carucci and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2013. 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
1.6field-weighted citation impact, top 17% 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, 24 citations in OpenAlex.

  1. Ensartinib (X-396) in ALK-Positive Non-Small Cell Lung Cancer: Results from a First-in-Human Phase I/II, Multicenter Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Trial
  2. Article
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  7. [Pharmacology and Clinical Evaluation of Ensartinib Hydrochloride Capsule].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020
    Review
  8. OncogenicLife science alliance · 2020
    Article
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  10. Review
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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

11 authors at 4 institutions in 1 country.

Hanna NingLaboratory for Investigative Dermatology, The Rockefeller University, New York, NY.
Hiroshi Mitsui
Claire Q F Wang
Mayte Suárez-Fariñas
Juana Gonzalez
Kejal R Shah
Jie Chen
Israel Coats
Diane Felsen
John A Carucci
James G Krueger
Rockefeller University · USCornell University · USBaylor University Medical Center · USNYU Langone Health · US

Funding

Transforming Translational Science and Education to Benefit Human HealthUL1TR000043 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2012 to 2015
$26.8M
Transforming Translational Science and Education to Benefit Human HealthKL2TR000151 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 2012 to 2015
$2.1M
NCATS NIH HHS 8 KL2 TR000151NCATS NIH HHS 8 UL1B TR000043NCATS NIH HHS KL2 TR000151NCATS NIH HHS UL1 TR000043
6 · The paper itself

Abstract

The pathogenesis of BCC is associated with sonic hedgehog (SHH) signaling. Vismodegib, a smoothened inhibitor that targets this pathway, is now in clinical use for advanced BCC patients, but its efficacy is limited. Therefore, new therapeutic options for this cancer are required. We studied gene expression profiling of BCC tumour tissues coupled with laser capture microdissection to identify tumour specific receptor tyrosine kinase expression that can be targeted by small molecule inhibitors. We found a >250 fold increase (FDR<10-4) of the oncogene, anaplastic lymphoma kinase (ALK) as well as its ligands, pleiotrophin and midkine in BCC compared to microdissected normal epidermis. qRT-PCR confirmed increased expression of ALK (p<0.05). Stronger expression of phosphorylated ALK in BCC tumour nests than normal skin was observed by immunohistochemistry. Crizotinib, an FDA-approved ALK inhibitor, reduced keratinocyte proliferation in culture, whereas a c-Met inhibitor did not. Crizotinib significantly reduced the expression of GLI1 and CCND2 (members of SHH-pathway) mRNA by approximately 60% and 20%, respectively (p<0.01). Our data suggest that ALK may increase GLI1 expression in parallel with the conventional SHH-pathway and promote keratinocyte proliferation. Hence, an ALK inhibitor alone or in combination with targeting SHH-pathway molecules may be a potential treatment for BCC patients.

Indexed as

Anaplastic Lymphoma KinaseAnimalsBasal Cell CarcinomaCrizotinibGene Expression ProfilingGene Expression Regulation, NeoplasticHedgehog ProteinsHumansKeratinocytesLaser Capture MicrodissectionMiceMice, TransgenicMolecular Targeted TherapyPyrazolesPyridinesReceptor Protein-Tyrosine KinasesALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseCrizotinibGLI1 protein, humanHedgehog ProteinsPyrazolesPyridinesReceptor Protein-Tyrosine KinasesTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID24163262
PMCPMC3926823
OpenAlexW1789174000

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.