Evidence map›Paper›PMID 28906000›Full record

ArticleInternational journal of cancer2018

A phosphoarray platform is capable of personalizing kinase inhibitor therapy in head and neck cancers.

Konrad Klinghammer, James Keller, Jonathan George, Jens Hoffmann, Edward L Chan, Michael J Hayman

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 3 institutions in 2 countries.

Konrad KlinghammerDepartment of Hematology and Oncology, Charite University Medicine, Berlin, Germany.ORCID 0000-0001-6425-4833
James KellerDepartment of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, NY, 11794.
Jonathan GeorgeDepartment of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, NY, 11794.
Jens HoffmannEPO-Experimental Pharmacology and Oncology GmbH, Berlin, Germany.
Edward L ChanDepartment of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, NY, 11794.
Michael J HaymanDepartment of Microbiology and Molecular Genetics, Stony Brook University, Stony Brook, NY, 11794.ORCID 0000-0002-9245-1583
Stony Brook University · USZero to Three · USExperimental Pathology Laboratories · US

Funding

Validating the prognostic value of EGFR768 in neuroblastomaR21CA187554 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI HAYMAN, MICHAEL JOHN · 2014 to 2015
$374k
NCI NIH HHS R21 CA187554
6 · The paper itself

Abstract

Tyrosine kinase inhibitors are effective treatments for cancers. Knowing the specific kinase mutants that drive the underlying cancers predict therapeutic response to these inhibitors. Thus, the current protocol for personalized cancer therapy involves genotyping tumors in search of various driver mutations and subsequently individualizing the tyrosine kinase inhibitor to the patients whose tumors express the corresponding driver mutant. While this approach works when known driver mutations are found, its limitation is the dependence on driver mutations as predictors for response. To complement the genotype approach, we hypothesize that a phosphoarray platform is equally capable of personalizing kinase inhibitor therapy. We selected head and neck squamous cell carcinoma as the cancer model to test our hypothesis. Using the receptor tyrosine kinase phosphoarray, we identified the phosphorylation profiles of 49 different tyrosine kinase receptors in five different head and neck cancer cell lines. Based on these results, we tested the cell line response to the corresponding kinase inhibitor therapy. We found that this phosphoarray accurately informed the kinase inhibitor response profile of the cell lines. Next, we determined the phosphorylation profiles of 39 head and neck cancer patient derived xenografts. We found that absent phosphorylated EGFR signal predicted primary resistance to cetuximab treatment in the xenografts without phosphorylated ErbB2. Meanwhile, absent ErbB2 signaling in the xenografts with phosphorylated EGFR is associated with a higher likelihood of response to cetuximab. In summary, the phosphoarray technology has the potential to become a new diagnostic platform for personalized cancer therapy.

Indexed as

AnimalsAntineoplastic AgentsCetuximabDrug Resistance, NeoplasmHead and Neck NeoplasmsHigh-Throughput Screening AssaysHumansMicePhosphorylationPrecision MedicineProtein Kinase InhibitorsProtein-Tyrosine KinasesXenograft Model Antitumor AssaysAntineoplastic AgentsCetuximabProtein Kinase InhibitorsProtein-Tyrosine Kinasescetuximab responsehead and neck squamous cell carcinomakinase inhibitorspersonalized medicinephosphoarray

Identifiers

PMID28906000
PMCPMC5765765
OpenAlexW2756383817

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.