Evidence map›Paper›PMID 28352186›Full record

ArticleOncoTargets and therapy2017

Tyrosine kinase domain mutations of

Chittibabu Vatte, Ali M Al Amri, Cyril Cyrus, Shahanas Chathoth, Sadananda Acharya, Tariq Mohammad Hashim, Zhara Al Ali, Saleh Tawfeeq Alshreadah, Ahmed Alsayyah, Amein K Al-Ali

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  9. International journal of molecular sciences · 2022
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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

10 authors at 3 institutions in 2 countries.

Chittibabu VatteDepartment of Genetic Research, Institute for Research and Medical Consultation, University of Dammam, Dammam.
Ali M Al AmriDepartment of Internal Medicine, King Fahd Hospital of the University, University of Dammam, Al-Khobar.
Cyril CyrusDepartment of Genetic Research, Institute for Research and Medical Consultation, University of Dammam, Dammam.
Shahanas ChathothDepartment of Genetic Research, Institute for Research and Medical Consultation, University of Dammam, Dammam.
Sadananda AcharyaDepartment of Stemcell Research, Institute for Research and Medical Consultation.
Tariq Mohammad HashimDepartment of Pathology, King Fahd Hospital of the University, University of Dammam, Al-Khobar.
Zhara Al AliDepartment of Internal Medicine, King Fahd Hospital of the University, University of Dammam, Al-Khobar.
Saleh Tawfeeq AlshreadahDepartment of Internal Medicine, King Fahd Hospital of the University, University of Dammam, Al-Khobar.
Ahmed AlsayyahDepartment of Pathology, King Fahd Hospital of the University, University of Dammam, Al-Khobar.
Amein K Al-AliDepartment of Biochemistry, College of Medicine, University of Dammam, Dammam, Kingdom of Saudi Arabia.
King Fahd Hospital of the University · SADammam Central Hospital · SAApplied StemCell (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpidermal growth factor receptor (

objectiveThe objective of this study was to investigate the spectrum of mutations in exons 18, 19, 20, and 21 of the MATERIALS AND

methodsThis retrospective study included 47 confirmed HNSCC cases. Mutations in the TK domain, exons 18, 19, 20, and 21 of the

resultsThe tumors exhibited EGFR-TK domain mutations in 57% of cases. Four cases of T790M mutations were reported for the first time among HNSCC patients. Out of the total mutations, L861Q (exon 21), exon 20 insertions and deletions of exon 19 accounted for the majority of mutations (21%, 19%, and 17%, respectively).

conclusionHigher frequency of EGFR-TK domain mutations together with the presence of the T790M mutation suggests that identification of these mutations might streamline the therapy and provide a better prognosis in HNSCC cases.

Indexed as

deletionsinsertionsreal-time PCRsomatic mutationsT790Mtherapy

Identifiers

PMID28352186
PMCPMC5359136
OpenAlexW2596816223

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.