Evidence map›Paper›PMID 26209091›Full record

ArticleJournal of translational medicine2015

Epidermal growth factor receptor pathway mutation and expression profiles in cervical squamous cell carcinoma: therapeutic implications.

Sureewan Bumrungthai, Kavita Munjal, Shirish Nandekar, Kumarasen Cooper, Tipaya Ekalaksananan, Chamsai Pientong, Mark Francis Evans

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

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  12. AnOncoTargets and therapy · 2020
    Article
  13. Differential effects of GLI2 and GLI3 in regulating cervical cancer malignancy in vitro and in vivo.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  14. Article
  15. Mutation analysis of EGFR and its correlation with the HPV in Indian cervical cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
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

7 authors at 4 institutions in 3 countries.

Sureewan BumrungthaiDepartment of Microbiology, Khon Kaen University, Khon Kaen, 40002, Thailand. sureewan.b@windowslive.com.
Kavita MunjalDepartment of Pathology, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh, 453555, India. kavita_munjal@rediffmail.com.
Shirish NandekarDepartment of Pathology, Sri Aurobindo Institute of Medical Sciences, Indore, Madhya Pradesh, 453555, India. shirishnandedkar@yahoo.co.in.
Kumarasen CooperDepartment of Pathology and Laboratory Medicine, Pearlman School of Medicine, University of Pennsylvania, Philadelphia, 19104-4283, USA. Kumarasen.Cooper@uphs.upenn.edu.
Tipaya EkalaksanananDepartment of Microbiology, Khon Kaen University, Khon Kaen, 40002, Thailand. tipeka@kku.ac.th.
Chamsai PientongDepartment of Microbiology, Khon Kaen University, Khon Kaen, 40002, Thailand. chapie@kku.ac.th.
Mark Francis EvansDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, 05405, VT, USA. mark.evans@uvm.edu.
Khon Kaen University · THSri Aurobindo Institute of Medical Sciences · INUniversity of Pennsylvania · USUniversity of Vermont · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical squamous cell carcinoma (CSCC) is a major cause of female mortality worldwide. This study has examined epidermal growth factor receptor (EGFR) pathway markers that represent actionable pharmacological targets.

methodsHPV16 positive CSCCs (n = 105 patients) from Madhya Pradesh, India were screened for KRAS and PIK3CA mutations by PNA-clamp real-time PCR. Immunohistochemistry (IHC) was performed for EGFR, PIK3CA, PTEN, phospho-AKT, phospho-mTOR and phospho-44/42 MAPK (ERK1/2).

resultsKRAS mutations were detected in 0/91 (0%) and PIK3CA mutations in 19/95 (20.0%) informative specimens: exon 9, E542 (n = 3) and E545 (n = 15); exon 20, H1047R (n = 1). PIK3CA mutation detection was associated with older mean patient age [48.2 vs. 56.6 years (P = 0.007)] and with post-menopausal age: 5/45 (11.1%) patients <50 years vs. 14/50 (28.0%) patients ≥50 years (P = 0.045; OR = 3.11). EGFR expression was present in 60/101 (59.4%) CSCCs and was associated with PIK3CA mutation detection (P < 0.05) but not age (P > 0.05). EGFR and phospho-AKT staining showed associations with tumor grade and/or lymph node status (P < 0.05). Significant associations were not found for the other study markers (P > 0.05).

conclusionThese data show that PIK3CA mutation acquisition is related to patient age and EGFR expression. The absence of KRAS mutations supports the potential of anti-EGFR therapies for CSCC treatment. The relatively high PIK3CA mutation rates indicate that PI3K may be a therapeutic target for a significant subset of CSCC patients. Qualitatively distinct IHC staining profiles for the marker panel were noted patient to patient; however, across patients, consistent linear relationships between up- and downstream pathway markers were not observed. Evaluation of the expression status of potential cancer pathway targets may be of value in addition to molecular profiling for choosing among therapeutic options.

Indexed as

Gene Expression ProfilingAdultAgedAged, 80 and overBiomarkers, TumorCarcinoma, Squamous CellClass I Phosphatidylinositol 3-KinasesCohort StudiesDNA Mutational AnalysisErbB ReceptorsExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryMiddle AgedBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesKRAS protein, humanPhosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID26209091
PMCPMC4513684
OpenAlexW1605849959

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LicenceCC BY
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Registered trials

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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.