Evidence map›Paper›PMID 29902261›Full record

ArticlePloS one2018

PIK3CA copy number aberration and activation of the PI3K-AKT-mTOR pathway in varied disease states of penile cancer.

Anthony Adimonye, Elzbieta Stankiewicz, Susannah La-Touche, Sakunthala Kudahetti, Giorgia Trevisan, Brendan Tinwell, Cathy Corbishley, Yong-Jie Lu, Nick Watkin, Daniel Berney

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
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 1 country.

Anthony AdimonyeBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID 0000-0002-0789-5279
Elzbieta StankiewiczBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Susannah La-ToucheBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Sakunthala KudahettiBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Giorgia TrevisanDepartment of Histopathology, Royal London Hospital, Barts Health NHS Trust, London, United Kingdom.
Brendan TinwellDepartment of Cellular Pathology, St George's Hospital, London, United Kingdom.
Cathy CorbishleyDepartment of Cellular Pathology, St George's Hospital, London, United Kingdom.
Yong-Jie LuBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Nick WatkinDepartment of Urology, St George's Hospital, London, United Kingdom.
Daniel BerneyBarts Cancer Institute, Centre for Molecular Oncology, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GBSt George's Hospital · GBBarts Health NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTherapeutic targeting of the PI3K-AKT-mTOR pathway may benefit patients with advanced penile squamous cell carcinoma (PSCC).

objectivesTo determine the prevalence of PIK3CA copy number gain and correlate this with the activity status of PI3K-AKT-mTOR pathway in pre-malignant penile intraepithelial neoplasia (PeIN) and invasive PSCC. MATERIALS AND

methodsArchival tissue blocks were obtained from 58 PeIN and 244 primary PSCC patients treated at St George's Hospital. PIK3CA copy number status (CNS) was assessed by fluorescence in-situ hybridisation. High-risk HPV DNA was detected with INNO-LiPA assay. p16INK4A, p-AKT and p-mTOR protein expression were assessed using immunohistochemistry (IHC).

resultsIncreased prevalence of PIK3CA copy number gain was seen in PSCC in comparison to PeIN (84/199 (42%) vs. 10/58 (17%); p = 0.0009). Analysis of the p-AKT and p-mTOR revealed a tendency to a more common expression of cytoplasmic p-AKT (p = 0.1318), nuclear p-AKT (p<0.0001) and cytoplasmic mTOR (p = 0.0006) in PeIN than PSCC. A significant association between p-AKT cytoplasmic immunoexpression and PIK3CA CNS (p = 0.0404) was found in PeIN.

conclusionOverall, PIK3CA copy number gain correlated with activation of the PI3K-AKT-mTOR pathway in PeIN and activation of this pathway is primarily involved in early penile carcinogenesis. Based on these results therapeutic targeting of this pathway in advanced PSCC is unlikely to produce significant clinical benefit. Future studies will need to focus on alternative therapeutic targets.

Indexed as

DNA Copy Number VariationsClass I Phosphatidylinositol 3-KinasesHumansMaleNeoplasm InvasivenessPapillomaviridaePenile NeoplasmsPhosphorylationProto-Oncogene Proteins c-aktRetrospective StudiesSignal TransductionTOR Serine-Threonine KinasesClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID29902261
PMCPMC6002057
OpenAlexW2807827931

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.