Evidence map›Paper›PMID 26887047›Full record

ArticleOncotarget2016

Retrospective study testing next generation sequencing of selected cancer-associated genes in resected prostate cancer.

Marco Lo Iacono, Consuelo Buttigliero, Valentina Monica, Enrico Bollito, Diletta Garrou, Susanna Cappia, Ida Rapa, Francesca Vignani, Valentina Bertaglia, Cristian Fiori and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Androgen Signaling in Prostate Cancer: When a Friend Turns Foe.Endocrine, metabolic & immune disorders drug targets · 2025
    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

15 authors at 1 institution in 1 country.

Marco Lo IaconoUniversity of Turin, Department of Oncology, Orbassano, Italy.
Consuelo ButtiglieroUniversity of Turin, Department of Oncology, Orbassano, Italy.
Valentina MonicaUniversity of Turin, Department of Oncology, Orbassano, Italy.
Enrico BollitoUniversity of Turin, Department of Oncology, Orbassano, Italy.
Diletta GarrouUniversity of Turin, Department of Oncology, Orbassano, Italy.
Susanna CappiaUniversity of Turin, Department of Oncology, Orbassano, Italy.
Ida RapaUniversity of Turin, Department of Oncology, Orbassano, Italy.
Francesca VignaniUniversity of Turin, Department of Oncology, Orbassano, Italy.
Valentina BertagliaUniversity of Turin, Department of Oncology, Orbassano, Italy.
Cristian FioriUniversity of Turin, Department of Oncology, Orbassano, Italy.
Mauro PapottiUniversity of Turin, Department of Oncology, Orbassano, Italy.
Marco VolanteUniversity of Turin, Department of Oncology, Orbassano, Italy.
Giorgio V ScagliottiUniversity of Turin, Department of Oncology, Orbassano, Italy.
Francesco PorpigliaUniversity of Turin, Department of Oncology, Orbassano, Italy.
Marcello TucciUniversity of Turin, Department of Oncology, Orbassano, Italy.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeProstate cancer (PCa) has a highly heterogeneous outcome. Beyond Gleason Score, Prostate Serum Antigen and tumor stage, nowadays there are no biological prognostic factors to discriminate between indolent and aggressive tumors.The most common known genomic alterations are the TMPRSS-ETS translocation and mutations in the PI3K, MAPK pathways and in p53, RB and c-MYC genes.The aim of this retrospective study was to identify by next generation sequencing the most frequent genetic variations (GVs) in localized and locally advanced PCa underwent prostatectomy and to investigate their correlation with clinical-pathological variables and disease progression.

resultsIdentified non-synonymous GVs included TP53 p.P72R (78% of tumors), two CSFR1 SNPs, rs2066934 and rs2066933 (70%), KDR p.Q472H (67%), KIT p.M541L (28%), PIK3CA p.I391M (19%), MET p.V378I (10%) and FGFR3 p.F384L/p.F386L (8%). TP53 p.P72R, MET p.V378I and CSFR1 SNPs were significantly associated with the HI risk group, TP53 and MET variations with T≥T2c. FGFR3 p.F384L/p.F386L was correlated with T≤T2b. MET p.V378I mutation, detected in 20% of HI risk patients, was associated with early biochemical recurrence. EXPERIMENTAL

designNucleic acids were obtained from tissue samples of 30 high (HI) and 30 low-intermediate (LM) risk patients, according to D'Amico criteria. Genomic DNA was explored with the Ion_AmpliSeq_Cancer_Hotspot_Panel_v.2 including 50 cancer-associated genes. GVs with allelic frequency (AF) ≥10%, affecting protein function or previously associated with cancer, were correlated with clinical-pathological variables.

conclusionOur results confirm a complex mutational profile in PCa, supporting the involvement of TP53, MET, FGFR3, CSF1R GVs in tumor progression and aggressiveness.

Indexed as

Genetic VariationAgedBiomarkers, TumorDisease ProgressionFollow-Up StudiesHigh-Throughput Nucleotide SequencingHumansMaleNeoplasm GradingNeoplasm InvasivenessNeoplasm Recurrence, LocalNeoplasm StagingPrognosisProstatectomyProstatic NeoplasmsRetrospective StudiesBiomarkers, Tumorgenetic characterizationnext generation sequencingprecision medicineprognostic factorsprostate cancer

Identifiers

PMID26887047
PMCPMC4924723
OpenAlexW2309982992

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.