Evidence map›Paper›PMID 26497122›Full record

ArticleHistopathology2016

Infiltrating epitheliosis of the breast: characterization of histological features, immunophenotype and genomic profile.

Carey A Eberle, Salvatore Piscuoglio, Emad A Rakha, Charlotte K Y Ng, Felipe C Geyer, Marcia Edelweiss, Rita A Sakr, Britta Weigelt, Jorge S Reis-Filho, Ian O Ellis

Open access · greenAbstract read
In one paragraph

Article in Histopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 38 citations in OpenAlex.

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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 2 institutions in 3 countries.

Carey A EberleDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Salvatore PiscuoglioDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Emad A RakhaDepartment of Histopathology, Nottingham University Hospitals, Nottingham, UK.
Charlotte K Y NgDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Felipe C GeyerDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Marcia EdelweissDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Rita A SakrDepartment of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Britta WeigeltDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Jorge S Reis-FilhoDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ian O EllisDepartment of Histopathology, Nottingham University Hospitals, Nottingham, UK.
Memorial Sloan Kettering Cancer Center · USNottingham University Hospitals NHS Trust · GB

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

aimsInfiltrating epitheliosis is a rare complex sclerosing lesion (CSL) of the breast, characterized by infiltrating ducts immersed in a scleroelastotic stroma and filled with cells having architectural and cytological patterns reminiscent of those of usual ductal hyperplasia. In this study we sought to define the molecular characteristics of infiltrating epitheliosis. METHODS AND

resultsEight infiltrating epitheliosis, adjacent breast lesions (one usual ductal hyperplasia, one papilloma, one micropapillary ductal carcinoma in situ and one low-grade adenosquamous carcinoma), and corresponding normal breast tissue from each case were microdissected and subjected to massively parallel sequencing analysis targeting all coding regions of 254 genes mutated recurrently in breast cancer and/or related to DNA repair. Mutations in components of the PI3K pathway were found in all infiltrating epitheliosis samples, seven of which harboured PIK3CA hotspot mutations, while the remaining case displayed a PIK3R1 somatic mutation.

conclusionsSomatic mutations affecting PI3K pathway genes were found to be highly prevalent in infiltrating epitheliosis, suggesting that these lesions may be neoplastic rather than hyperplastic. The landscape of somatic genetic alterations found in infiltrating epitheliosis is similar to that of radial scars/CSLs, suggesting that infiltrating epitheliosis may represent one end of this spectrum of lesions.

Indexed as

AgedAged, 80 and overBreastBreast NeoplasmsCarcinoma, AdenosquamousCarcinoma, Intraductal, NoninfiltratingClass I Phosphatidylinositol 3-KinasesFemaleFibrocystic Breast DiseaseHigh-Throughput Nucleotide SequencingHumansHyperplasiaImmunophenotypingMiddle AgedMutationPapillomaClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humancomplex sclerosing lesionsimmunohistochemistryinfiltrating epitheliosismassively parallel sequencing

Identifiers

PMID26497122
PMCPMC4957818
OpenAlexW2135017264

What OpenQuestion holds

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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.