Evidence map›Paper›PMID 38104042›Full record

ReviewMedical oncology (Northwood, London, England)2023

Epithelial to mesenchymal transition (EMT) in metaplastic breast cancer and phyllodes breast tumors.

Ioanna Akrida, Francesk Mulita, Kerasia-Maria Plachouri, Nikolaos Benetatos, Ioannis Maroulis, Helen Papadaki

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  4. Paclitaxel drives TREM2Nature communications · 2026
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  13. [Mechanism ofSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
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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

6 authors at 2 institutions in 1 country.

Ioanna AkridaDepartment of General Surgery, University General Hospital of Patras, Rion, Greece. joannakrida@yahoo.gr.ORCID http://orcid.org/0000-0001-5939-5041
Francesk MulitaDepartment of General Surgery, University General Hospital of Patras, Rion, Greece.
Kerasia-Maria PlachouriUniversity of Patras Medical School, Rion, Greece.
Nikolaos BenetatosDepartment of General Surgery, University General Hospital of Patras, Rion, Greece.
Ioannis MaroulisDepartment of General Surgery, University General Hospital of Patras, Rion, Greece.
Helen PapadakiDepartment of Anatomy-Histology-Embryology, University of Patras Medical School, Rion, Greece.
General University Hospital of Patras · GRUniversity of Patras · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT), a transdifferentiation program whereby epithelial cells acquire mesenchymal phenotype, is essential during embryonic development. EMT has also been implicated in cancer progression by conferring migratory and metastatic potential, as well as cell plasticity and stem cell like traits, to cancer cells. Metaplastic breast carcinoma (MBC) is a rare aggressive type of breast cancer characterized by the presence of heterologous elements, typically by the existence of epithelial and mesenchymal components. Phyllodes tumors (PTs) are uncommon fibroepithelial neoplasms consisting of epithelial and mesenchymal elements. Although various hypotheses have been proposed on the pathogenesis of these biphasic tumors, there is growing evidence supporting the theory that PTs and MBC could both correlate with cancer related EMT. This review summarizes the existing literature on the emerging role of EMT in the pathogenesis of MBC and PTs. Both malignant PTs and MBC are characterized by poor prognosis. Therefore, several anti-EMT targeting strategies such as blocking upstream signaling pathways, targeting the molecular drivers of EMT and targeting mesenchymal cells and the extracellular matrix, could potentially represent a promising therapeutic approach for patients suffering from these aggressive neoplasms.

Indexed as

Breast NeoplasmsPhyllodes TumorCell TransdifferentiationEpithelial-Mesenchymal TransitionFemaleHumansStem CellsBreast cancerEpithelial–mesenchymal transition (EMT)Metaplastic breast carcinomaPhyllodes breast tumors

Identifiers

PMID38104042
OpenAlexW4389831830

What OpenQuestion holds

Textmetadata
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.