Evidence map›Paper›PMID 31610171›Full record

ReviewThe American journal of pathology2020

Cell of Origin and Immunologic Events in the Pathogenesis of Breast Implant-Associated Anaplastic Large-Cell Lymphoma.

Suzanne D Turner, Giorgio Inghirami, Roberto N Miranda, Marshall E Kadin

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  9. Silicone breast implant-associated pathologies and T cell-mediated responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

4 authors at 4 institutions in 2 countries.

Suzanne D TurnerDivision of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, United Kingdom. Electronic address: sdt36@cam.ac.uk.
Giorgio InghiramiDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York.
Roberto N MirandaDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Marshall E KadinDepartment of Dermatology, Roger Williams Medical Center, Providence, Rhode Island; Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts.
Cornell University · USRoger Williams Medical Center · USThe University of Texas MD Anderson Cancer Center · USUniversity of Cambridge · GB

Funding

Preclinical Models and Therapeutics CoreP01CA229100 · NCI · MAYO CLINIC ARIZONA · PI SCOTT, DAVID WILLIAM · 2018 to 2022
$10.2M
6 · The paper itself

Abstract

Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma. Nearly all cases have been associated with textured implants. Most cases are of effusion-limited, indolent disease, with an excellent prognosis after implant and capsule removal. However, capsular invasion and tumor mass have a more aggressive course and a fatal outcome risk. This review summarizes the current knowledge on BIA-ALCL cell of origin and immunologic factors underlying its pathogenesis. Cytokine expression profiling of BIA-ALCL cell lines and clinical specimens reveals a predominantly type 17 helper T-cell (Th17)/Th1 signature, implicating this as its cell of origin. However, a Th2 allergic inflammatory response is suggested by the presence of IL-13, with infiltration of eosinophils and IgE-coated mast cells in clinical specimens of BIA-ALCL. The microenvironment-induced T-cell plasticity, a factor increasingly appreciated, may partially explain these divergent results. Mutations resulting in constitutive Janus kinase (JAK)-STAT activation have been detected and associated with BIA-ALCL pathogenesis in a small number of cases. One possible scenario is that an inflammatory microenvironment stimulates an immune response, followed by polyclonal expansion of Th17/Th1 cell subsets with release of inflammatory cytokines and chemokines and accumulation of seroma. JAK-STAT3 gain-of-function mutations within this pathway and others may subsequently lead to monoclonal T-cell proliferation and clinical BIA-ALCL. Current research suggests that therapies targeting JAK proteins warrant investigation in BIA-ALCL.

Indexed as

Cell LineageBreast ImplantsBreast NeoplasmsFemaleHumansLymphoma, Large-Cell, Anaplastic

Identifiers

PMID31610171
PMCPMC7298558
OpenAlexW2973689811

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.