Evidence map›Paper›PMID 34824220›Full record

ArticleNature communications2021

High endogenous CCL2 expression promotes the aggressive phenotype of human inflammatory breast cancer.

Anita Rogic, Ila Pant, Luca Grumolato, Ruben Fernandez-Rodriguez, Andrew Edwards, Suvendu Das, Aaron Sun, Shen Yao, Rui Qiao, Shabnam Jaffer and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Reprogramming the Immune Landscape of Inflammatory Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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 5 institutions in 4 countries.

Anita RogicLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0001-6750-5159
Ila Pant *Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0003-0517-6542
Luca Grumolato *Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0001-8231-3032
Ruben Fernandez-RodriguezLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0001-9127-1735
Andrew EdwardsLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Suvendu DasLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Aaron SunLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0002-5773-3382
Shen YaoDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Rui QiaoDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Shabnam JafferDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0001-9843-7427
Ravi SachidanandamDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Guray AkturkTisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.ORCID http://orcid.org/0000-0001-7032-8085
Rosa KarlicBioinformatics group, Division of Molecular Biology, Department of Biology, Faculty of Science, University of Zagreb, Zagreb, Croatia.ORCID http://orcid.org/0000-0002-1291-2897
Mihaela SkobeLaboratory of Cancer Lymphangiogenesis, Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA. mihaela.skobe@mssm.edu.ORCID http://orcid.org/0000-0003-1583-6487
Stuart A AaronsonDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA. stuart.aaronson@mssm.edu.ORCID http://orcid.org/0000-0002-4643-0474
Icahn School of Medicine at Mount Sinai · USTisch Hospital · USIndian Institute of Advanced Research · INInserm · FRUniversity of Zagreb · HR

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
Impact of WTC dust on immune functions and prostate cancer promotionU01OH011328 · OH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AARONSON, STUART A · 2016 to 2020
$3.0M
Defining mechanisms and targets in Wnt addicted human malignancies (PQ22)R01CA170702 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AARONSON, STUART A · 2012 to 2015
$1.4M
NCI NIH HHS P01 CA080058NCI NIH HHS P30 CA196521NCI NIH HHS R01 CA170702NIOSH CDC HHS U01 OH011328
6 · The paper itself

Abstract

Inflammatory Breast Cancer (IBC) is a highly aggressive malignancy with distinct clinical and histopathological features whose molecular basis is unresolved. Here we describe a human IBC cell line, A3250, that recapitulates key IBC features in a mouse xenograft model, including skin erythema, diffuse tumor growth, dermal lymphatic invasion, and extensive metastases. A3250 cells express very high levels of the CCL2 chemokine and induce tumors enriched in macrophages. CCL2 knockdown leads to a striking reduction in macrophage densities, tumor proliferation, skin erythema, and metastasis. These results establish IBC-derived CCL2 as a key factor driving macrophage expansion, and indirectly tumor growth, with transcriptomic analysis demonstrating the activation of multiple inflammatory pathways. Finally, primary human IBCs exhibit macrophage infiltration and an enriched macrophage RNA signature. Thus, this human IBC model provides insight into the distinctive biology of IBC, and highlights potential therapeutic approaches to this deadly disease.

Indexed as

AnimalsCell Line, TumorChemokine CCL2FemaleGene Expression Regulation, NeoplasticHumansInflammationInflammatory Breast NeoplasmsMiceMice, SCIDMyeloid CellsNeoplasm MetastasisReceptors, CCR2Transplantation, HeterologousTumor-Associated MacrophagesTumor MicroenvironmentCCL2 protein, humanCCR2 protein, humanChemokine CCL2Receptors, CCR2

Identifiers

PMID34824220
PMCPMC8617270
OpenAlexW3215037340

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.