Evidence map›Paper›PMID 29259013›Full record

ArticleCancer research2018

The CARMA3-Bcl10-MALT1 Signalosome Drives NFκB Activation and Promotes Aggressiveness in Angiotensin II Receptor-Positive Breast Cancer.

Prasanna Ekambaram, Jia-Ying Lloyd Lee, Nathaniel E Hubel, Dong Hu, Saigopalakrishna Yerneni, Phil G Campbell, Netanya Pollock, Linda R Klei, Vincent J Concel, Phillip C Delekta and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.2field-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

65 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Angiotensin II type 1 receptor signaling promotes bladder cancer progression and its inhibition by Losartan.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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  6. Discovery ofActa pharmaceutica Sinica. B · 2025
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5 more citing papers are in PubMed but not listed here.

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

18 authors at 4 institutions in 1 country.

Prasanna EkambaramDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Jia-Ying Lloyd LeeDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Nathaniel E HubelDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Dong HuDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Saigopalakrishna YerneniDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania.
Phil G CampbellDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, Pennsylvania.
Netanya PollockDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Linda R KleiDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Vincent J ConcelDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Phillip C DelektaDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Arul M ChinnaiyanDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Scott A TomlinsDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Daniel R RhodesDepartment of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Nolan PriedigkeitWomen's Cancer Research Center, Magee-Womens Research Institute, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Adrian V LeeWomen's Cancer Research Center, Magee-Womens Research Institute, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Steffi OesterreichWomen's Cancer Research Center, Magee-Womens Research Institute, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Linda M McAllister-LucasDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. lucaspc@upmc.edu linda.mcallister@chp.edu.
Peter C LucasDepartments of Pathology and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. lucaspc@upmc.edu linda.mcallister@chp.edu.
University of Pittsburgh · USUniversity of Michigan · USCarnegie Mellon University · USMcGowan Institute for Regenerative Medicine · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
GPCR Signaling Through a Novel NF-kB PathwayR01HL082914 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LUCAS, PETER C, MCALLISTER-LUCAS, LINDA M · 2008 to 2017
$3.6M
New mechanisms for modulating the MALT1 oncoproteinR01CA207196 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LUCAS, PETER C, MCALLISTER-LUCAS, LINDA M · 2018 to 2022
$2.2M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA207196NHLBI NIH HHS R01 HL082914
6 · The paper itself

Abstract

The angiotensin II receptor AGTR1, which mediates vasoconstrictive and inflammatory signaling in vascular disease, is overexpressed aberrantly in some breast cancers. In this study, we established the significance of an AGTR1-responsive NFκB signaling pathway in this breast cancer subset. We documented that AGTR1 overexpression occurred in the luminal A and B subtypes of breast cancer, was mutually exclusive of HER2 expression, and correlated with aggressive features that include increased lymph node metastasis, reduced responsiveness to neoadjuvant therapy, and reduced overall survival. Mechanistically, AGTR1 overexpression directed both ligand-independent and ligand-dependent activation of NFκB, mediated by a signaling pathway that requires the triad of CARMA3, Bcl10, and MALT1 (CBM signalosome). Activation of this pathway drove cancer cell-intrinsic responses that include proliferation, migration, and invasion. In addition, CBM-dependent activation of NFκB elicited cancer cell-extrinsic effects, impacting endothelial cells of the tumor microenvironment to promote tumor angiogenesis. CBM/NFκB signaling in AGTR1

Indexed as

AnimalsApoptosisB-Cell CLL-Lymphoma 10 ProteinBiomarkers, TumorBreast NeoplasmsCARD Signaling Adaptor ProteinsCell MovementCell ProliferationChick EmbryoFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMiceMice, NudeMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinAGTR1 protein, humanB-Cell CLL-Lymphoma 10 ProteinBCL10 protein, humanBiomarkers, TumorCARD10 protein, humanCARD Signaling Adaptor ProteinsMALT1 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNF-kappa BReceptor, Angiotensin, Type 1Receptors, AngiotensinRNA, Small Interfering

Identifiers

PMID29259013
PMCPMC6436094
OpenAlexW2779506403

What OpenQuestion holds

Textmetadata
LicenceTDM
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.