Evidence map›Paper›PMID 26876172›Full record

ArticleCell reports2016

Satb1 Overexpression Drives Tumor-Promoting Activities in Cancer-Associated Dendritic Cells.

Amelia J Tesone, Melanie R Rutkowski, Eva Brencicova, Nikolaos Svoronos, Alfredo Perales-Puchalt, Tom L Stephen, Michael J Allegrezza, Kyle K Payne, Jenny M Nguyen, Jayamanna Wickramasinghe and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 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

15 authors at 4 institutions in 2 countries.

Amelia J TesoneTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Melanie R RutkowskiTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Eva BrencicovaTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Nikolaos SvoronosTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Alfredo Perales-PuchaltTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Tom L StephenTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Michael J AllegrezzaTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Kyle K PayneTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Jenny M NguyenTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA.
Jayamanna WickramasingheCenter for Systems and Computational Biology, the Wistar Institute, Philadelphia, PA 19104, USA.
Julia TchouDivision of Endocrine and Oncologic Surgery, Department of Surgery, University of Pennsylvania, Philadelphia, PA 19104-1693, USA.
Mark E BorowskyHelen F. Graham Cancer Center, Christiana Care Health System, 4701 Ogletown-Stanton Road, Newark, DE 19713, USA.
Gabriel A RabinovichLaboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME-CONICET), C1428ADN Buenos Aires, Argentina.
Andrew V KossenkovCenter for Systems and Computational Biology, the Wistar Institute, Philadelphia, PA 19104, USA.
Jose R Conejo-GarciaTumor Microenvironment and Metastasis Program, the Wistar Institute, Philadelphia, PA 19104, USA. Electronic address: jrconejo@wistar.org.
The Wistar Institute · USChristiana Care Health System · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Pennsylvania · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
Toxicology, Pathology and Biodistribution Core (TPB Core)U54CA151662 · NCI · DARTMOUTH COLLEGE · PI POGUE, BRIAN WILLIAM · 2010 to 2014
$11.6M
Vascular Leukocytes Influence the Tumor MicroenvironmentR01CA124515 · NCI · WISTAR INSTITUTE · PI Jose R Conejo-Garcia · 2007 to 2026
$7.1M
Initiation and Evolution of the Ovarian Cancer MicroenvironmentR01CA157664 · NCI · WISTAR INSTITUTE · PI CONEJO-GARCIA, JOSE R · 2011 to 2020
$3.8M
Effects of Common Polymorphisms in Immune Sensors in Tumor ImmunosurveillanceR01CA178687 · NCI · WISTAR INSTITUTE · PI CONEJO-GARCIA, JOSE R · 2013 to 2017
$1.9M
Integrative Approach to Comprehensive Analysis of High Throughput Data on a Cancer Center LevelR50CA211199 · NCI · WISTAR INSTITUTE · PI Andrew V Kossenkov · 2016 to 2026
$1.6M
NCI NIH HHS CA010815NCI NIH HHS P30 CA010815NCI NIH HHS P30CA10815NCI NIH HHS R01 CA124515NCI NIH HHS R01CA124515NCI NIH HHS R01 CA157664NCI NIH HHS R01CA157664NCI NIH HHS R01 CA178687NCI NIH HHS R01CA178687NCI NIH HHS R50 CA211199NCI NIH HHS T32 CA009140NCI NIH HHS T32 CA009171NCI NIH HHS T32CA009171NCI NIH HHS U54 CA151662NCI NIH HHS U54CA151662
6 · The paper itself

Abstract

Special AT-rich sequence-binding protein 1 (Satb1) governs genome-wide transcriptional programs. Using a conditional knockout mouse, we find that Satb1 is required for normal differentiation of conventional dendritic cells (DCs). Furthermore, Satb1 governs the differentiation of inflammatory DCs by regulating major histocompatibility complex class II (MHC II) expression through Notch1 signaling. Mechanistically, Satb1 binds to the Notch1 promoter, activating Notch expression and driving RBPJ occupancy of the H2-Ab1 promoter, which activates MHC II transcription. However, tumor-driven, unremitting expression of Satb1 in activated Zbtb46(+) inflammatory DCs that infiltrate ovarian tumors results in an immunosuppressive phenotype characterized by increased secretion of tumor-promoting Galectin-1 and IL-6. In vivo silencing of Satb1 in tumor-associated DCs reverses their tumorigenic activity and boosts protective immunity. Therefore, dynamic fluctuations in Satb1 expression govern the generation and immunostimulatory activity of steady-state and inflammatory DCs, but continuous Satb1 overexpression in differentiated DCs converts them into tolerogenic/pro-inflammatory cells that contribute to malignant progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell DifferentiationCell ProliferationCell Transformation, NeoplasticDendritic CellsFemaleGalectin 1Histocompatibility Antigens Class IIHistonesHumansImmune ToleranceImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukin-6Matrix Attachment Region Binding ProteinsMiceGalectin 1Histocompatibility Antigens Class IIhistone H2B type 1-AHistonesImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukin-6interleukin-6, mouseMatrix Attachment Region Binding ProteinsNotch1 protein, mouseRbpj protein, mouseReceptor, Notch1RNA, Small InterferingSatb1 protein, mouseTranscription FactorsZbtb46 protein, mouse

Identifiers

PMID26876172
PMCPMC4767618
OpenAlexW2259350898

What OpenQuestion holds

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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.