Evidence map›Paper›PMID 33013860›Full record

ArticleFrontiers in immunology2020

HMGB1 Promotes Myeloid Egress and Limits Lymphatic Clearance of Malignant Pleural Effusions.

Adam C Soloff, Katherine E Jones, Amy A Powers, Pranav Murthy, Yue Wang, Kira L Russell, Miranda Byrne-Steele, Amanda W Lund, Jian-Min Yuan, Sara E Monaco and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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

13 authors at 5 institutions in 1 country.

Adam C SoloffDepartment of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Katherine E JonesDepartment of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Amy A PowersDepartment of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Pranav MurthyDepartment of Surgery, Division of Surgical Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Yue WangDepartment of Surgery, Division of Surgical Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Kira L RussellDepartment of Surgery, Division of Surgical Oncology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Miranda Byrne-SteeleiRepertoire, Inc., Huntsville, AL, United States.
Amanda W LundDepartment of Cell, Developmental and Cancer Biology, Oregon Health and Science University, Portland, OR, United States.
Jian-Min YuanDivision of Cancer Control and Population Sciences, UPMC Hillman Cancer Center, Pittsburgh, PA, United States.
Sara E MonacoDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Jian HaniRepertoire, Inc., Huntsville, AL, United States.
Rajeev DhuparDepartment of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Michael T LotzeCancer Immunology and Immunotherapy Program, UPMC Hillman Cancer Center, Pittsburgh, PA, United States.
University of Pittsburgh · USiRepertoire (United States) · USOregon Health & Science University · USUPMC Hillman Cancer Center · USVA Pittsburgh Healthcare System · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
(PQ5) Mitochondria are endocellular symbionts that serve as targets for immune recognitionR01CA206012 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FACCIABENE, ANDREA · 2016 to 2020
$2.0M
Pancreatic Ductal Adenocarcinoma is a disease of constitutive autophagyR01CA181450 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LOTZE, MICHAEL T, ZEH, HERBERT J · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA181450NCI NIH HHS R01 CA206012
6 · The paper itself

Abstract

Pleural effusions, when benign, are attributed to cardiac events and suffusion of fluid within the pleural space. When malignant, lymphatic obstruction by tumor and failure to absorb constitutively produced fluid is the predominant formulation. The prevailing view has been challenged recently, namely that the lymphatics are only passive vessels, carrying antigenic fluid to secondary lymphoid sites. Rather, lymphatic vessels can be a selective barrier, efficiently coordinating egress of immune cells and factors within tissues, limiting tumor spread and immune pathology. An alternative explanation, offered here, is that damage associated molecular pattern molecules, released in excess, maintain a local milieu associated with recruitment and retention of immune cells associated with failed lymphatic clearance and functional lymphatic obstruction. We found that levels of high mobility group box 1 (HMGB1) were equally elevated in both benign and malignant pleural effusions (MPEs) and that limited diversity of T cell receptor expressing gamma and delta chain were inversely associated with these levels in MPEs. Acellular fluid from MPEs enhanced γδ T cell proliferation

Indexed as

BiomarkersCell CountCytokinesHMGB1 ProteinHumansLeukocytes, MononuclearLymphatic SystemMonocytesMyeloid CellsPleural Effusion, MalignantReceptors, Antigen, T-CellBiomarkersCytokinesHMGB1 ProteinReceptors, Antigen, T-Celladaptomebenign pleural effusionsHMGB1immune repertoiremalignant pleural effusionsmonocytestumor immunologyγδ T cells

Identifiers

PMID33013860
PMCPMC7498625
OpenAlexW3083685119

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.