Evidence map›Paper›PMID 31435021›Full record

ArticleOncogene2019

The dysfunction of BP180/collagen XVII in keratinocytes promotes melanoma progression.

Bin-Jin Hwang, Yang Zhang, Jaime M Brozowski, Zhen Liu, Susan Burette, Kendall Lough, Christof C Smith, Yue Shan, Jinbo Chen, Ning Li and 5 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 15 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 2 institutions in 2 countries.

Bin-Jin Hwang *Department of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Yang Zhang *Department of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Jaime M BrozowskiDepartment of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Zhen LiuDepartment of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Susan BuretteDepartment of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Kendall LoughDepartment of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Christof C SmithDepartment of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Yue ShanDepartment of Biostatistics, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Jinbo ChenDepartment of Dermatology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ning LiDepartment of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Scott WilliamsDepartment of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.ORCID http://orcid.org/0000-0001-9975-7334
Maureen SuDepartment of Pediatrics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Paul GoogeDepartment of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Nancy E ThomasDepartment of Dermatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Zhi LiuDepartment of Microbiology and Immunology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. zhi_liu@med.unc.edu.
University of North Carolina at Chapel Hill · USWuhan No.1 Hospital · CN

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Sex Differences in Methylome Alterations and Mutational Burden in Early Stage MelanomaP01CA206980 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BERWICK, MARIANNE, THOMAS, NANCY E. · 2017 to 2022
$10.1M
IMMUNOPATHOGENESIS OF BULLOUS PEMPHIGOIDR01AI040768 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2001 to 2016
$4.1M
Eosinophils in Bullous PemphigoidR01AR070276 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI · 2017 to 2021
$1.9M
Inflammasome-gasdermin axis in bullous pemphigoidR01AR072694 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LIU, ZHI, MIAO, EDWARD A · 2018 to 2022
$1.9M
NCI NIH HHS P01 CA206980NCI NIH HHS P30 CA016086NIAID NIH HHS R01 AI040768NIAMS NIH HHS R01 AR070276NIAMS NIH HHS R01 AR072694U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01 AI61430
6 · The paper itself

Abstract

BP180, also termed collagen XVII, is a hemidesmosomal transmembrane glycoprotein expressed in basal keratinocytes, and functions as a cell-matrix adhesion molecule in the dermal-epidermal junction of the skin. Its function, other than cell-matrix adhesion, remains unclear. We generated a mouse strain with BP180 dysfunction (termed ∆NC16A), which develops spontaneous skin inflammation accompanied by an influx of myeloid derived suppressor cells (MDSCs). We used the B16 mouse melanoma model to demonstrate that BP180 dysfunction in either skin or basal keratinocytes promotes MDSC influx into skin and tumor progression. MDSC depletion reduced tumor progression in ∆NC16A mice, demonstrating a critical role for BP180 dysfunction-driven MDSCs in melanoma progression. This study provides the first direct evidence that BP180, a cell-cell matrix adhesion molecule, possesses antitumor function through modulating infiltration of MDSCs. Basal keratinocytes actively participate in skin microenvironment changes caused by BP180 dysfunction. ∆NC16A mice could be a new animal model to study the melanoma microenvironment.

Indexed as

AnimalsAutoantigensCell AdhesionCollagen Type XVIIDisease Models, AnimalDisease ProgressionHumansKeratinocytesMelanomaMelanoma, ExperimentalMiceMyeloid-Derived Suppressor CellsNon-Fibrillar CollagensSkinTumor MicroenvironmentAutoantigensCollagen Type XVIINon-Fibrillar Collagens

Identifiers

PMID31435021
PMCPMC6908749
OpenAlexW2969843984

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.