Evidence map›Paper›PMID 31912614›Full record

ArticleMolecular carcinogenesis2020

Loss of myeloid-specific lamin A/C drives lung metastasis through Gfi-1 and C/EBPε-mediated granulocytic differentiation.

Hiroki Ishii, Woo-Yong Park, Jaeyoung So, Skyler Kuhn, Vishal N Koparde, Yanli Pang, Tim F Greten, M Christine Hollander, Li Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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

9 authors at 2 institutions in 1 country.

Hiroki IshiiLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Woo-Yong ParkLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Jaeyoung SoLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Skyler KuhnCCR Collaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Vishal N KopardeCCR Collaborative Bioinformatics Resource, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Yanli PangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Tim F GretenThoracic and Gastrointestinal Malignancies Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
M Christine HollanderLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.
Li YangLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland.ORCID 0000-0002-0930-206X
National Cancer Institute · USFrederick National Laboratory for Cancer Research · US

Funding

CCR Collaborative Bioinformatics ResourceZICBC011532 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MALIK, MARIAM · 2013 to 2025
$33.7M
Myeloid TGFbeta signaling in breast cancer metastasis and dormancyZIABC011163 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YANG, LI · 2009 to 2025
$14.5M
Immune suppressor mechanisms in patients with GI cancerZIABC011344 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GRETEN, TIM · 2010 to 2025
$2.2M
Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

The immune-suppressive tumor microenvironment promotes metastatic spread and outgrowth. One of the major contributors is tumor-associated myeloid cells. However, the molecular mechanisms regulating their differentiation and function are not well understood. Here we report lamin A/C, a nuclear lamina protein associated with chromatin remodeling, was one of the critical regulators in cellular reprogramming of tumor-associated myeloid cells. Using myeloid-specific lamin A/C knockout mice and triple-negative breast cancer (TNBC) mouse models, we discovered that the loss of lamin A/C drives CD11b

Indexed as

AnimalsCCAAT-Enhancer-Binding ProteinsCell DifferentiationCells, CulturedChemokinesDisease Models, AnimalFemaleGranulocytesHumansInflammationLamin Type ALeukocytes, MononuclearLung NeoplasmsMiceMice, Inbred BALB CMice, Inbred C57BLCCAAT-Enhancer-Binding ProteinsCEBPE protein, humanChemokinesGFI1B protein, humanLamin Type ALMNA protein, humanProto-Oncogene ProteinsRepressor Proteinsgranulocytic differentiationimmunosuppressionlamin A/Cmetastasismyeloid cells

Identifiers

PMID31912614
PMCPMC7282947
OpenAlexW3000377980

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.