Evidence map›Paper›PMID 37055410›Full record

ArticleNature communications2023

Targeting CXCL16 and STAT1 augments immune checkpoint blockade therapy in triple-negative breast cancer.

Bhavana Palakurthi, Shaneann R Fross, Ian H Guldner, Emilija Aleksandrovic, Xiyu Liu, Anna K Martino, Qingfei Wang, Ryan A Neff, Samantha M Golomb, Cheryl Lewis and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 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

13 authors at 2 institutions in 1 country.

Bhavana PalakurthiDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Shaneann R FrossDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Ian H GuldnerDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Emilija AleksandrovicDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.ORCID 0000-0001-6698-2893
Xiyu LiuDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Anna K MartinoDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.ORCID 0000-0002-9014-2867
Qingfei WangDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.ORCID 0000-0003-2503-0639
Ryan A NeffDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Samantha M GolombDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Cheryl LewisDepartment of Pathology and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, 75235, USA.ORCID 0000-0003-2685-6475
Yan PengDepartment of Pathology and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, 75235, USA.
Erin N HoweDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA.
Siyuan ZhangDepartment of Biological Sciences, College of Science, University of Notre Dame, Notre Dame, IN, 46556, USA. Siyuan.Zhang@UTSouthwestern.edu.ORCID 0000-0003-0910-3666
University of Notre Dame · USThe University of Texas Southwestern Medical Center · US

Funding

Unfolded Protein Response and Autophagy in T Helper Cell Effector FunctionP20GM121176 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Monica Rosas Lemus · 2017 to 2026
$24.9M
NIGMS NIH HHS P20 GM121176
6 · The paper itself

Abstract

Chemotherapy prior to immune checkpoint blockade (ICB) treatment appears to improve ICB efficacy but resistance to ICB remains a clinical challenge and is attributed to highly plastic myeloid cells associating with the tumor immune microenvironment (TIME). Here we show by CITE-seq single-cell transcriptomic and trajectory analyses that neoadjuvant low-dose metronomic chemotherapy (MCT) leads to a characteristic co-evolution of divergent myeloid cell subsets in female triple-negative breast cancer (TNBC). Specifically, we identify that the proportion of CXCL16 + myeloid cells increase and a high STAT1 regulon activity distinguishes Programmed Death Ligand 1 (PD-L1) expressing immature myeloid cells. Chemical inhibition of STAT1 signaling in MCT-primed breast cancer sensitizes TNBC to ICB treatment, which underscores the STAT1's role in modulating TIME. In summary, we leverage single-cell analyses to dissect the cellular dynamics in the tumor microenvironment (TME) following neoadjuvant chemotherapy and provide a pre-clinical rationale for modulating STAT1 in combination with anti-PD-1 for TNBC patients.

Indexed as

Triple Negative Breast NeoplasmsChemokine CXCL16FemaleHumansImmune Checkpoint InhibitorsMyeloid CellsRadioimmunotherapySTAT1 Transcription FactorTumor MicroenvironmentChemokine CXCL16CXCL16 protein, humanImmune Checkpoint InhibitorsSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID37055410
PMCPMC10101955
OpenAlexW4365450820

What OpenQuestion holds

Textmetadata
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.