Evidence map›Paper›PMID 27405665›Full record

ArticleScientific reports2016

Therapeutic targeting of myeloid-derived suppressor cells involves a novel mechanism mediated by clusterin.

Junmin Zhou, Sarah S Donatelli, Danielle L Gilvary, Melba M Tejera, Erika A Eksioglu, Xianghong Chen, Domenico Coppola, Sheng Wei, Julie Y Djeu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  5. Tumor-associated myeloid cells in cancer immunotherapy.Journal of hematology & oncology · 2023
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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

9 authors at 1 institution in 1 country.

Junmin ZhouDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Sarah S DonatelliDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Danielle L GilvaryDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Melba M TejeraDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Erika A EksiogluDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Xianghong ChenDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Domenico CoppolaDepartment of Pathology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Sheng WeiDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Julie Y DjeuDepartment of Immunology, H. Lee Moffitt Cancer Center, Tampa, FL 33612, USA.
Moffitt Cancer Center · US

Funding

Tumor Immunology Training Program -1 T32 CA115308-A1T32CA115308 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI WRIGHT, KENNETH LYNN · 2007 to 2017
$2.8M
Modulation of the S100A9/CD33 Pathway by the Flavonoids ICA and ICT on the TumorK01CA187020 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI EKSIOGLU, ERIKA ADRIANA · 2014 to 2018
$456k
NCI NIH HHS K01 CA187020NCI NIH HHS T32 CA115308
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) constitute a key checkpoint that impedes tumor immunity against cancer. Chemotherapeutic intervention of MDSCs has gained ground as a strategy for cancer therapy but its mechanism remains obscure.We report here a unique mechanism by which monocytic (M)-MDSCs are spared, allowing them to polarize towards M1 macrophages for reactivation of immunity against breast cancer. We first demonstrated that curcumin, like docetaxel (DTX), can selectively target CD11b(+)Ly6G(+)Ly6C(low) granulocytic (G)-MDSCs, sparing CD11b(+)Ly6G(-)Ly6C(high) M-MDSCs, with reduced tumor burden in 4T1-Neu tumor-bearing mice. Curcumin treatment polarized surviving M-MDSCs toward CCR7(+) Dectin-1(-)M1 cells, accompanied by IFN-γ production and cytolytic function in T cells. Selective M-MDSC chemoresistence to curcumin and DTX was mediated by secretory/cytoplasmic clusterin (sCLU). sCLU functions by trapping Bax from mitochondrial translocation, preventing the apoptotic cascade. Importantly, sCLU was only found in M-MDSCs but not in G-MDSCs. Knockdown of sCLU in M-MDSCs and RAW264.7 macrophages was found to reverse their natural chemoresistance. Clinically, breast cancer patients possess sCLU expression only in mature CD68(+) macrophages but not in immature CD33(+) immunosuppressive myeloid cells infiltrating the tumors. We thus made the seminal discovery that sCLU expression in M-MDSCs accounts for positive immunomodulation by chemotherapeutic agents.

Indexed as

AnimalsAntigens, LyAntineoplastic AgentsCD11b AntigenCell DifferentiationCell Line, TumorCell ProliferationClusterinCurcuminFemaleInterferon-gammaMammary Neoplasms, ExperimentalMiceMyeloid-Derived Suppressor CellsRAW 264.7 CellsXenograft Model Antitumor AssaysAntigens, LyAntineoplastic AgentsCD11b AntigenClu protein, mouseClusterinCurcuminIFNG protein, mouseInterferon-gammaLy-6C antigen, mouseLy6G antigen, mouse

Identifiers

PMID27405665
PMCPMC4942787
OpenAlexW2472901304

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.