Evidence map›Paper›PMID 25922428›Full record

Trial reportClinical cancer research : an official journal of the American Association for Cancer Research2015

Myeloid-Derived Suppressor Cells as an Immune Parameter in Patients with Concurrent Sunitinib and Stereotactic Body Radiotherapy.

Hui-Ming Chen, Ge Ma, Neil Gildener-Leapman, Samuel Eisenstein, Brian A Coakley, Junko Ozao, John Mandeli, Celia Divino, Myron Schwartz, Max Sung and 6 more

Open access · greenAbstract readClinical Trial, Phase IClinical Trial, Phase II
In one paragraph

Trial report in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

74 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
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  4. Harnessing myeloid cells in cancer.Molecular cancer · 2025
    Review
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  9. Radiation Therapy and Myeloid-Derived Suppressor Cells: Breaking Down Their Cancerous Partnership.International journal of radiation oncology, biology, physics · 2024
    Review
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14 more citing papers are in PubMed but not listed here.

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

16 authors at 1 institution in 1 country.

Hui-Ming Chen *Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Ge Ma *Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Neil Gildener-LeapmanDepartment of Otolaryngology and Radiation Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Samuel EisensteinDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Brian A CoakleyDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Junko OzaoDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
John MandeliDepartment of Preventive Medicine, Mount Sinai School of Medicine, New York, New York.
Celia DivinoDepartment of Surgery, Mount Sinai School of Medicine, New York, New York.
Myron SchwartzDepartment of Surgery, Mount Sinai School of Medicine, New York, New York.
Max SungDepartment of Medicine, Mount Sinai School of Medicine, New York, New York.
Robert FerrisDepartment of Otolaryngology and Radiation Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Johnny KaoDepartment of Radiation Oncology, Good Samaritan Hospital Medical Center, West Islip, New York.
Lu-Hai WangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, 35 Keyan Road, Zhunan, Miaoli County 350, Taiwan.
Ping-Ying PanDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Eric C KoDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Shu-Hsia ChenDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, New York.
Icahn School of Medicine at Mount Sinai · US

Funding

Intervention of immune tolerance by small molecules to enhance immune therapyR01CA127483 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, SHU-HSIA · 2008 to 2018
$3.4M
Myeloid Suppressor Cell-Mediated Immune Suppression of Tumor Specific T CellsR01CA109322 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHEN, SHU-HSIA · 2006 to 2015
$3.2M
Combination gene therapy for metastatic colon cancerR01CA070337 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHEN, SHU-HSIA · 2002 to 2010
$2.7M
Novel therapy targeting refractory colon cancerR01CA188610 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI PAN, PING-YING · 2015 to 2019
$1.8M
HSC Derived MDSC for the Prevention of GHVD Without Suppressing GvLR01CA140243 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PAN, PING-YING · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA070337NCI NIH HHS R01 CA109322NCI NIH HHS R01 CA127483NCI NIH HHS R01 CA140243NCI NIH HHS R01 CA188610
6 · The paper itself

Abstract

purposeThe clinical effects of sunitinib on human myeloid-derived suppressor cell (MDSC) subsets and correlation of the T-cell-mediated immune responses and clinical outcomes in patients with oligometastases treated by stereotactic body radiotherapy (SBRT) have been evaluated. EXPERIMENTAL

designThe numbers of granulocytic and monocytic MDSC subsets, effector T cells, and regulatory T cells in the peripheral blood were evaluated pre- and post-sunitinib treatment and concurrent with SBRT. Correlations between MDSC, Treg, and T-cell responses and clinical outcomes were analyzed.

resultsPatients with oligometastases of various cancer types had elevated granulocytic MDSC and certain subsets of monocytic MDSC population. Sunitinib treatment resulted in a significant reduction in monocytic MDSC, phosphorylated STAT3, and arginase levels in monocytic MDSC (CD33(+)CD14(+)CD16(+)), and an increase in T-cell proliferative activity in cancer patients. Interestingly, the effects of sunitinib on reducing the accumulation and immune-suppressive function of MDSC were significantly correlated with Treg reduction, in responders but not in nonresponding patients. SBRT synergized the therapeutic effects of sunitinib, especially as related to decreased numbers of monocytic MDSC, Treg, and B cells, and augmented Tbet expression in primary CD4 and CD8 T cells. These effects were not observed in patients receiving radiation therapy alone. Most interestingly, the responders, defined by sunitinib-mediated reduction in CD33(+)CD11b(+) myeloid cell populations, tend to exhibit improved progression-free survival and cause-specific survival.

conclusionsSunitinib treatment increased the efficacy of SBRT in patients with oligometastases by reversing MDSC and Treg-mediated immune suppression and may enhance cancer immune therapy to prevent tumor recurrence post-SBRT.

Indexed as

RadiosurgeryAntineoplastic AgentsCD11b AntigenCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationCell SurvivalDisease ProgressionFlow CytometryHumansImmune SystemImmunosuppressive AgentsIndolesLeukocytes, MononuclearMonocytesMyeloid CellsAntineoplastic AgentsCD11b AntigenImmunosuppressive AgentsIndolesPyrrolesSialic Acid Binding Ig-like Lectin 3STAT3 protein, humanSTAT3 Transcription FactorSunitinib

Identifiers

PMID25922428
PMCPMC4720266
OpenAlexW2029880452

What OpenQuestion holds

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Registered trials

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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.