Evidence map›Paper›PMID 34253827›Full record

ArticleCommunications biology2021

Immune checkpoint blockade in triple negative breast cancer influenced by B cells through myeloid-derived suppressor cells.

Alyssa Vito, Omar Salem, Nader El-Sayes, Ian P MacFawn, Ana L Portillo, Katy Milne, Danielle Harrington, Ali A Ashkar, Yonghong Wan, Samuel T Workenhe and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Leveraging preclinical models of metastatic breast cancer.Biochimica et biophysica acta. Reviews on cancer · 2024
    Review
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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 5 institutions in 2 countries.

Alyssa VitoMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.ORCID 0000-0002-2197-4395
Omar SalemMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.
Nader El-SayesMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.
Ian P MacFawnDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Ana L PortilloMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.ORCID 0000-0002-4191-4859
Katy MilneDeeley Research Centre, BC Cancer, Victoria, BC, Canada.
Danielle HarringtonDeeley Research Centre, BC Cancer, Victoria, BC, Canada.
Ali A AshkarMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.ORCID 0000-0003-1139-1468
Yonghong WanMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada.
Samuel T WorkenheDepartment of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.ORCID 0000-0001-9521-3903
Brad H NelsonDeeley Research Centre, BC Cancer, Victoria, BC, Canada.
Tullia C BrunoDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Karen L MossmanMcMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada. mossk@mcmaster.ca.ORCID 0000-0002-1725-5873
McMaster University · CAUniversity of Pittsburgh · USMcMaster University Medical Centre · CAUniversity of British Columbia · CAUniversity of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple negative breast cancer holds a dismal clinical outcome and as such, patients routinely undergo aggressive, highly toxic treatment regimens. Clinical trials for TNBC employing immune checkpoint blockade in combination with chemotherapy show modest prognostic benefit, but the percentage of patients that respond to treatment is low, and patients often succumb to relapsed disease. Here, we show that a combination immunotherapy platform utilizing low dose chemotherapy (FEC) combined with oncolytic virotherapy (oHSV-1) increases tumor-infiltrating lymphocytes, in otherwise immune-bare tumors, allowing 60% of mice to achieve durable tumor regression when treated with immune checkpoint blockade. Whole-tumor RNA sequencing of mice treated with FEC + oHSV-1 shows an upregulation of B cell receptor signaling pathways and depletion of B cells prior to the start of treatment in mice results in complete loss of therapeutic efficacy and expansion of myeloid-derived suppressor cells. Additionally, RNA sequencing data shows that FEC + oHSV-1 suppresses genes associated with myeloid-derived suppressor cells, a key population of cells that drive immune escape and mediate therapeutic resistance. These findings highlight the importance of tumor-infiltrating B cells as drivers of antitumor immunity and their potential role in the regulation of myeloid-derived suppressor cells.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsB-LymphocytesCell Line, TumorChlorocebus aethiopsCombined Modality TherapyFemaleHumansImmune Checkpoint InhibitorsImmunotherapyKaplan-Meier EstimateLymphocytes, Tumor-InfiltratingMiceMice, Inbred C57BLMyeloid-Derived Suppressor CellsOncolytic VirotherapyImmune Checkpoint Inhibitors

Identifiers

PMID34253827
PMCPMC8275624
OpenAlexW3178402802

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.