Evidence map›Paper›PMID 37991442›Full record

ArticleCancer science2023

Eribulin is an immune potentiator in breast cancer that upregulates human leukocyte antigen class I expression via the induction of NOD-like receptor family CARD domain-containing 5.

Asaka Wada, Yoshihiko Hirohashi, Goro Kutomi, Kenji Murata, Sadahiro Iwabuchi, Yuka Mizue, Aiko Murai, Daisuke Kyuno, Hiroaki Shima, Tomoyuki Minowa and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.4field-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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. 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

19 authors at 3 institutions in 1 country.

Asaka WadaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yoshihiko HirohashiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-0608-3914
Goro KutomiDepartment of Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kenji MurataDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sadahiro IwabuchiDepartment of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
Yuka MizueDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Aiko MuraiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Daisuke KyunoDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroaki ShimaDepartment of Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tomoyuki MinowaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kenta SasakiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Terufumi KuboDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takayuki KanasekiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0001-7294-6880
Tomohide TsukaharaDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-3678-4359
Munehide NakatsugawaDepartment of Pathology, Tokyo Medical University Hachioji Medical Center, Tokyo, Japan.
Shinichi HashimotoDepartment of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
Makoto OsanaiDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0003-1754-252X
Toshihiko TorigoeDepartment of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Ichiro TakemasaDepartment of Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sapporo Medical University · JPWakayama Medical University · JPTokyo Medical University Hachioji Medical Center · JP

Funding

Core Research for Evolutional Science and Technology JPMJCR15G3Japan Agency for Medical Research and Development 20cm0106352h0002Japan Agency for Medical Research and Development 21cm0106309h0006Japan Agency for Medical Research and Development 22ama221317h0001Japan Society for the Promotion of Science 20H03460Japan Society for the Promotion of Science 21K18257
6 · The paper itself

Abstract

Eribulin inhibits microtubule polymerization and improves the overall survival of patients with recurrent metastatic breast cancer. A subgroup analysis revealed a low neutrophil to lymphocyte ratio (NLR) (<3) to be a prognostic factor of eribulin treatment. We thus hypothesized that eribulin might be related to the immune response for breast cancer cells and we analyzed the effects of eribulin on the immune system. Immunohistochemical staining revealed that human leukocyte antigen (HLA) class I expression was increased in clinical samples after eribulin treatment. In vitro assays revealed that eribulin treatment increased HLA class I expression in breast cancer line cells. RNA-sequencing demonstrated that eribulin treatment increased the expression of the NOD-like family CARD domain-containing 5 (NLRC5), a master regulator of HLA class I expression. Eribulin treatment increased the NY-ESO-1-specific T-cell receptor (TCR) transduced T (TCR-T) cell response for New York oesophageal squamous cell carcinoma 1 (NY-ESO-1) overexpressed breast cancer cells. The eribulin and TCR-T combined therapy model revealed that eribulin and immunotherapy using TCR-T cells has a synergistic effect. In summary, eribulin increases the expression of HLA class 1 via HLA class 1 transactivatior NLRC5 and eribulin combination with immunotherapy can be effective for the treatment of breast cancer.

Indexed as

Breast NeoplasmsAntigens, NeoplasmCaspase Activation and Recruitment DomainFemaleFuransHLA AntigensHumansIntracellular Signaling Peptides and ProteinsKetonesNeoplasm Recurrence, LocalNLR ProteinsPolyether PolyketidesReceptors, Antigen, T-CellAntigens, NeoplasmeribulinFuransHLA AntigensIntracellular Signaling Peptides and ProteinsKetonesNLRC5 protein, humanNLR ProteinsPolyether PolyketidesReceptors, Antigen, T-Cellcombination therapycytotoxic T lymphocyteseribulinHLA class INLRC5

Identifiers

PMID37991442
PMCPMC10728009
OpenAlexW4388922050

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.