Evidence map›Paper›PMID 34545658›Full record

ArticleCancer science2021

MK-6, a novel not-α IL-2, elicits a potent antitumor activity by improving the effector to regulatory T cell balance.

Maki Kobayashi, Katsuhiko Kojima, Kazutaka Murayama, Yuji Amano, Takashi Koyama, Naoko Ogama, Toshikazu Takeshita, Tatsuro Fukuhara, Nobuyuki Tanaka

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 9 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

9 authors at 3 institutions in 1 country.

Maki KobayashiDivision of Tumor Immunobiology, Miyagi Cancer Center Research Institute, Natori, Japan.
Katsuhiko KojimaDepartment of Microbiology and Immunology, Shinshu University School of Medicine, Matsumoto, Japan.
Kazutaka MurayamaDivision of Biomedical Measurements and Diagnostics, Tohoku University Graduate School of Biomedical Engineering, Sendai, Japan.
Yuji AmanoDepartment of Microbiology and Immunology, Shinshu University School of Medicine, Matsumoto, Japan.ORCID https://orcid.org/0000-0002-1588-3120
Takashi KoyamaDivision of Tumor Immunobiology, Miyagi Cancer Center Research Institute, Natori, Japan.
Naoko OgamaDivision of Tumor Immunobiology, Miyagi Cancer Center Research Institute, Natori, Japan.
Toshikazu TakeshitaDepartment of Microbiology and Immunology, Shinshu University School of Medicine, Matsumoto, Japan.
Tatsuro FukuharaDivision of Respiratory Oncology, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID https://orcid.org/0000-0003-0440-470X
Nobuyuki TanakaDivision of Tumor Immunobiology, Miyagi Cancer Center Research Institute, Natori, Japan.ORCID https://orcid.org/0000-0002-0229-8061
Tohoku University · JPShinshu University · JPMiyagi Prefectural Hospital Organization · JP

Funding

Core Research for Evolutional Science and Technology JPMJCR17H4Japan Agency for Medical Research and Development 21cm0106387h0001Japan Society for the Promotion of Science 18H04056Japan Society for the Promotion of Science 18K08643Japan Society for the Promotion of Science 19K08609Japan Society for the Promotion of Science 20K08203Japan Society for the Promotion of Science 20K08580Japan Society for the Promotion of Science 20K17766
6 · The paper itself

Abstract

IL-2 is a pleiotropic cytokine that regulates immune cell homeostasis. Its immunomodulatory function has been used clinically as an active immunotherapy agent for metastatic cancers. However, severe adverse effects, including the vascular leak syndrome and the preferential stimulation of anti-immunogenic Treg rather than effector T cells, have been obstacles. We newly designed a mutein IL-2, Mutakine-6 (MK-6), with reduced IL-2Rα-binding capability. MK-6 induced comparable cell growth potential toward IL-2Rβγ-positive T cells but was far less efficient in in vitro Treg proliferation and STAT5 activation. Unlike IL-2, in vivo administration of MK-6 produced minimal adverse effects. Using CT26 and B16F10-syngeneic tumor models, we found MK-6 was highly efficacious on tumor regression. Serum albumin conjugation to MK-6 prolonged in vivo half-life and accumulated in CT26 tumors, showing enhanced antitumor effect. Tumor-infiltrating leukocytes analysis revealed that albumin-fused MK-6 increased the ratio of effector CD8

Indexed as

AnimalsCD4-Positive T-LymphocytesCell Line, TumorCell ProliferationDisease Models, AnimalFemaleHalf-LifeImmunity, CellularImmunologic FactorsInterleukin-2Interleukin-2 Receptor alpha SubunitInterleukin-2 Receptor beta SubunitInterleukin Receptor Common gamma SubunitLymphocytes, Tumor-InfiltratingMiceMice, Inbred BALB CImmunologic FactorsInterleukin-2Interleukin-2 Receptor alpha SubunitInterleukin-2 Receptor beta SubunitInterleukin Receptor Common gamma SubunitSerum AlbuminSTAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor Proteinscancer immunotherapycytokinesIL-2 Muteinregulatory T cellstumor-infiltrating lymphocytes

Identifiers

PMID34545658
PMCPMC8586658
OpenAlexW3200750007

What OpenQuestion holds

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LicenceCC BY-NC
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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.