Evidence map›Paper›PMID 35443621›Full record

ArticleBMC cancer2022

Baseline soluble MICA levels act as a predictive biomarker for the efficacy of regorafenib treatment in colorectal cancer.

Jun Arai, Yumi Otoyama, Ken-Ichi Fujita, Kaku Goto, Masayuki Tojo, Atsushi Katagiri, Hisako Nozawa, Yutaro Kubota, Takehiro Takahashi, Hiroo Ishida and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. 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
0.4field-weighted citation impact, top 43% 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, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
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

17 authors at 4 institutions in 2 countries.

Jun AraiDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan. araiguma10@med.showa-u.ac.jp.
Yumi OtoyamaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.
Ken-Ichi FujitaDivision of Cancer Genome and Pharmacotherapy, Department of Clinical Pharmacy, Showa University School of Pharmacy, Tokyo, Japan.
Kaku GotoInstitut de Recherche Sur Les Maladies Virales Et Hépatiques, INSERM, Strasbourg, France.
Masayuki TojoDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.
Atsushi KatagiriDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.
Hisako NozawaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.
Yutaro KubotaDivision of Medical Oncology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Takehiro TakahashiDivision of Medical Oncology, Showa University Fujigaoka Hospital, Yokohama, Japan.
Hiroo IshidaDivision of Internal Medicine, Department of Medicine, Showa University Hokubu Hospital, Yokohama, Japan.
Takuya TsunodaDivision of Medical Oncology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.
Natsumi MatsumotoDivision of Cancer Genome and Pharmacotherapy, Department of Clinical Pharmacy, Showa University School of Pharmacy, Tokyo, Japan.
Keita OgawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Ryo NakagawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Ryosuke MuroyamaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Naoya KatoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hitoshi YoshidaDivision of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.
Showa University · JPChiba University · JPInserm · FRShowa University Fujigaoka Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo evaluate the effect of regorafenib on soluble MHC class I polypeptide-related sequence A (MICA) (sMICA) level in vitro. In addition, we clinically examined whether its plasma levels were associated with regorafenib activity in terms of progression-free survival (PFS) in patients with CRC.

methodsHuman CRC cell line HCT116 and HT29 cells were treated with regorafenib and its pharmacologically active metabolites, M2 or M5 at the same concentrations as those in sera of patients. We also examined the sMICA levels and the area under the plasma concentration-time curve of regorafenib, M2 and M5.

resultsRegorafenib, M2, and M5 significantly suppressed shedding of MICA in human CRC cells without toxicity. This resulted in the reduced production of sMICA. In the clinical examination, patients with CRC who showed long median PFS (3.7 months) had significantly lower sMICA levels than those with shorter median PFS (1.2 months) (p = 0.045).

conclusionsMICA is an attractive agent for manipulating the immunological control of CRC and baseline sMICA levels could be a predictive biomarker for the efficacy of regorafenib treatment.

Indexed as

Colorectal NeoplasmsHistocompatibility Antigens Class IBiomarkersHumansPhenylurea CompoundsPyridinesBiomarkersHistocompatibility Antigens Class IPhenylurea CompoundsPyridinesregorafenibColorectal CancerMHC class I polypeptide-related sequence ANatural killer cellRegorafenib

Identifiers

PMID35443621
PMCPMC9019943
OpenAlexW4224282810

What OpenQuestion holds

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LicenceCC BY
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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.