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


Journal

BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800

Informations de publication

Date de publication:
20 Apr 2022
Historique:
received: 25 12 2021
accepted: 04 04 2022
entrez: 21 4 2022
pubmed: 22 4 2022
medline: 23 4 2022
Statut: epublish

Résumé

To 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. Human 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. Regorafenib, 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). MICA 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.

Sections du résumé

BACKGROUND BACKGROUND
To 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.
METHODS METHODS
Human 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.
RESULTS RESULTS
Regorafenib, 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).
CONCLUSIONS CONCLUSIONS
MICA 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.

Identifiants

pubmed: 35443621
doi: 10.1186/s12885-022-09512-5
pii: 10.1186/s12885-022-09512-5
pmc: PMC9019943
doi:

Substances chimiques

Biomarkers 0
Histocompatibility Antigens Class I 0
Phenylurea Compounds 0
Pyridines 0
regorafenib 24T2A1DOYB

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

428

Informations de copyright

© 2022. The Author(s).

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Auteurs

Jun Arai (J)

Division 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 Otoyama (Y)

Division of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

Ken-Ichi Fujita (KI)

Division of Cancer Genome and Pharmacotherapy, Department of Clinical Pharmacy, Showa University School of Pharmacy, Tokyo, Japan.

Kaku Goto (K)

Institut de Recherche Sur Les Maladies Virales Et Hépatiques, INSERM, Strasbourg, France.

Masayuki Tojo (M)

Division of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

Atsushi Katagiri (A)

Division of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

Hisako Nozawa (H)

Division of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

Yutaro Kubota (Y)

Division of Medical Oncology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.

Takehiro Takahashi (T)

Division of Medical Oncology, Showa University Fujigaoka Hospital, Yokohama, Japan.

Hiroo Ishida (H)

Division of Internal Medicine, Department of Medicine, Showa University Hokubu Hospital, Yokohama, Japan.

Takuya Tsunoda (T)

Division of Medical Oncology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan.

Natsumi Matsumoto (N)

Division of Cancer Genome and Pharmacotherapy, Department of Clinical Pharmacy, Showa University School of Pharmacy, Tokyo, Japan.

Keita Ogawa (K)

Department of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Ryo Nakagawa (R)

Department of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Ryosuke Muroyama (R)

Department of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Naoya Kato (N)

Department of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.

Hitoshi Yoshida (H)

Division of Gastroenterology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

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