Evidence map›Paper›PMID 32086539›Full record

ArticleCancer immunology, immunotherapy : CII2020

Phosphorylated vimentin as an immunotherapeutic target against metastatic colorectal cancer.

Mizuho Ohara, Kenzo Ohara, Takumi Kumai, Takayuki Ohkuri, Toshihiro Nagato, Yui Hirata-Nozaki, Akemi Kosaka, Marino Nagata, Ryusuke Hayashi, Shohei Harabuchi and 6 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Targeting cytoskeletal phosphorylation in cancer.Exploration of targeted anti-tumor therapy · 2021
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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

16 authors at 2 institutions in 1 country.

Mizuho OharaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Kenzo OharaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Takumi KumaiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan. t-kumai@asahikawa-med.ac.jp.ORCID http://orcid.org/0000-0002-3411-671X
Takayuki OhkuriDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan. ohkurit@asahikawa-med.ac.jp.
Toshihiro NagatoDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Yui Hirata-NozakiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Akemi KosakaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Marino NagataDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Ryusuke HayashiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Shohei HarabuchiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Yuki YajimaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Kensuke OikawaDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Yasuaki HarabuchiDepartment of Otolaryngology-Head and Neck surgery, Asahikawa Medical University, Asahikawa, Japan.
Yasuo SumiDepartment of Surgery, Asahikawa Medical University, Asahikawa, Japan.
Hiroyuki FurukawaDepartment of Surgery, Asahikawa Medical University, Asahikawa, Japan.
Hiroya KobayashiDepartment of Pathology, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, 0788510, Japan.
Asahikawa Medical University · JPAsahikawa Medical College Hospital · JP

Funding

Japan Society for the Promotion of Science 17K16884Japan Society for the Promotion of Science 19K07452
6 · The paper itself

Abstract

Colorectal cancer (CRC) patients with metastatic lesions have low 5-year survival rates. During metastasis, cancer cells often obtain unique characteristics such as epithelial-mesenchymal transition (EMT). Vimentin a biomarker contributes to EMT by changing cell shape and motility. Since abnormal phosphorylation is a hallmark of malignancy, targeting phosphorylated vimentin is a feasible approach for the treatment of metastatic tumors while sparing non-tumor cells. Recent evidence has revealed that both CD8 cytotoxic T lymphocytes (CTLs) and also CD4 helper T lymphocytes (HTLs) can distinguish post-translationally modified antigens from normal antigens. Here, we showed that the expression of phosphorylated vimentin was upregulated in metastatic sites of CRC. We also showed that a chemotherapeutic reagent augmented the expression of phosphorylated vimentin. The novel phosphorylated helper peptide epitopes from vimentin could elicit a sufficient T cell response. Notably, precursor lymphocytes that specifically reacted to these phosphorylated vimentin-derived peptides were detected in CRC patients. These results suggest that immunotherapy targeting phosphorylated vimentin could be promising for metastatic CRC patients.

Indexed as

AdultAgedCell LineCell Line, TumorColorectal NeoplasmsFemaleHumansImmunotherapyMaleMiddle AgedNeoplasm MetastasisVimentinVimentinCD4 T cellColorectal cancerEpitopePhosphorylationPost-translational modificationVimentin

Identifiers

PMID32086539
PMCPMC11027720
OpenAlexW3008740818

What OpenQuestion holds

Textmetadata
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.