Evidence map›Paper›PMID 38449302›Full record

ArticleBMB reports2024

Targeting cell surface glucose-regulated protein 94 in gastric cancer with an anti-GRP94 human monoclonal antibody.

Hyun Jung Kim, Yea Bin Cho, Kyun Heo, Ji Woong Kim, Ha Gyeong Shin, Eun-Bi Lee, Seong-Min Park, Jong Bae Park, Sukmook Lee

Abstract readNews
In one paragraph

Article in BMB reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. ATM interaction with GRP94 modulates oncogenic receptor expression and signaling and microglial activation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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.

Hyun Jung KimDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707, Korea.
Yea Bin ChoDepartment of Chemistry, Kookmin University, Seoul 02707, Korea.
Kyun HeoDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707; Department of Chemistry, Kookmin University, Seoul 02707; Antibody Research Institute, Kookmin University, Seoul 02707, Korea.
Ji Woong KimDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707, Korea.
Ha Gyeong ShinDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707, Korea.
Eun-Bi LeeDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707, Korea.
Seong-Min ParkDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Jong Bae ParkDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Sukmook LeeDepartment of Biopharmaceutical Chemistry, Kookmin University, Seoul 02707; Department of Chemistry, Kookmin University, Seoul 02707; Antibody Research Institute, Kookmin University, Seoul 02707, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC), a leading cause of cancer-related mortality, remains a significant challenge despite recent therapeutic advancements. In this study, we explore the potential of targeting cell surface glucose-regulated protein 94 (GRP94) with antibodies as a novel therapeutic approach for GC. Our comprehensive analysis of GRP94 expression across various cancer types, with a specific focus on GC, revealed a substantial overexpression of GRP94, highlighting its potential as a promising target. Through in vitro and in vivo efficacy assessments, as well as toxicological analyses, we found that K101.1, a fully human monoclonal antibody designed to specifically target cell surface GRP94, effectively inhibits GC growth and angiogenesis without causing in vivo toxicity. Furthermore, our findings indicate that K101.1 promotes the internalization and concurrent downregulation of cell surface GRP94 on GC cells. In conclusion, our study suggests that cell surface GRP94 may be a potential therapeutic target in GC, and that antibody-based targeting of cell surface GRP94 may be an effective strategy for inhibiting GRP94-mediated GC growth and angiogenesis. [BMB Reports 2024; 57(4): 188-193].

Indexed as

Antibodies, MonoclonalStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationHumansMembrane GlycoproteinsMiceMice, NudeNeovascularization, PathologicAntibodies, MonoclonalendoplasminMembrane Glycoproteins

Identifiers

PMID38449302
PMCPMC11058359

What OpenQuestion holds

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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.