Evidence map›Paper›PMID 21163950›Full record

ArticleThe Journal of biological chemistry2011

Growth suppression of human hepatocellular carcinoma xenografts by a monoclonal antibody CH12 directed to epidermal growth factor receptor variant III.

Hua Jiang, Huamao Wang, Zhonghua Tan, Suwen Hu, Hai Wang, Bizhi Shi, Lin Yang, Peiyong Li, Jianren Gu, Hongyang Wang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. The Dietary SupplementOxidative medicine and cellular longevity · 2021
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  7. A Fusion Receptor as a Safety Switch, Detection, and Purification Biomarker for Adoptive Transferred T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
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  11. EGFR Signaling in Liver Diseases.International journal of molecular sciences · 2015
    Review
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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

11 authors at 4 institutions in 1 country.

Hua JiangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Medical School of Shanghai Jiaotong University, Shanghai 200032, China.
Huamao Wang
Zhonghua Tan
Suwen Hu
Hai Wang
Bizhi Shi
Lin Yang
Peiyong Li
Jianren Gu
Hongyang Wang
Zonghai Li
State Key Laboratory of Oncogene and Related Genes · CNShanghai Cancer Institute · CNRuijin Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human hepatocellular carcinoma (HCC) is considered difficult to cure because it is resistant to radio- and chemotherapy and has a high recurrence rate after curative liver resection. Epidermal growth factor receptor variant III (EGFRvIII) has been reported to express in HCC tissues and cell lines. This article describes the efficacy of an anti-EGFRvIII monoclonal antibody (mAb CH12) in the treatment of HCC xenografts with EGFRvIII expression and the underlying mechanism of EGFRvIII as an oncogene in HCC. The results demonstrated that CH12 bound preferentially to EGFRvIII with a dissociation constant (K(d)) of 1.346 nm/liter. In addition, CH12 induces strong antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity in Huh7-EGFRvIII (with exogenous expression of EGFRvIII) and SMMC-7721 (with endogenous expression of EGFRvIII) cells. Notably, CH12 significantly inhibited the growth of Huh7-EGFRvIII and SMMC-7721 xenografts in vivo with a growth inhibition ratio much higher than C225, a U. S. Food and Drug Administration-approved anti-EGFR antibody. Treatment of the two HCC xenografts with CH12 significantly suppressed tumor proliferation and angiogenesis. Mechanistically, in vivo treatment with CH12 reduced the phosphorylation of constitutively active EGFRvIII, Akt, and ERK. Down-regulation of the apoptotic protectors Bcl-x(L), Bcl-2, and the cell cycle regulator cyclin D1, as well as up-regulation of the cell-cycle inhibitor p27, were also observed after in vivo CH12 treatment. Collectively, these results indicate that the monoclonal antibody CH12 is a promising therapeutic agent for HCC with EGFRvIII expression.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, Neoplasmbcl-X ProteinCarcinoma, HepatocellularCyclin D1Cyclin-Dependent Kinase Inhibitor p27CytotoxinsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHumansIntracellular Signaling Peptides and ProteinsLiver Neoplasms, ExperimentalMiceNeoplasm TransplantationPhosphorylationAntibodies, MonoclonalAntibodies, NeoplasmBCL2L1 protein, humanbcl-X ProteinCDKN1B protein, humanCyclin D1Cyclin-Dependent Kinase Inhibitor p27Cytotoxinsepidermal growth factor receptor VIIIErbB ReceptorsExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID21163950
PMCPMC3037704
OpenAlexW1991775632

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.