Evidence map›Paper›PMID 25949918›Full record

ArticleOncoimmunology2015

Combating HER2-overexpressing breast cancer through induction of calreticulin exposure by Tras-Permut CrossMab.

Fan Zhang, Jie Zhang, Moyan Liu, Lichao Zhao, RuiXia LingHu, Fan Feng, Xudong Gao, Shunchang Jiao, Lei Zhao, Yi Hu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  4. IFI16-dependent STING signaling is a crucial regulator of anti-HER2 immune response in HER2+ breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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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 3 countries.

Fan ZhangDepartment of Oncology; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Jie ZhangNursing Department; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Moyan LiuDepartment of Nephrology; General Hospital of Jinan Military Command ; Jinan, People's Republic of China.
Lichao ZhaoMedical Department; General Hospital of Jinan Military Command ; Jinan, People's Republic of China.
RuiXia LingHuDepartment of Oncology; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Fan FengDepartment of Pharmacy; General Hospital of Shenyang Military Command ; Shenyang, People's Republic of China.
Xudong GaoDepartment of Gastroenterology ; PLA 302 Hospital ; Beijing, People's Republic of China.
Shunchang JiaoDepartment of Oncology; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Lei ZhaoPLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China ; Institute for Translational Medicine; Second Military Medical University ; Shanghai, People's Republic of China.
Yi HuDepartment of Oncology; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Junlan YangDepartment of Oncology; PLA General Hospital; PLA School of Medicine ; Beijing, People's Republic of China.
Chinese PLA General Hospital · CNSecond Military Medical University · CNGeneral Hospital of Jinan Military Command · CNGeneral Hospital of Shenyang Military Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although trastuzumab has succeeded in breast cancer treatment, acquired resistance is one of the prime obstacles for breast cancer therapies. There is an urgent need to develop novel HER2 antibodies against trastuzumab resistance. Here, we first rational designed avidity-imporved trastuzumab and pertuzumab variants, and explored the correlation between the binding avidity improvement and their antitumor activities. After characterization of a pertuzumab variant L56TY with potent antitumor activities, a bispecific immunoglobulin G-like CrossMab (Tras-Permut CrossMab) was generated from trastuzumab and binding avidity-improved pertuzumab variant L56TY. Although, the antitumor efficacy of trastuzumab was not enhanced by improving its binding avidity, binding avidity improvement could significantly increase the anti-proliferative and antibody-dependent cellular cytotoxicity (ADCC) activities of pertuzumab. Further studies showed that Tras-Permut CrossMab exhibited exceptional high efficiency to inhibit the progression of trastuzumab-resistant breast cancer. Notably, we found that calreticulin (CRT) exposure induced by Tras-Permut CrossMab was essential for induction of tumor-specific T cell immunity against tumor recurrence. These data indicated that simultaneous blockade of HER2 protein by Tras-Permut CrossMab could trigger CRT exposure and subsequently induce potent tumor-specific T cell immunity, suggesting it could be a promising therapeutic strategy against trastuzumab resistance.

Indexed as

ADCCantibody-dependent cellular cytotoxicitycalreticulin exposureCDR, complementarity determining regionCH1, constant heavy chain 1CL, constant light chainCrossMabCRT, calreticulinFCM, flow cytometryHER2-ECD, extracellular domain of HER2HER2-overexpressing breast cancerHER, human epidermal growth factor receptorLDH, lactate dehydrogenasemAb, monoclonal antibodyPBMCs, peripheral blood mononuclear cellspertuzumabPI3K, phosphatidylinositol 3-kinaseSEC, size-exclusion chromatographyT cell immunitytrastuzumab

Identifiers

PMID25949918
PMCPMC4404837
OpenAlexW2091477909

What OpenQuestion holds

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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.