Evidence map›Paper›PMID 32002122›Full record

ArticleOncotarget2020

Novel functional anti-HER3 monoclonal antibodies with potent anti-cancer effects on various human epithelial cancers.

Kouki Okita, Shogo Okazaki, Shinya Uejima, Erina Yamada, Hiroki Kaminaka, Misa Kondo, Shiho Ueda, Ryo Tokiwa, Nami Iwata, Akitaka Yamasaki and 7 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. HER3 in cancer: from the bench to the bedside.Journal of experimental & clinical cancer research : CR · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. 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

17 authors at 5 institutions in 1 country.

Kouki Okita *Cell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Shogo Okazaki *Cell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Shinya UejimaCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Erina YamadaCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Hiroki KaminakaCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Misa KondoCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Shiho UedaCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Ryo TokiwaCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Nami IwataCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Akitaka YamasakiCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Natsumi HayashiCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Dai OguraLink Genomics, Inc., Chuo-ku, Tokyo, Japan.
Kenji HirotaniOncology Clinical Development Department, R&D Division, Daiichi Sankyo Co., Ltd., Tokyo, Japan.
Toshiaki YoshiokaField of Basic Science, Department of Occupational therapy, Graduate School of Health Sciences, Akita University, Akita, Japan.
Masahiro InoueDepartment of Clinical Bio-Resource Research and Development, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kazue MasukoCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Takashi MasukoCell Biology Laboratory, School of Pharmacy, Kindai University, Higashiosaka, Osaka, Japan.
Kindai University · JPAkita University · JPDaiichi-Sankyo (Japan) · JPKyoto University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resistance of progressive cancers against chemotherapy is a serious clinical problem. In this context, human epidermal growth factor receptor 3 (HER3) can play important roles in drug resistance to HER1- and HER2- targeted therapies. Since clinical testing of anti-HER3 monoclonal antibodies (mAbs) such as patritumab could not show remarkable effect compared with existing drugs, we generated novel mAbs against anti-HER3. Novel rat mAbs reacted with HEK293 cells expressing HER3, but not with cells expressing HER1, HER2 or HER4. Specificity of mAbs was substantiated by the loss of mAb binding with knockdown by siRNA and knockout of CRISPR/Cas9-based genome-editing. Analyses of CDR sequence and germline segment have revealed that seven mAbs are classified to four groups, and the binding of patritumab was inhibited by one of seven mAbs. Seven mAbs have shown reactivity with various human epithelial cancer cells, strong internalization activity of cell-surface HER3, and inhibition of NRG1 binding, NRG1-dependent HER3 phosphorylation and cell growth. Anti-HER3 mAbs were also reactive with

Indexed as

CDRHER3internalizationmAbNRG1

Identifiers

PMID32002122
PMCPMC6967776
OpenAlexW2999025536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.