Evidence map›Paper›PMID 33983573›Full record

ArticleAdvances in experimental medicine and biology2021

HER2 Signaling in Breast Cancer.

Incheol Shin

Abstract read
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In one paragraph

Article in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
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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

1 author at 1 institution in 1 country.

Incheol ShinDepartment of Life Science, Hanyang University, Seoul, South Korea. shin.incheol@gmail.com.
Hanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HER2 gene amplification occurs in many breast cancer patients and is associated with poor clinical prognosis. Trastuzumab is a therapeutic monoclonal antibody binding to HER2 and inhibits growth of HER2-positive breast cancer cells and used as a principal treatment for HER2-positive breast cancer. Unfortunately, some HER2-positive breast cancers eventually relapse after trastuzumab treatment. To investigate the molecular mechanism of trastuzumab resistance, we generated trastuzumab-resistant cells using a mouse model and found ECM1 protein is increased in trastuzumab-resistant cells. ECM1 was shown to increase EGFR signaling via upregulated matrix metalloproteinase 9/galectin-3/mucin pathway. To further find the novel mediators of HER2-driven signaling pathways in breast cancer, we investigated the upregulated proteins in HER2-overexpressing breast cancer cells using a proteomics approach and found that KRT19 is strongly upregulated in HER2-positive breast cancer cells and it activates HER2 signaling by binding to HER2 and stabilizes the receptor on the cell membrane. Moreover, we found that treatment of KRT19 antibody resulted in reduced cell viability of trastuzumab-resistant HER2-positive breast cancer cells as well as trastuzumab-sensitive cancer cells both in vitro and in vivo.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCell Line, TumorDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesExtracellular Matrix ProteinsHumansNeoplasm Recurrence, LocalTrastuzumabAntineoplastic AgentsECM1 protein, humanErb-b2 Receptor Tyrosine KinasesExtracellular Matrix ProteinsTrastuzumabECM1EGFRHER2KRT19Trastuzumab

Identifiers

PMID33983573
OpenAlexW3163013392

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.