Evidence map›Paper›PMID 26064441›Full record

ArticleAmerican journal of translational research2015

A critical role for HER3 in HER2-amplified and non-amplified breast cancers: function of a kinase-dead RTK.

Nandini Dey, Casey Williams, Brain Leyland-Jones, Pradip De

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

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  15. PET and SPECT Imaging of the EGFR Family (RTK Class I) in Oncology.International journal of molecular sciences · 2021
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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

4 authors at 1 institution in 1 country.

Nandini DeyDepartment of Molecular and Experimental Medicine, Avera Cancer Institute Sioux Falls, SD ; Department of Internal Medicine, SSOM, University of South Dakota SD.
Casey WilliamsDepartment of Molecular and Experimental Medicine, Avera Cancer Institute Sioux Falls, SD ; Department of Internal Medicine, SSOM, University of South Dakota SD.
Brain Leyland-JonesDepartment of Molecular and Experimental Medicine, Avera Cancer Institute Sioux Falls, SD ; Department of Internal Medicine, SSOM, University of South Dakota SD.
Pradip DeDepartment of Molecular and Experimental Medicine, Avera Cancer Institute Sioux Falls, SD ; Department of Internal Medicine, SSOM, University of South Dakota SD.
Avera Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ERBB3/HER3 is the most intriguing RTK by virtue of its ability to transduce multiple cytosolic signals for the proliferation and growth of tumor cells in spite of being a "kinase dead" receptor that binds to its true ligand, heregulin. Although other members of the HER3 family like EGFR and HER2 have long been recognized to be associated with breast tumorigenesis and studied because of their predictive and prognostic value, the significance of HER3 as an irrefutable component of HER family signalosome is a relatively new development. The recent understanding of signals originating from the oncogenic partnership of HER3 with HER2 in the context of HER2 amplification/overexpression showed the critical clinical value for the treatment of HER2+BC. The downstream signaling cascade (included but not limited to the PI3K signaling) associated with signals originating from HER2:HER3 dimers play a vital role in the tumorigenesis, drug-resistance and tumor progression of HER2+BC. The upregulation of HER3 activity provides an alternate "escape route" via which tumor cells bypass either the inhibition of the HER family RTKs or the inhibition of the downstream PI3K-AKT-mTOR signaling pathway. By understanding the signaling that provides this "escape route" for these tumor cells treated with a targeted therapy (HER2 inhibitors or inhibitors of downstream PI3K-AKT-mTOR signaling pathway), we are just beginning to appreciate the prognostic value of HER3 in breast cancer. In this review, we will discuss the relevance of HER3 signaling in the context of, (1) downstream oncogenic signals and (2) therapeutic options in HER2 amplified BC.

Indexed as

Breast cancerHER2HER3neuregulinPI3K

Identifiers

PMID26064441
PMCPMC4455348
OpenAlexW2402692848

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.