Evidence map›Paper›PMID 28463969›Full record

ArticlePloS one2017

HER2-positive breast cancer cells expressing elevated FAM83A are sensitive to FAM83A loss.

Courtney A Bartel, Mark W Jackson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-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

30 citing papers in PubMed, 69 citations in OpenAlex.

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  16. Combining Neratinib with CDK4/6, mTOR, and MEK Inhibitors in Models of HER2-positive Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

2 authors at 1 institution in 1 country.

Courtney A BartelDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America.ORCID http://orcid.org/0000-0003-3249-5442
Mark W JacksonDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America.
Case Western Reserve University · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Amar Desai · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
RESEARCH ONCOLOGY TRAINING GRANTT32CA059366 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 1993 to 2025
$5.5M
Identification of a noval oncogene using validation-based insertional mutagenesisR01CA138421 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 2010 to 2020
$3.2M
Defining the role of FAM83A in Herceptin-resistant breast cancerR21CA194902 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI JACKSON, MARK W. · 2016 to 2017
$379k
NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA138421NCI NIH HHS R21 CA194902NCI NIH HHS T32 CA059366NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

HER2-positive breast cancer (HER2+ BC) is an aggressive subtype with a poor prognosis. Although the antibody trastuzumab, which targets the HER2 growth factor receptor, has improved survival rates, patients often present with de novo resistance or acquire resistance after an initial response. Identifying new ways to target HER2 signaling will be critical for overcoming trastuzumab resistance. FAM83A is a novel oncogene identified by its ability to confer resistance to EGFR therapies, a receptor closely related to HER2. Moreover, a prior study identified hyper-tyrosine phosphorylated FAM83A in trastuzumab-resistant HER2+ BC. Here, we find that FAM83A expression is elevated in 36% of HER2+ BC tumors. In a panel of HER2+ BC cell lines, FAM83A expression is significantly increased in the trastuzumab-resistant derivatives relative to parental controls. shRNA-mediated ablation of FAM83A in the panel of HER2+ BC cell lines suppresses HER2+ BC cell growth in both 2D and 3D cell cultures, elevates apoptosis markers, and suppresses PI3K signaling. Growth inhibition following FAM83A knock-down, however, was independent of trastuzumab sensitivity, suggesting that FAM83A is a key signaling component in HER2+ BCs that could serve as a novel therapeutic target in both trastuzumab-resistant and trastuzumab-sensitive cancers.

Indexed as

Antineoplastic AgentsApoptosisBreast NeoplasmsCell Culture TechniquesCell Line, TumorCell ProliferationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesGene Knockdown TechniquesGenetic VectorsHumansLentivirusNeoplasm ProteinsRNA, Small InterferingTrastuzumabAntineoplastic AgentsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesFAM83A protein, humanNeoplasm ProteinsRNA, Small InterferingTrastuzumab

Identifiers

PMID28463969
PMCPMC5413028
OpenAlexW2611669941

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.