Evidence map›Paper›PMID 36176751›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2022

Persistent EGFR/K-RAS/SIAH pathway activation drives chemo-resistance and early tumor relapse in triple-negative breast cancer.

Amy H Tang, Richard A Hoefer, Mary L Guye, Harry D Bear

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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 2 institutions in 1 country.

Amy H TangDepartment of Microbiology and Molecular Cell Biology, Leroy T. Canoles Jr. Cancer Research Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA.
Richard A HoeferSchool of Systems Biology, George Mason University, Manassas, VA 20110, USA.
Mary L GuyeSentara Cancer Network, Sentara Healthcare, Norfolk, VA 23507, USA.
Harry D BearDivision of Surgical Oncology, Departments of Surgery and Microbiology and Immunology, Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298-0011, USA.
Sentara Heart Hospital · USEastern Virginia Medical School · US

Funding

SIAH2-Dependent Proteolysis in Cell Migration, Tumor Growth and Cancer MetastasisR01CA140550 · NCI · EASTERN VIRGINIA MEDICAL SCHOOL · PI TANG, AMY H. · 2010 to 2014
$1.4M
NCI NIH HHS R01 CA140550
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. It disproportionately affects BRCA mutation carriers and young women, especially African American (AA) women. Chemoresistant TNBC is a heterogeneous and molecularly unstable disease that challenges our ability to apply personalized therapies. With the approval of immune checkpoint blockade (ICB) for TNBC, the addition of pembrolizumab to systemic chemotherapy has become standard of care (SOC) in neoadjuvant systemic therapy (NST) for high-risk early-stage TNBC. Pembrolizumab plus chemotherapy significantly increased the pathologic complete response (pCR) and improved event-free survival in TNBC. However, clinical uncertainties remain because similarly treated TNBC partial responders with comparable tumor responses to neoadjuvant therapy often experience disparate clinical outcomes. Current methods fall short in accurately predicting which high-risk patients will develop chemo-resistance and tumor relapse. Therefore, novel treatment strategies and innovative new research initiatives are needed. We propose that the EGFR-K-RAS-SIAH pathway activation is a major tumor driver in chemoresistant TNBC. Persistent high expression of SIAH in residual tumors following NACT/NST reflects that the EGFR/K-RAS pathway remains activated (ON), indicating an ineffective response to treatment. These chemoresistant tumor clones persist in expressing SIAH (SIAH

Indexed as

and treatment optimizationchemo-resistancedetection of chemo-resistanceEGFR/K-RAS/SIAH pathway activation in TNBCneoadjuvant chemotherapy prognosispatient risk stratificationprecision quantification of therapy efficacyseven in absentia (SINA) and human homologs of SINA (SIAH) E3 ligaseTriple-negative breast cancer (TNBC)ubiquitin-mediated proteolysis

Identifiers

PMID36176751
PMCPMC9511813
OpenAlexW4285141407

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.