Evidence map›Paper›PMID 31767884›Full record

ArticleScientific reports2019

Expression of the BAD pathway is a marker of triple-negative status and poor outcome.

Bernadette M Boac, Forough Abbasi, Roohi Ismail-Khan, Yin Xiong, Atif Siddique, Hannah Park, Mingda Han, Daryoush Saeed-Vafa, Hatem Soliman, Brendon Henry and 11 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 27 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

21 authors at 5 institutions in 1 country.

Bernadette M BoacDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Forough AbbasiCedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.
Roohi Ismail-KhanDepartment of Oncologic Sciences, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Yin XiongDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Atif SiddiqueDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Hannah ParkDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Mingda HanDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Daryoush Saeed-VafaDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Hatem SolimanDepartment of Oncologic Sciences, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Brendon HenryDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
M Juliana PenaDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
E Clair McClungUniversity of Arizona Cancer Center, Obstetrics and Gynecology, Tucson, AZ, 85724, USA.
Sharon E RobertsonIndiana University Health, Indianapolis, IN, 46202, USA.
Sarah L ToddDepartment of Women's Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Alex LopezDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Weihong SunDepartment of Women's Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Susmitha ApuriDepartment of Women's Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.
Johnathan M LancasterMyriad Genetics, Salt Lake City, UT, 84108, USA.
Anders E BerglundDepartment of Bioinformatics and Biostatistics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA.ORCID http://orcid.org/0000-0002-0393-3530
Anthony M MaglioccoProtean Diagnostics, Tampa, FL, 33612, USA.
Douglas C MarchionDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, 33612, USA. dcmarchion@gmail.com.
Moffitt Cancer Center · USCedars-Sinai Medical Center · USIndiana University Health · USMyriad Genetics · USUniversity of Arizona · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI Christine O'Connell · 1998 to 2026
$93.5M
Development of a Genomic Expression Signature Associated with ChemoresistanceR21CA181617 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MARCHION, DOUGLAS C · 2014 to 2015
$403k
NCI NIH HHS P30 CA076292NCI NIH HHS R21 CA181617
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) has few therapeutic targets, making nonspecific chemotherapy the main treatment. Therapies enhancing cancer cell sensitivity to cytotoxic agents could significantly improve patient outcomes. A BCL2-associated agonist of cell death (BAD) pathway gene expression signature (BPGES) was derived using principal component analysis (PCA) and evaluated for associations with the TNBC phenotype and clinical outcomes. Immunohistochemistry was used to determine the relative expression levels of phospho-BAD isoforms in tumour samples. Cell survival assays evaluated the effects of BAD pathway inhibition on chemo-sensitivity. BPGES score was associated with TNBC status and overall survival (OS) in breast cancer samples of the Moffitt Total Cancer Care dataset and The Cancer Genome Atlas (TCGA). TNBC tumours were enriched for the expression of phospho-BAD isoforms. Further, the BPGES was associated with TNBC status in breast cancer cell lines of the Cancer Cell Line Encyclopedia (CCLE). Targeted inhibition of kinases known to phosphorylate BAD protein resulted in increased sensitivity to platinum agents in TNBC cell lines compared to non-TNBC cell lines. The BAD pathway is associated with triple-negative status and OS. TNBC tumours were enriched for the expression of phosphorylated BAD protein compared to non-TNBC tumours. These findings suggest that the BAD pathway it is an important determinant of TNBC clinical outcomes.

Indexed as

Gene Regulatory Networksbcl-Associated Death ProteinBiomarkers, TumorCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiddle AgedOligonucleotide Array Sequence AnalysisPhosphorylationPrincipal Component AnalysisPrognosisSignal TransductionSurvival AnalysisTriple Negative Breast NeoplasmsBAD protein, humanbcl-Associated Death ProteinBiomarkers, Tumor

Identifiers

PMID31767884
PMCPMC6877530
OpenAlexW2990259066

What OpenQuestion holds

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Registered trials

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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.