Evidence map›Paper›PMID 29608984›Full record

ArticleCancer letters2018

Sorafenib improves alkylating therapy by blocking induced inflammation, invasion and angiogenesis in breast cancer cells.

Alfeu Zanotto-Filho, Subapriya Rajamanickam, Eva Loranc, V Pragathi Masamsetti, Aparna Gorthi, July Carolina Romero, Sonal Tonapi, Rosangela Mayer Gonçalves, Robert L Reddick, Raymond Benavides and 3 more

Abstract read
In one paragraph

Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Design, synthesis and biological evaluation of a new thieno[2,3-Journal of enzyme inhibition and medicinal chemistry · 2020
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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

13 authors at 4 institutions in 2 countries.

Alfeu Zanotto-FilhoGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA; Departamento de Farmacologia, Universidade Federal de Santa Catarina (UFSC), Florianópolis, SC, Brazil.
Subapriya RajamanickamGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA.
Eva LorancGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA.
V Pragathi MasamsettiGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA.
Aparna GorthiGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA; Department of Cell Systems and Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA.
July Carolina RomeroGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA; Department of Cell Systems and Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA.
Sonal TonapiGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA; Department of Cell Systems and Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA.
Rosangela Mayer GonçalvesDepartamento de Farmacologia, Universidade Federal de Santa Catarina (UFSC), Florianópolis, SC, Brazil.
Robert L ReddickDepartment of Pathology, University of Texas Health at San Antonio, San Antonio, TX, USA.
Raymond BenavidesDepartment of Pathology, University of Texas College of Pharmacy, Austin, TX, USA.
John KuhnDepartment of Pathology, University of Texas Health at San Antonio, San Antonio, TX, USA; Department of Pathology, University of Texas College of Pharmacy, Austin, TX, USA.
Yidong ChenDepartment of Epidemiology and Biostatistics, University of Texas Health at San Antonio, San Antonio, TX, USA.
Alexander J R BishopGreehey Children's Cancer Research Institute, University of Texas Health at San Antonio, San Antonio, TX, USA; Department of Cell Systems and Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA. Electronic address: bishopa@uthscsa.edu.
The University of Texas at San Antonio · USThe University of Texas Health Science Center at San Antonio · USUniversidade Federal de Santa Catarina · BRTexas College · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Cancer Biology Training ProgramT32CA148724 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Pei Wang, Feng-Chun Yang · 2011 to 2026
$3.3M
Improving etoposide treatment of Ewing's sarcomaR01CA152063 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BISHOP, ALEXANDER JAMES · 2011 to 2015
$1.5M
High Throughput DNA Sequencer: Illumina HiSeq 3000 SequencerS10OD021805 · OD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LAI, ZHAO · 2016 to 2016
$600k
Comparing and contrasting the biology of damage survival at a genomic levelR15ES019128 · NIEHS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BISHOP, ALEXANDER JAMES · 2010 to 2010
$446k
A screen for damage response genes using recombinationK22ES012264 · NIEHS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BISHOP, ALEXANDER JAMES · 2004 to 2006
$321k
NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA152063NCI NIH HHS T32 CA148724NIEHS NIH HHS K22 ES012264NIEHS NIH HHS R15 ES019128NIH HHS S10 OD021805
6 · The paper itself

Abstract

Molecular targeted compounds are emerging as a strategy to improve classical chemotherapy. Herein, we describe that using low dose of the multikinase inhibitor sorafenib improves cyclophosphamide antitumor activity by inhibiting angiogenesis, metastasis and promoting tumor healing in MDA-MB231 xenografts and the 4T1-12B syngeneic breast cancer metastasis model. Mechanistic studies in MDA-MB231 cells revealed that alkylation upregulates inflammatory genes/proteins such as COX-2, IL8, CXCL2 and MMP1 in a MEK1/2-ERK1/2-dependent manner. These proteins enrich the secretome of cancer cells, stimulating cell invasion and angiogenesis via autocrine and paracrine mechanisms. Sorafenib inhibits MEK1/2-ERK1/2 pathway thereby decreasing inflammatory genes and mitigating cell invasion and angiogenesis at basal and alkylation-induced conditions whereas NRF2 and ER stress pathways involved in alkylation survival are not affected. In non-invasive/non-angiogenic breast cancer cells (SKBR3 and MCF7), alkylation did not elicit inflammatory responses with the only sorafenib effect being ERK1/2-independent ROS-dependent cytotoxicity when using higher drug concentrations. In summary, our data show that alkylating agents may elicit inflammatory responses that seems to contribute to malignant progression in specific breast cancer cells. Identifying and targeting drivers of this phenotype may offer opportunities to optimize combined drug regimens between classical chemotherapeutics and targeted agents.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalCyclophosphamideDrug SynergismFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceNeovascularization, PathologicSignal TransductionAntineoplastic Agents, AlkylatingCyclophosphamideSorafenibAlkylationInflammationMEK1/2-ERK1/2SecretomeSorafenib

Identifiers

PMID29608984
PMCPMC5930000
OpenAlexW2794710392

What OpenQuestion holds

Textmetadata
LicenceTDM
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.