Evidence map›Paper›PMID 25117814›Full record

ArticleBritish journal of cancer2014

Fascin is involved in the chemotherapeutic resistance of breast cancer cells predominantly via the PI3K/Akt pathway.

H Ghebeh, S Al-Khaldi, S Olabi, A Al-Dhfyan, F Al-Mohanna, R Barnawi, A Tulbah, T Al-Tweigeri, D Ajarim, M Al-Alwan

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 86 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

10 authors at 2 institutions in 1 country.

H GhebehStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
S Al-KhaldiThe Joint Center for Genomics Research, King Abdulaziz City for Sciences and Technology, Riyadh, Saudi Arabia.
S OlabiStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
A Al-DhfyanStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
F Al-MohannaDepartment of Comparative Medicine, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
R BarnawiStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
A TulbahDepartment of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
T Al-TweigeriDepartment of Oncology, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
D AjarimDepartment of Oncology, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
M Al-AlwanStem Cell and Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Centre, MBC: 03-99, P.O. Box: 3354, Riyadh 11211, Saudi Arabia.
King Faisal Specialist Hospital & Research Centre · SAKing Abdulaziz City for Science and Technology · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA major therapeutic challenge for breast cancer is the ability of cancer cells to evade killing of conventional chemotherapeutic agents. We have recently reported the actin-bundling protein (fascin) as a major regulator of breast cancer metastasis and survival.

methodsSurvival of breast cancer patients that received chemotherapy and xenograft tumour model was used to assess the effect of chemotherapy on fascin-positive and -negative breast cancer cells. Molecular and cellular assays were used to gain in-depth understanding of the relationship between fascin and chemoresistance.

resultsWe showed a significant correlation between fascin expression and shorter survival in breast cancer patients who received chemotherapy. In xenograft experiments, fascin-positive cancer cells displayed significantly more resistance to chemotherapy-mediated apoptotic cell death than fascin-negative counterparts. This increased chemoresistance was at least partially mediated through PI3K/Akt signalling, and was paralleled by increased FAK phosphorylation, enhanced expression of the inhibitor of apoptosis proteins (XIAP and Livin) and suppression of the proapoptotic markers (caspase 9, caspase 3 and PARP).

conclusionsThis is the first report to demonstrate fascin involvement in breast cancer chemotherapeutic resistance, supporting the development of fascin-targeting drugs for better treatment of chemoresistance breast cancer.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsApoptosisBreast NeoplasmsCarrier ProteinsCell Line, TumorFemaleHumansMiceMice, NudeMicrofilament ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSurvival AnalysisXenograft Model Antitumor AssaysAntineoplastic AgentsCarrier ProteinsfascinMicrofilament ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25117814
PMCPMC4200093
OpenAlexW2037769763

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.