Evidence map›Paper›PMID 35954391›Full record

ArticleCancers2022

Identification of Src as a Therapeutic Target in Oesophageal Adenocarcinoma through Functional Genomic and High-Throughput Drug Screening Approaches.

Niamh H McCabe, Leanne Stevenson, Enya Scanlon, Rosalie Douglas, Susanna Kennedy, Oliver Keminer, Björn Windshügel, Daniela Zisterer, Richard D Kennedy, Jaine K Blayney and 1 more

Abstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

11 authors.

Niamh H McCabePatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.
Leanne StevensonPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.
Enya ScanlonPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.ORCID 0000-0002-1952-511X
Rosalie DouglasPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.
Susanna KennedyPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.
Oliver KeminerFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Discovery Research ScreeningPort, 22525 Hamburg, Germany.ORCID 0000-0003-1473-469X
Björn WindshügelFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Discovery Research ScreeningPort, 22525 Hamburg, Germany.ORCID 0000-0002-4835-3134
Daniela ZistererTrinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, D08 XW7X Dublin, Ireland.
Richard D KennedyAlmac Diagnostics Ltd., Craigavon BT63 5QD, UK.
Jaine K BlayneyPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.
Richard C TurkingtonPatrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast BT9 7AE, UK.ORCID 0000-0003-3164-1890

Funding

Cancer Research UK C50880/A29831HSC R&D Division, Public Health Agency, Northern Ireland EAT/5106/14Marie Sklodowska-curie: Training in Cancer Mechanisms and Therapeutics (TRACT) 721906
6 · The paper itself

Abstract

Drug resistance limits the effectiveness of oesophageal adenocarcinoma (OAC) chemotherapies, leading to a poor prognosis for this disease. Elucidation of the underlying resistance mechanisms is key to enabling the identification of more effective treatments. This study, therefore, aims to identify novel therapeutic and/or chemotherapy sensitising drug targets in OAC. Transcriptional data from a cohort of 273 pre-treatment OAC biopsies, from patients who received neoadjuvant chemotherapy followed by surgical resection, were analysed using gene set enrichment analysis (GSEA) to determine differential gene expression between responding and non-responding OAC tumours. From this, 80 genes were selected for high-throughput siRNA screening in OAC cell lines with or without standard chemotherapy treatment. In parallel, cell viability assays were performed using a panel of FDA-approved drugs and combination index (CI) values were calculated to evaluate drug synergy with standard chemotherapy. Mechanisms of synergy were investigated using western blot, propidium iodide flow cytometry, and proliferation assays. Taken together, the screens identified that targeting Src, using either siRNA or the small molecule inhibitor dasatinib, enhanced the efficacy of chemotherapy in OAC cells. Further in vitro functional analysis confirmed Src inhibition to be synergistic with standard OAC chemotherapies, 5-fluorouracil (5-FU), and cisplatin (CDDP). In conclusion, a compound screen together with a functional genomic approach identified Src as a potential chemosensitising target in OAC, which could be assessed in a clinical study for poor prognosis OAC patients.

Indexed as

chemotherapydrug resistanceoesophageal cancersiRNA screen

Identifiers

PMID35954391
PMCPMC9367554

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.