Evidence map›Paper›PMID 35929603›Full record

ArticleBiochemical Society transactions2022

Focal adhesion kinase priming in pancreatic cancer, altering biomechanics to improve chemotherapy.

Kendelle J Murphy, Jessie Zhu, Michael Trpceski, Brooke A Pereira, Paul Timpson, David Herrmann

Open access · hybridAbstract read
In one paragraph

Article in Biochemical Society transactions, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

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  12. The role of molecular testing in pancreatic cancer.Therapeutic advances in gastroenterology · 2023
    Review
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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

6 authors at 1 institution in 1 country.

Kendelle J MurphyGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.ORCID 0000-0002-3234-3812
Jessie ZhuGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.
Michael TrpceskiGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.
Brooke A PereiraGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.ORCID 0000-0003-3513-1214
Paul TimpsonGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.ORCID 0000-0002-5514-7080
David HerrmannGarvan Institute of Medical Research and The Kinghorn Cancer Centre, Darlinghurst, NSW 2010, Australia.ORCID 0000-0002-9514-7501
Garvan Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dense desmoplastic and fibrotic stroma is a characteristic feature of pancreatic ductal adenocarcinoma (PDAC), regulating disease progression, metastasis and response to treatment. Reciprocal interactions between the tumour and stroma are mediated by bidirectional integrin-mediated signalling, in particular by Focal Adhesion Kinase (FAK). FAK is often hyperactivated and overexpressed in aggressive cancers, promoting stromal remodelling and inducing tissue stiffness which can accelerate cancer cell proliferation, survival and chemoresistance. Therapeutic targeting of the PDAC stroma is an evolving area of interest for pre-clinical and clinical research, where a subtle reshaping of the stromal architecture prior to chemotherapy may prove promising in the clinical management of disease and overall patient survival. Here, we describe how transient stromal manipulation (or 'priming') via short-term FAK inhibition, rather than chronic treatment, can render PDAC cells exquisitely vulnerable to subsequent standard-of-care chemotherapy. We assess how our priming publication fits with the recent literature and describe in this perspective how this could impact future cancer treatment. This highlights the significance of treatment timing and warrants further consideration of anti-fibrotic therapies in the clinical management of PDAC and other fibrotic diseases.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsBiomechanical PhenomenaCell Line, TumorFibrosisFocal Adhesion Protein-Tyrosine KinasesHumansFocal Adhesion Protein-Tyrosine KinasesbiomechanicsFAKfibrosispancreatic cancerpriming

Identifiers

PMID35929603
PMCPMC9444069
OpenAlexW4289993951

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.