Evidence map›Paper›PMID 29937990›Full record

ArticleOncotarget2018

Targeting autophagy sensitises lung cancer cells to Src family kinase inhibitors.

Ewa Rupniewska, Rajat Roy, Francesco A Mauri, Xinxue Liu, Maciej Kaliszczak, Guido Bellezza, Lucio Cagini, Mattia Barbareschi, Stefano Ferrero, Anna M Tommasi and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. A Novel Peptide that Disrupts the Lck-IPArchives of microbiology & immunology · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Beyond TCR Signaling: Emerging Functions of Lck in Cancer and Immunotherapy.International journal of molecular sciences · 2019
    Review
  17. 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

13 authors at 5 institutions in 2 countries.

Ewa RupniewskaDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Rajat RoyDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Francesco A MauriDepartment of Histopathology and Imperial College London, London, United Kingdom.
Xinxue LiuStatistical Advisory Service, Imperial College London, London, United Kingdom.
Maciej KaliszczakDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Guido BellezzaInstitute of Pathology, Division of Cancer Research, Perugia Medical School, University of Perugia, Perugia, Italy.
Lucio CaginiDepartment of Thoracic Surgery, Division of Cancer Research, Perugia Medical School, University of Perugia, Perugia, Italy.
Mattia BarbareschiUnit of Surgical Pathology, Laboratory of Molecular Pathology S. Chiara Hospital, Trento, Italy.
Stefano FerreroDivision of Pathology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy.
Anna M TommasiDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Eric AboagyeDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Michael J SecklDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Olivier E PardoDivision of Cancer, Department of Surgery and Cancer, Imperial College London, London, United Kingdom.
Imperial College London · GBUniversity of Perugia · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITOspedale Santa Chiara · ITRoyal Statistical Society · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the main cancer killer in both men and women, mostly due to the rapid development of drug resistant metastatic disease. Here, we evaluate the potential involvement of SRC family kinases (SFK) in lung cancer biology and assess the possible benefits of their inhibition as a therapeutic approach. We demonstrated that various SRC family members, including LYN and LCK, normally expressed solely in hematopoietic cells and neural tissues, are overexpressed and activated in a panel of SCLC and NSCLC cell lines. This was clinically relevant as LYN and FYN are also overexpressed in lung cancer clinical specimens. Moreover, LYN overexpression correlated with decreased patient survival on univariate and multivariate analysis. Dasatinib (BMS-354825), a SRC/ABL inhibitor, effectively blocked SFK activation at nanomolar concentrations which correlated with a significant decrease in cell numbers of multiple lung cancer cell lines. This effect was matched by a decrease in DNA synthesis, but only moderate induction of apoptosis. Indeed, dasatinib as well as PP2, another SFK inhibitor, strongly induced autophagy that likely prevented apoptosis. However, inhibition of this autophagic response induced robust apoptosis and sensitised lung cancer cells to dasatinib

Indexed as

apoptosisdasatiniblung cancerresistanceSRC

Identifiers

PMID29937990
PMCPMC6007948
OpenAlexW2805980353

What OpenQuestion holds

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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.