Evidence map›Paper›PMID 35884511›Full record

ReviewCancers2022

Alternative Treatment Options to ALK Inhibitor Monotherapy for EML4-ALK-Driven Lung Cancer.

Savvas Papageorgiou, Sarah L Pashley, Laura O'Regan, Sam Khan, Richard Bayliss, Andrew M Fry

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Clinical difference on the variants and co-mutation in a Chinese cohort with ALK-positive advanced non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. 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

6 authors at 2 institutions in 1 country.

Savvas PapageorgiouDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.ORCID 0000-0002-3447-0276
Sarah L PashleyDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.
Laura O'ReganDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.
Sam KhanLeicester Cancer Research Centre (LCRC), Department of Genetics and Genome Biology, University of Leicester, Robert Kilpatrick Clinical Sciences Building, Leicester LE2 7LX, UK.
Richard BaylissAstbury Centre for Structural Molecular Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK.
Andrew M FryDepartment of Molecular and Cell Biology, University of Leicester, Lancaster Road, Leicester LE1 7RH, UK.ORCID 0000-0003-4417-7329
University of Leicester · GBUniversity of Leeds · GB

Funding

Cancer Research UK C24461/A23302Medical Research Council MC_PC_17171Wellcome Trust 204801/Z/16/ZWorldwide Cancer Research 13-0042Worldwide Cancer Research 16-0119
6 · The paper itself

Abstract

EML4-ALK is an oncogenic fusion protein that accounts for approximately 5% of NSCLC cases. Targeted inhibitors of ALK are the standard of care treatment, often leading to a good initial response. Sadly, some patients do not respond well, and most will develop resistance over time, emphasizing the need for alternative treatments. This review discusses recent advances in our understanding of the mechanisms behind EML4-ALK-driven NSCLC progression and the opportunities they present for alternative treatment options to ALK inhibitor monotherapy. Targeting ALK-dependent signalling pathways can overcome resistance that has developed due to mutations in the ALK catalytic domain, as well as through activation of bypass mechanisms that utilise the same pathways. We also consider evidence for polytherapy approaches that combine targeted inhibition of these pathways with ALK inhibitors. Lastly, we review combination approaches that use targeted inhibitors of ALK together with chemotherapy, radiotherapy or immunotherapy. Throughout this article, we highlight the importance of alternative breakpoints in the

Indexed as

ALK inhibitorschemotherapyEML4-ALKimmunotherapymicrotubule poisonsNSCLCradiotherapyTKIs

Identifiers

PMID35884511
PMCPMC9325236
OpenAlexW4285733396

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.