Evidence map›Paper›PMID 28835699›Full record

ArticleScientific reports2017

Differential responsiveness of MET inhibition in non-small-cell lung cancer with altered CBL.

Yi-Hung Carol Tan, Tamara Mirzapoiazova, Brian M Won, Li Zhu, Minu K Srivastava, Everett E Vokes, Aliya N Husain, Surinder K Batra, Sherven Sharma, Ravi Salgia

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Improvement of Diagnostics in NSCLC Patients withInternational journal of molecular sciences · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Journal of personalized medicine · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. 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

10 authors at 4 institutions in 1 country.

Yi-Hung Carol TanDepartment of Medicine, Section of Hematology/Oncology, The University of Chicago Medicine and Biologic Sciences, Chicago, IL, USA.
Tamara MirzapoiazovaDepartment of Medical Oncology and Therapeutic Research, City of Hope, Duarte, CA, USA.
Brian M WonDepartment of Medicine, Section of Hematology/Oncology, The University of Chicago Medicine and Biologic Sciences, Chicago, IL, USA.
Li ZhuDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Minu K SrivastavaDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Everett E VokesDepartment of Medicine, Section of Hematology/Oncology, The University of Chicago Medicine and Biologic Sciences, Chicago, IL, USA.
Aliya N HusainDepartment of Pathology, The University of Chicago Medicine and Biologic Sciences, Chicago, IL, USA.
Surinder K BatraDepartment of Biochemistry and Molecular Biology, University of Nebraska College of Medicine, Omaha, NE, USA.
Sherven SharmaDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Ravi SalgiaDepartment of Medical Oncology and Therapeutic Research, City of Hope, Duarte, CA, USA. rsalgia@coh.org.
University of Chicago · USUniversity of California, Los Angeles · USCity of Hope · USUniversity of Nebraska Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Casitas B-lineage lymphoma (CBL) is an E3 ubiquitin ligase and a molecule of adaptor that we have shown is important for non-small-cell lung cancer (NSCLC). We investigated if MET is a target of CBL and if enhanced in CBL-altered NSCLC. We showed that CBL wildtype cells have lower MET expression than CBL mutant cells. Ubiquitination of MET was also decreased in CBL mutant cells compared to wildtype cells. Mutant cells were also more sensitive to MET inhibitor SU11274 than wild-type cells. sh-RNA-mediated knockdown of CBL enhanced cell motility and colony formation in NSCLC cells, and these activities were inhibited by SU11274. Assessment of the phospho-kinome showed decreased phosphorylation of pathways involving MET, paxillin, EPHA2, and VEGFR. When CBL was knocked down in the mutant cell line H1975 (erlotinib-resistant), it became sensitive to MET inhibition. Our findings suggest that CBL status is a potential positive indicator for MET-targeted therapeutics in NSCLC.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell MovementCell SurvivalDisease Models, AnimalDrug Resistance, NeoplasmErbB ReceptorsGene ExpressionGene Knockdown TechniquesHumansLung NeoplasmsMiceMutationNeoplasm MetastasisPhosphorylationAntineoplastic AgentsErbB ReceptorsProtein Kinase InhibitorsProto-Oncogene Proteins c-cblProto-Oncogene Proteins c-metRNA, Small Interfering

Identifiers

PMID28835699
PMCPMC5569108
OpenAlexW2749616691

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.