Evidence map›Paper›PMID 34665336›Full record

ReviewMedical oncology (Northwood, London, England)2021

Overcoming resistance to targeted therapy using MET inhibitors in solid cancers: evidence from preclinical and clinical studies.

Nehad M Ayoub, Dalia R Ibrahim, Amer E Alkhalifa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 8 citations in OpenAlex.

  1. The impact of the PI3K/AKT/mTOR signaling pathway on trastuzumab resistance in HER2-positive gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  6. The Impact of the Coexpression ofThe breast journal · 2024
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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

3 authors at 1 institution in 1 country.

Nehad M AyoubDepartment of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology (JUST), P.O. Box 3030, Irbid, 22110, Jordan. nmayoub@just.edu.jo.ORCID http://orcid.org/0000-0003-2284-4370
Dalia R IbrahimDepartment of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology (JUST), P.O. Box 3030, Irbid, 22110, Jordan.
Amer E AlkhalifaDepartment of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology (JUST), P.O. Box 3030, Irbid, 22110, Jordan.ORCID http://orcid.org/0000-0002-6872-4780
Jordan University of Science and Technology · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted therapy is a hallmark of cancer treatment that has changed the landscape of cancer management and enabled a personalized treatment approach. Nevertheless, the development of cancer resistance is a major challenge that is currently threatening the effective utilization of targeted therapies. The hepatocyte growth factor receptor, MET, is a receptor tyrosine kinase known for its oncogenic activity and tumorigenic potential. MET is a well-known driver of cancer resistance. A growing body of evidence revealed a major role of MET in mediating acquired resistance to several classes of targeted therapies. Deregulations of MET commonly associated with the development of cancer resistance include gene amplification, overexpression, autocrine activation, and crosstalk with other signaling pathways. Small-molecule tyrosine kinase inhibitors of MET are currently approved for the treatment of different solid cancers. This review summarizes the current evidence regarding MET-mediated cancer resistance toward targeted therapies. The molecular mechanisms associated with resistance are described along with findings from preclinical and clinical studies on using MET inhibitors to restore the anticancer activity of targeted therapies for the treatment of solid tumors.

Indexed as

Molecular Targeted TherapyAnimalsDrug Resistance, NeoplasmGene AmplificationHumansMutationNeoplasmsProto-Oncogene Proteins c-metMET protein, humanProto-Oncogene Proteins c-metAmplificationMETResistanceTargeted therapyTyrosine kinase inhibitors

Identifiers

PMID34665336
OpenAlexW3206336676

What OpenQuestion holds

Textmetadata
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.