Evidence map›Paper›PMID 40543507›Full record

ArticleCell reports. Medicine2025

MET pathway inhibition increases chemo-immunotherapy efficacy in small cell lung cancer.

Raúl Del Rey-Vergara, Miguel Alejandro Galindo-Campos, Pedro Rocha, Marina Carpes, Carlos Martínez, Laura Masfarré, Silvia Menéndez, Fabricio Quimis, Adrià Rossell, Albert Iñañez and 17 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. The Five-Decade Journey of Small Cell Lung Cancer.Cancer communications (London, England) · 2026
    Review
  2. Review
  3. 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

27 authors.

Raúl Del Rey-VergaraCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Miguel Alejandro Galindo-CamposCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Pedro RochaCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain; Department of Medical Oncology, Hospital del Mar, Barcelona, Spain.
Marina CarpesInstituto Murciano de Investigación Biosanitaria IMIB-Pascual Parrilla, Pathology Core, Murcia, Spain.
Carlos MartínezInstituto Murciano de Investigación Biosanitaria IMIB-Pascual Parrilla, Pathology Core, Murcia, Spain; Department of Anatomy and Comparative Pathology, Facultad de Veterinaria, Universidad de Murcia, Murcia, Spain.
Laura MasfarréDepartment of Medical Oncology, Hospital del Mar, Barcelona, Spain.
Silvia MenéndezCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Fabricio QuimisCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Adrià RossellCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Albert IñañezCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain.
Sandra Pérez-BuiraDepartment of Pathology, IIS-Fundación Jiménez Díaz-CIBERONC, Madrid, Spain.
Federico RojoDepartment of Pathology, IIS-Fundación Jiménez Díaz-CIBERONC, Madrid, Spain.
Ramon GimenoTranslational Clinical Research Program, Hospital del Mar Research Institute, Barcelona, Spain; Department of Pathology, Hospital del Mar, Barcelona, Spain.
Dolores IslaMedical Oncology Department, Hospital Universitario Lozano Blesa, IIS Aragón, Zaragoza, Spain.
Jon ZugazagoitiaDepartment of Medical Oncology, Hospital Universitario 12 de Octubre, Madrid, Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Madrid, Spain.
Cristina Martí BlancoMedical Oncology, Hospital Universitari Sant Joan de Reus, Reus, Spain.
Rosario García-CampeloDepartment of Medical Oncology, Hospital Universitario A Coruña, Health Research Institute, INIBIC, A Coruña, Spain.
Alberto Moreno-VegaMedical Oncology, Hospital Universitario Reina Sofía, Córdoba, Spain.
Luis León-MateosDepartment of Medical Oncology, Complexo Hospitalario Universitario de Santiago de Compostela (SERGAS), Santiago de Compostela, Spain.
Ángel Callejo MellénOBU Medical Department, AstraZeneca, Madrid, Spain.
Kwon-Sik ParkDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, VA 22903, USA.
Simon HeekeDepartment of Thoracic/Head & Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
John V HeymachDepartment of Thoracic/Head & Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Álvaro TausDepartment of Medical Oncology, Hospital del Mar, Barcelona, Spain.
Luis Paz-AresDepartment of Medical Oncology, Hospital Universitario 12 de Octubre, Madrid, Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Madrid, Spain.
Ana RoviraCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain; Department of Medical Oncology, Hospital del Mar, Barcelona, Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Madrid, Spain.
Edurne ArriolaCancer Research Program, Hospital del Mar Research Institute, Barcelona, Spain; Department of Medical Oncology, Hospital del Mar, Barcelona, Spain; Centro de Investigación Biomédica en Red de Oncología, CIBERONC-ISCIII, Madrid, Spain. Electronic address: earriola@hmar.cat.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The introduction of immunotherapy as a first-line treatment for advanced small cell lung cancer (SCLC) represents significant progress, yet there remains an opportunity to further improve patient outcomes. Hepatocyte growth factor (HGF) receptor (MET) pathway activation promotes epithelial-mesenchymal transition, driving chemoresistance and potentially impairing the efficacy of immunotherapy. In SCLC mouse models, adding MET inhibition to chemo-immunotherapy (anti-PD-L1) reduces tumor growth, extends survival, and reshapes the tumor microenvironment by decreasing suppressive myeloid cell infiltration and enhancing the immune response. Analysis of pretreatment human SCLC tumor samples reveals that myeloid-enriched immune infiltrates may contribute to chemo-immunotherapy resistance. Elevated serum HGF levels are associated with a mesenchymal and inflamed phenotype, suggesting that patients with these characteristics might benefit from MET inhibitor-based therapeutic strategies. These findings provide strong preclinical and translational evidence supporting MET inhibition as a therapeutic approach to overcome treatment resistance, enhancing the immune response and improving outcomes in biomarker-defined subsets of SCLC patients.

Indexed as

ImmunotherapyLung NeoplasmsProto-Oncogene Proteins c-metSmall Cell Lung CarcinomaAnimalsB7-H1 AntigenCell Line, TumorDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHepatocyte Growth FactorHumansMiceSignal TransductionTumor MicroenvironmentXenograft Model Antitumor AssaysB7-H1 AntigenHepatocyte Growth FactorMET protein, humanProto-Oncogene Proteins c-metepithelial-mesenchymal transitionimmune checkpoint inhibitorMET inhibitormyeloid-derived suppressor cellssmall cell lung cancer

Identifiers

PMID40543507
PMCPMC12281364

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Registered trials

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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.