ArticleClinical cancer research : an official journal of the American Association for Cancer Research2020
Dual Blockade of c-MET and the Androgen Receptor in Metastatic Castration-resistant Prostate Cancer: A Phase I Study of Concurrent Enzalutamide and Crizotinib.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- ADT and activation of HGF and WNT axes in double-null prostate cancer.Nature reviews. Urology · 2026Review
- The HGF/MET Axis in Advanced Prostate Cancer: From Context-Dependent Biology to Biomarker-Driven Therapeutic Strategies.Cancers · 2026Review
- Mechanism and therapeutic significance of ARV-110 combined with a PDGFR inhibitor for the induction of apoptosis in castration-resistant prostate cancer cells through the ROS/JNK pathway.Cell death & disease · 2026Article
- Deciphering molecular pathways in urological cancers: A gateway to precision therapeutics.Journal of advanced research · 2026Review
- Molecular mechanisms and classification of castration-resistant prostate cancer: Insights into androgen receptor, cancer stem cells, and neuroendocrine features.Current urology · 2026Article
- Novel hormone therapies for advanced prostate cancer: Understanding and countering drug resistance.Journal of pharmaceutical analysis · 2025Review
- Article
- Crizotinib Inhibits Viability, Migration, and Invasion by Suppressing theCurrent oncology (Toronto, Ont.) · 2025Article
- Functional interaction between receptor tyrosine kinase MET and ETS transcription factors promotes prostate cancer progression.Molecular oncology · 2025Article
- Integrative multi-omics and drug-response characterization of patient-derived prostate cancer primary cells.Signal transduction and targeted therapy · 2023Article
- Targeting c-Met in the treatment of urologic neoplasms: Current status and challenges.Frontiers in oncology · 2023Review
- The MST1R/RON Tyrosine Kinase in Cancer: Oncogenic Functions and Therapeutic Strategies.Cancers · 2022Review
- Autophagy Inhibition by Targeting PIKfyve Potentiates Response to Immune Checkpoint Blockade in Prostate Cancer.Nature cancer · 2021Article
- Androgen Receptor Signaling Pathway in Prostate Cancer: From Genetics to Clinical Applications.Cells · 2020Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 1 country.
Funding
Abstract
purposeAndrogen receptor (AR) inhibition can upregulate c-MET expression, which may be a resistance mechanism driving progression of castration-resistant prostate cancer (CRPC). We conducted a phase I trial investigating the safety and pharmacokinetics of a potent c-MET inhibitor, crizotinib, with the AR antagonist, enzalutamide, in CRPC. PATIENTS AND
methodsEmploying a 3+3 dose-escalation design, we tested three dose levels of crizotinib (250 mg daily, 200 mg twice a day, and 250 mg twice a day) with standard-dose enzalutamide (160 mg daily). The primary endpoint was rate of dose-limiting toxicities (DLTs). Tolerability and pharmacokinetics profile were secondary endpoints.
resultsTwenty-four patients were enrolled in the dose-escalation (
conclusionsConcurrent administration of enzalutamide and crizotinib resulted in a clinically significant 74% decrease in systemic crizotinib exposure. Further investigation of this combination in CRPC is not planned. Our results highlight the importance of evaluating pharmacokinetics interactions when evaluating novel combination strategies in CRPC.
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Registered trials
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.