ReviewJournal of enzyme inhibition and medicinal chemistry2026
Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.
Review in Journal of enzyme inhibition and medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
11 authors.
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Abstract
Bone Marrow Tyrosine Kinase on Chromosome X (BMX), also known as epithelial/endothelial cell kinase (ETK), is a core member of the Tec family of non-receptor tyrosine kinases. Structurally, BMX kinase contains an N-terminal PH domain, a BH domain, a SH2 domain, a SH3 domain and a C-terminal catalytic tyrosine kinase domain. This distinctive modular architecture enables BMX to engage in diverse cellular signalling cascades. It has been reported that BMX is highly expressed and plays an oncogenic role in various cancers. In this paper, we mainly explore the function and mechanism of BMX in tumour cell proliferation, apoptosis, invasion, metastasis, cancer stem cell properties, angiogenesis and drug resistance. Furthermore, the research focus on summarising the research progress of BMX inhibitors for cancer treatment. This review aims to provide a theoretical framework for cancer therapy by targeting BMX.
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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 Socratic graph.