ArticleFrontiers in oncology2025
Targeting the N-cadherin/
Article in Frontiers in oncology, 2025. 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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5 authors.
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Abstract
Introduction: The molecular mechanisms underlying chronic myeloid leukemia (CML) progression from chronic phase (CP) to blast crisis (BC) remain incompletely understood. This study aimed to identify progression-specific genes and elucidate the role of N-cadherin (CDH2) in BC transformation. Methods: We analyzed the GSE4170 dataset to identify differentially expressed genes (DEGs) across CML phases. Functional annotations were performed via GSEA, GO, and KEGG analyses. The role of N-cadherin was validated using Results: Transcriptomic analysis identified 1,294 DEGs during CML progression, with 41 "progression-specific" genes showing consistent expression trends. Among these, N-cadherin was significantly upregulated in BC patient samples. Overexpression of N-cadherin in KU812 cells promoted cell cycle entry, accelerated tumor growth Discussion: Our findings elucidate the role of CDH2 in CML progression through activation of the Wnt/
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