Publications by authors named "P V Dunaev"

The design of fluorescent probes based on biocompatible luminophores for medical diagnostics is one of the rapidly developing areas worldwide. Here, we report the synthesis of a novel BODIPYs containing a propanoic acid residue at the α-position of one of the pyrrole rings conjugated to (+)-myrtenol or thiotherpenoid. Both conjugates are quite photostable (t ∼ 40 h) and exhibit high fluorescence efficiency (φ ∼ 77-90 %).

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We showed previously that the autocrine activation of the FGFR-mediated pathway in GIST lacking secondary mutations was a result of the inhibition of KIT signaling. We show here that the FGF2/FGFR pathway regulates VEGF-A/VEGFR signaling in IM-resistant GIST cells. Indeed, recombinant FGF2 increased the production of VEGF-A by IM-naive and resistant GIST cells.

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The widespread occurrence of breast cancer and its propensity to develop drug resistance highlight the need for a comprehensive understanding of the molecular mechanisms involved. This study investigates the intricate pathways associated with secondary resistance to taxol in triple-negative breast cancer (TNBC) cells, with a particular focus on the changes observed in the cytoplasmic actin isoforms. By studying a taxol-resistant TNBC cell line, we revealed a shift between actin isoforms towards γ-actin predominance, accompanied by increased motility and invasive properties.

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The overall survival of patients with the advanced and recurrent gastric cancer (GC) remains unfavorable. In particular, this is due to cancer spreading and resistance to chemotherapy associated with the epithelial-mesenchymal transition (EMT) of tumor cells. EMT can be identified by the transcriptome profiling of GC for EMT markers.

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Article Synopsis
  • The study reveals that inhibiting KIT signaling in gastrointestinal stromal tumors (GISTs) activates the FGFR signaling pathway, leading to resistance against imatinib (Gleevec) despite no secondary mutations present.
  • Long-term culture of imatinib-resistant GISTs shows reduced KIT expression and increased activation of FGFR signaling, making them more sensitive to pan-FGFR inhibitors like BGJ 398.
  • The findings highlight that targeting the FGF-2/FGFR2 signaling pathway could be a promising strategy for overcoming imatinib resistance in GISTs.
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