Blar i forfatter "Seip, Kotryna"

Viser treff 1-3 av 3

    • Detection of phenotype-specific therapeutic vulnerabilities in breast cells using a CRISPR loss-of-function screen 

      Barkovskaya, Anna; Goodwin, Craig; Seip, Kotryna; Hilmarsdòttir, Bylgja; Pettersen, Solveig; Stalnecker, Clint; Engebraaten, Olav; Briem, Eirikur; Der, Channing J; Moestue, Siver Andreas; Guðjónsson, Þórarinn; Mælandsmo, Gunhild Mari; Prasmickaite, Lina (Journal article; Tidsskriftartikkel; Peer reviewed, 2021-03-24)
      Cellular phenotype plasticity between the epithelial and mesenchymal states has been linked to metastasis and heterogeneous responses to cancer therapy, and remains a challenge for the treatment of triple-negative breast cancer (TNBC). Here, we used isogenic human breast epithelial cell lines, D492 and D492M, representing the epithelial and mesenchymal phenotypes, respectively. We employed a CRISPR-Cas9 ...

    • O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes 

      Barkovskaya, Anna; Seip, Kotryna; Hilmarsdòttir, Bylgja; Mælandsmo, Gunhild Mari; Moestue, Siver Andreas; Itkonen, Harri (Journal article; Tidsskriftartikkel; Peer reviewed, 2019-04-05)
      Post-translational modifcation of intracellular proteins with a single N-acetylglucosamine sugar (O-GlcNAcylation) regulates signaling, proliferation, metabolism and protein stability. In breast cancer, expression of the enzyme that catalyzes O-GlcNAcylation – O-GlcNAc-transferase (OGT), and the extent of protein O-GlcNAcylation, are upregulated in tumor tissue, and correlate with cancer progression. ...

    • Stroma-induced phenotypic plasticity offers phenotype-specific targeting to improve melanoma treatment 

      Seip, Kotryna; Jørgensen, Kjetil Nordbø; Haselager, Marco Vincent; Albrecht, Marco; Haugen, Mads Haugland; Egeland, Eivind Valen; Lucarelli, Philippe; Engebråten, Olav; Sauter, Thomas; Mælandsmo, Gunhild Mari; Prasmickaite, Lina (Journal article; Tidsskriftartikkel; Peer reviewed, 2018-09-18)
      Cancer cells' phenotypic plasticity, promoted by stromal cells, contributes to intra-tumoral heterogeneity and affects response to therapy. We have disclosed an association between fibroblast-stimulated phenotype switching and resistance to the clinically used BRAF inhibitor (BRAFi) vemurafenib in malignant melanoma, revealing a challenge in targeting the fibroblast-induced phenotype. Here we compared ...