Magdalena Mieszkowska

ORCID: 0000-0003-1429-6693
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About
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Research Areas
  • Cancer Cells and Metastasis
  • Fibroblast Growth Factor Research
  • Cancer Immunotherapy and Biomarkers
  • Estrogen and related hormone effects
  • Cell Adhesion Molecules Research
  • Cancer, Stress, Anesthesia, and Immune Response
  • HER2/EGFR in Cancer Research
  • Monoclonal and Polyclonal Antibodies Research
  • Growth Hormone and Insulin-like Growth Factors
  • Inflammatory mediators and NSAID effects
  • Cancer, Hypoxia, and Metabolism
  • Protein Tyrosine Phosphatases
  • Hippo pathway signaling and YAP/TAZ
  • Cytokine Signaling Pathways and Interactions
  • Cellular Mechanics and Interactions

Gdańsk Medical University
2014-2020

RELX Group (Netherlands)
2019

Daejeon University
2019

Signaling mediated by growth factors receptors has long been suggested as one of the key responsible for failure endocrine treatment in breast cancer (BCa). Herein we present that presence tamoxifen, FGFs (Fibroblast Growth Factors) promote BCa cell with strongest effect being produced FGF7. FGFR2 was identified a mediator FGF7 action and FGFR2-induced signaling found to underlie cancer-associated fibroblasts-dependent resistance tamoxifen. FGF7/FGFR2-triggered pathway shown induce ER...

10.1016/j.neo.2017.07.006 article EN cc-by-nc-nd Neoplasia 2017-09-02

We have recently demonstrated that, fibroblast growth factor 2 (FGFR2), signalling via ribosomal S6 kinase (RSK2), promotes progression of breast cancer (BCa). Loss progesterone receptor (PR), whose activity in BCa cells can be stimulated by receptors (GFRs), is associated with poor patient outcome. Here we showed that FGF7/FGFR2 triggered phosphorylation PR at Ser294, ubiquitination and subsequent receptor`s degradation the 26S proteasome pathway cells. further RSK2 mediated...

10.18632/oncotarget.13322 article EN Oncotarget 2016-11-12

The members of p90 ribosomal S6 kinase (RSK) family Ser/Thr kinases are downstream effectors MAPK/ERK pathway that regulate diverse cellular processes including cell growth, proliferation and survival. In carcinogenesis, RSKs thought to modulate motility, invasion metastasis. Herein, we have studied an involvement in FGF2/FGFR2-driven behaviours mammary epithelial breast cancer cells. We found both silencing inhibiting FGFR2 attenuated phosphorylation RSKs, whereas overexpression and/or its...

10.1016/j.bbamcr.2014.06.022 article EN cc-by-nc-nd Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2014-07-08

The proposed involvement of CD151 in breast cancer (BCa) progression is based on findings from studies invasive ductal carcinoma (IDC). IDC and lobular (ILC) represent distinct disease entities. Here we evaluated clinical significance alone association with integrin α3β1 patients ILC context the data our recent study. Expression and/or was samples (N=117) using immunohistochemistry. were analysed relation to results an cohort (N=182) demonstrating a prognostic value expression CD151/integrin...

10.1038/bjc.2015.344 article EN cc-by-nc-sa British Journal of Cancer 2015-09-29

There are data to suggest that some ductal carcinoma in situ (DCIS) may evolve through an evolutionary bottleneck, where minor clones susceptible the imposed selective pressure drive disease progression. Here, we tested hypothesis impact of inflammatory environment on DCIS evolution is HER2-dependent, conferring proliferative dominance HER2-negative cells. In tissue samples, density tumour-infiltrating immune cells (TIICs) was associated only with high tumour nuclear grade, but 9%...

10.1016/j.neo.2020.09.003 article EN cc-by-nc-nd Neoplasia 2020-09-25

Breast cancer (BCa) is the most common affecting women worldwide. Overexpression of human epidermal growth factor receptor 2 (HER2) occurs in ~20‑25% invasive ductal breast carcinomas and associated with more aggressive phenotype. Herceptin, a humanized antibody against HER2, standard therapy HER2‑overexpressing cases. Approximately one‑third patients relapse despite treatment. Therefore numerous studies have investigated molecular mechanisms Herceptin resistance. An interaction between HER2...

10.3892/ol.2017.7493 article EN Oncology Letters 2017-11-27
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