Publications by authors named "T Lagerweij"

Article Synopsis
  • Cancer-secreted extracellular vesicles (EVs) induce a unique type of mesenchymal stem cells (iMSCs) that contribute to therapy resistance in bone cancers like osteosarcoma and multiple myeloma.
  • EVs alter the MSC transcriptome and drive the development of iMSCs, which can eliminate the benefits of therapies aimed at reducing metastasis.
  • Targeting EV-induced pathways with a combination of drugs has shown promise in overcoming iMSC-induced resistance, providing potential strategies to enhance treatment effectiveness in patients.
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Background Appropriate treatment of pulmonary hypertension (PH) is critically dependent on accurate discrimination between pre- and postcapillary PH. However, clinical discrimination is challenging and frequently requires a right heart catheterization. Existing risk scores to detect postcapillary PH have suboptimal discriminatory strength.

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Introduction: Glioblastoma (GBM) is an incurable cancer type. New therapeutic options are investigated, including targeting the mitogen-activated protein kinase (MAPK) pathway using MEK inhibitors as radio-sensitizers. In this study, we investigated whether MEK inhibition via PD0325901 leads to radio-sensitization in experimental in vitro and in vivo models of GBM.

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: Recent studies suggested that extracellular vesicles (EVs) play a role both in the metastatic niche formation and in the progression of several tumors, including pancreatic cancer. In particular, the effects of EVs on metastasis should be studied in model systems that take into account both the tumor cells and the metastatic site/tumor microenvironment. Studies with labeled EVs or EV-secreting cells in models will reflect the physiological and pathological functions of EVs.

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Background: Pancreatic ductal adenocarcinoma (PDAC) is a very lethal disease, with minimal therapeutic options. Aberrant tyrosine kinase activity influences tumor growth and is regulated by phosphorylation. We investigated phosphorylated kinases as target in PDAC.

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