Publications by authors named "M Bootsma"

In preclinical studies, p53 loss of function impacts chemotherapy response, but this has not been consistently validated clinically. We trained a TP53-loss phenocopy gene expression signature from pan-cancer clinical samples in the TCGA. In vitro, the TP53-loss phenocopy signature predicted chemotherapy response across cancer types.

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Therapies against cell-surface targets (CSTs) represent an emerging treatment class in solid malignancies. However, high-throughput investigations of CST expression across cancer types have been reliant on data sets of mostly primary tumors, despite therapeutic use most commonly in metastatic disease. We identified a total of 818 clinical trials of CST therapies with 78 CSTs.

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Background: Hypothesizing that early treatment yields improved prognosis, we aimed to investigate how the timing of immunosuppressive treatment relates to interstitial lung disease (ILD) development and the course of pulmonary function in systemic sclerosis (SSc).

Methods: A cohort was created using data from the EUSTAR database and Nijmegen Systemic Sclerosis cohort, including adult patients who started their first immunosuppressive treatment (ie mycophenolate mofetil, methotrexate, cyclophosphamide, tocilizumab or rituximab) after SSc diagnosis, and no signs of ILD on high-resolution CT. ILD-free survival and the course of forced vital capacity % predicted (ppFVC) were assessed for up to 5 years follow-up comparing patients who started early (disease duration ≤ 3 years) vs late with immunosuppression.

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Article Synopsis
  • The study explores how three-dimensional genomic structure variations impact gene expression and mutation rates in metastatic castration-resistant prostate cancer, using a combination of advanced sequencing techniques on 80 biopsy samples.
  • Findings revealed significant differences in gene expression, methylation patterns, and structural variations between different chromatin compartments, along with specific chromatin contact loss at the AR locus linked to poor treatment responses.
  • The research identified distinct subtypes of tumors based on their methylation and gene expression profiles, suggesting that DNA interactions could contribute to structural variant formation, ultimately enhancing understanding of tumor behavior and treatment outcomes.
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