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http://dx.doi.org/10.1001/jamadermatol.2023.5338 | DOI Listing |
Protein Pept Lett
January 2025
Scientific Research Center, Beijing ChosenMed Clinical Laboratory Co., Ltd. Beijing100176, China.
Background: The role of Zona pellucida glycoprotein 3 (ZP3) is unclear in pancreatic adenocarcinoma (PAAD).
Objective: This study aimed to explore the role of ZP3 in PAAD.
Methods: A comparative analysis of ZP3 gene expression was performed to discern differences between various types of cancer and PAAD, leveraging data sourced from The Cancer Genome Atlas (TCGA).
Nat Med
January 2025
Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
The MEK inhibitor selumetinib induces objective responses and provides clinical benefit in children with neurofibromatosis type 1 (NF1) and inoperable plexiform neurofibromas (PNs). To evaluate whether similar outcomes were possible in adult patients, in whom PN growth is generally slower than in pediatric patients, we conducted an open-label phase 2 study of selumetinib in adults with NF1 PNs. The study was designed to evaluate objective response rate (primary objective), tumor volumetric responses, patient-reported outcomes and pharmacodynamic effects in PN biopsies.
View Article and Find Full Text PDFJpn J Clin Oncol
January 2025
Department of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65-Tsurumai, Showa, Nagoya, 466-8560, Japan.
Objective: In Japan, selumetinib is used in pediatric patients with neurofibromatosis type 1 (NF1) and symptomatic inoperable plexiform neurofibroma (PN). However, there have been no real-world reports on Japanese patients. In this study, we reported a single-center, short-term experience with selumetinib after its approval in Japan.
View Article and Find Full Text PDFNat Commun
December 2024
Institute of Human Genetics, University Hospital, Friedrich-Schiller-Universität Jena, 07740, Jena, Germany.
Brain organoids offer unprecedented insights into brain development and disease modeling and hold promise for drug screening. Significant hindrances, however, are morphological and cellular heterogeneity, inter-organoid size differences, cellular stress, and poor reproducibility. Here, we describe a method that reproducibly generates thousands of organoids across multiple hiPSC lines.
View Article and Find Full Text PDFCancers (Basel)
November 2024
Institute of Biostructures and Bioimaging, National Research Council, 80145 Naples, Italy.
Background: Oncogene-driven NSCLC is usually treated with targeted therapies using tyrosine kinase inhibitors (TKIs) to inhibit oncogene downstream signaling pathways, affecting tumor survival and proliferation. EGFR- and KRAS-mutant NSCLCs are the most represented subtypes, and they are treated in clinical practice with oncogene-targeting drugs in the first and second line, respectively. Unfortunately, the development of oncogene-independent resistant clones limits TKI efficacy.
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