Currently, in the absence of BRAFV600 mutation, the management of advanced melanomas is based on immunotherapies, but only half of the patients are responders. RAF1 (also named CRAF) fusions occur in 1-2.1% of wild-type melanomas. Preclinical data suggest that the presence of RAF fusion may be sensitive to MEK inhibitors. We report the case of a patient with an advanced melanoma harboring an EFCC1-RAF1 fusion who showed a clinical benefit from and a partial response to a MEK inhibitor.
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http://dx.doi.org/10.1097/CMR.0000000000000882 | DOI Listing |
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 PDFSci Rep
January 2025
Department of Mechanical Engineering, Adama Science and Technology University, Adama, Ethiopia.
Recycled engine oil was produced from used engine oil (15W-40) using a combination of MEK and 1-butanol solvents with an activated carbon adsorbent through the adsorption process. The experimental design matrix was prepared using Box-Behnken design (BBD) package within RSM, and recycled engine oil is optimized by response surface methodology (RSM). By varying solvent-to-oil ratio, the temperature and contact duration optimal conditions were identified as a 5.
View Article and Find Full Text PDFTrends Cancer
December 2024
Department of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA; Immunology and Microbiology Program, University of Massachusetts Chan Medical School, Worcester, MA, USA; Cancer Center, University of Massachusetts Chan Medical School, Worcester, MA, USA. Electronic address:
Chronic damage following oncogene induction or cancer therapy can produce cellular senescence. Senescent cells not only exit the cell cycle but communicate damage signals to their environment that can trigger immune responses. Recent work has revealed that senescent tumor cells are highly immunogenic, leading to new ways to activate antitumor immunosurveillance and potentiate T cell-directed immunotherapies.
View Article and Find Full Text PDFCancer Sci
December 2024
Department of Molecular Oncology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Patient-derived organoids represent a novel platform to recapitulate the cancer cells in the patient tissue. While cancer heterogeneity has been extensively studied by a number of omics approaches, little is known about the spatiotemporal kinase activity dynamics. Here we applied a live imaging approach to organoids derived from 10 pancreatic ductal adenocarcinoma (PDAC) patients to comprehensively understand their heterogeneous growth potential and drug responses.
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December 2024
School of Medicine, Cardiff University, Henry Wellcome Building, Cardiff, CF14 4XN, UK.
Most pancreatic cancer patients are diagnosed at advanced stages, with poor survival rates and drug resistance making pancreatic cancer one of the highest causes of cancer death in the UK. Understanding the underlying mechanism behind its carcinogenesis, metastasis and drug resistance has become an essential task for researchers. We have discovered that a well-established tumour suppressor, EPLIN, has an oncogenic rather than suppressive role in pancreatic cancer.
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