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Evolving Immunotherapy Strategies in Gastrointestinal Neuroendocrine Neoplasms.
Curr Treat Options Oncol
January 2025
The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Treatment for neuroendocrine neoplasms (NENs) is tailored to the tumor's site of origin, grade, and differentiation. NENs are categorized into two main types: well-differentiated neuroendocrine tumors (NETs), which tend to grow more slowly and are less aggressive, and poorly differentiated neuroendocrine carcinomas (NECs), which are highly aggressive and harder to treat. Treatment options for NETs range from somatostatin analogues and mTOR inhibitors to peptide receptor radionuclide therapy (PRRT) with Lutetium-177 dotatate.
View Article and Find Full Text PDFGeneration of chimeric forms of rhesus macaque rhadinovirus expressing KSHV envelope glycoproteins gH and gL for utilization in an NHP model of infection.
J Virol
January 2025
Vaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton, Oregon, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with Kaposi's sarcoma and B cell malignancies. Like all herpesviruses, KSHV contains conserved envelope glycoproteins (gps) involved in virus binding, entry, assembly, and release from infected cells, which are also targets of the immune response. Due to the lack of a reproducible animal model of KSHV infection, the precise functions of the KSHV gps during infection are not completely known.
View Article and Find Full Text PDFPharmacologically induced proteolysis of histone deacetylase-6 attenuates influenza virus replication despite limited anti-tumor effects.
Life Sci
January 2025
Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Electronic address:
The protein deacetylase HDAC6 has been controversially linked to cancer cell proliferation and viral propagation. We analyzed whether a pharmacological depletion of HDAC6 with a recent proteolysis-targeting chimera (PROTAC) kills tumor cells. We show that low micromolar doses of the cereblon-based PROTAC TH170, but not its inactive analog TH170E, induce proteasomal degradation of HDAC6.
View Article and Find Full Text PDFArticle Synopsis
- FT596 is a novel cancer therapy using iPSC-derived CAR NK cells targeting CD19, designed to assess its safe dosage and effectiveness alone and with rituximab in patients with B-cell lymphoma.
- This phase 1 trial involved patients with relapsed or refractory B-cell lymphoma, administering FT596 after chemotherapy, with separate regimens for those receiving rituximab and those who did not.
- The study measured potential side effects while determining the optimal dose of FT596 and allowed modifications to the treatment based on patient tolerance and response.
Msh2-Msh3 DNA-binding is not sufficient to promote trinucleotide repeat expansions in Saccharomyces cerevisiae.
Genetics
January 2025
Department of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY 14203, USA.
Mismatch repair (MMR) is a highly conserved DNA repair pathway that recognizes mispairs that occur spontaneously during DNA replication and coordinates their repair. In Saccharomyces cerevisiae, Msh2-Msh3 and Msh2-Msh6 initiate MMR by recognizing and binding insertion deletion loops (in/dels) up to ∼ 17 nucleotides (nt.) and base-base mispairs, respectively; the two complexes have overlapping specificity for small (1-2 nt.
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