We studied the effect of cyclopentenyl cytosine (CPEC) on human neuroblastoma SK-N-BE(2)-C cell line cells. CPEC had an IC50 value of 100 nM for non-synchronised SK-N-BE(2)-C cells. These cells were arrested in G0/G1-phase or early S-phase of the cell cycle upon treatment with CPEC. After treatment of synchronised S-phase cells with 1 microM CPEC, the number of cells present after 3 days was less than 10% of that observed for the untreated cells. S-phase synchronised cells treated with CPEC and deoxycytidine showed an increased viability in comparison with cells treated with CPEC alone. Approximately 15% of the cells treated with CPEC and deoxycytidine traversed through one cell cycle. The amount of CTP declined to undetectable levels within 3 h after addition of 1 microM CPEC. The presence of cytidine prevented, to a large extent, the cytostatic effect of CPEC.
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http://dx.doi.org/10.1016/0959-8049(95)00071-p | DOI Listing |
Exp Hematol Oncol
January 2025
Department of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Background: Several approaches are being explored for engineering off-the-shelf chimeric antigen receptor (CAR) T cells. In this study, we engineered chimeric Fcγ receptor (FcγR) T cells and tested their potential as a versatile platform for universal T cell therapy.
Methods: Chimeric FcγR (CFR) constructs were generated using three distinct forms of FcγR, namely CD16A, CD32A, and CD64.
J Transl Med
January 2025
Department of Biomedical and Biotechnological Sciences, Division of Medical Biochemistry, University of Catania, Catania, Italy.
Background: Clonal myeloproliferation and fibrotic transformation of the bone marrow (BM) are the pathogenetic events most commonly occurring in myelofibrosis (MF). There is great evidence indicating that tumor microenvironment is characterized by high lactate levels, acting not only as an energetic source, but also as a signaling molecule.
Methods: To test the involvement of lactate in MF milieu transformation, we measured its levels in MF patients' sera, eventually finding a massive accumulation of this metabolite, which we showed to promote the expansion of immunosuppressive subsets.
J Exp Clin Cancer Res
January 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with limited treatment options and a poor prognosis. The critical role of epigenetic alterations such as changes in DNA methylation, histones modifications, and chromatin remodeling, in pancreatic tumors progression is becoming increasingly recognized. Moreover, in PDAC these aberrant epigenetic mechanisms can also limit therapy efficacy.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of Nephrology, Affiliated Hospital of Jiaxing University (The First Hospital of Jiaxing), No.1882, Zhonghuan North Road, Jiaxing, 314000, Zhejiang, China.
Background: Dysfunction in podocyte mitophagy has been identified as a contributing factor to the onset and progression of diabetic nephropathy (DN), and BMAL1 plays an important role in the regulation of mitophagy. Thus, this study intended to examine the impact of BMAL1 on podocyte mitophagy in DN and elucidate its underlying mechanisms.
Materials And Methods: High D-glucose (HG)-treated MPC5 cells was used as a podocyte injury model for investigating the potential roles of BMAL1 in DN.
Cancer Cell Int
January 2025
Department of Immuno-Oncology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China.
Background: Patients with lung adenocarcinoma (LUAD) receiving drug treatment often have an unpredictive response and there is a lack of effective methods to predict treatment outcome for patients. Dendritic cells (DCs) play a significant role in the tumor microenvironment and the DCs-related gene signature may be used to predict treatment outcome. Here, we screened for DC-related genes to construct a prognostic signature to predict prognosis and response to immunotherapy in LUAD patients.
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