Scientists demonstrated potent single-agent activity of anti-CD25 antibodies optimized to deplete Treg cells, while preserving IL-2-STAT5 signaling on effector T cells and show synergy with immune checkpoint blockade in vivo.
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CD25-T reg -depleting antibodies preserving IL-2 signaling on effector T cells enhance effector activation and antitumor immunity | Nature Cancer. (n.d.). Retrieved November 17, 2020, from https://www.nature.com/articles/s43018-020-00133-0 Cite
Investigators addressed the consequences of spleen tyrosine kinase (SYK) inhibition to leukemia stem-cell function and assessed SYK-associated pathways in acute myeloid leukemia cell biology.
[Cell Death & Disease]
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Researchers report that persistent activation of signal transducer and activator of transcription 5 in tumor-specific CD4+ T cells drives the development of polyfunctional T cells.
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Ding, Z.-C., Shi, H., Aboelella, N. S., Fesenkova, K., Park, E.-J., Liu, Z., Pei, L., Li, J., McIndoe, R. A., Xu, H., Piazza, G. A., Blazar, B. R., Munn, D. H., & Zhou, G. (2020). Persistent STAT5 activation reprograms the epigenetic landscape in CD4+ T cells to drive polyfunctionality and antitumor immunity. Science Immunology, 5(52). https://doi.org/10.1126/sciimmunol.aba5962 Cite
Using a recently developed specific inhibitor, the authors found that vacuolar protein sorting 34 inhibition induces apoptosis in acute myeloid leukemia cells but not in normal CD34+ hematopoietic cells.
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Scientists showed that STAT5 was the earliest factor binding and remodeling the Il9 locus to allow BATF binding in both mouse and human Th9 cultures.
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STAT5 promotes accessibility and is required for BATF-mediated plasticity at the Il9 locus | Nature Communications. (n.d.). Retrieved September 28, 2020, from https://www.nature.com/articles/s41467-020-18648-6 Cite
Scientists showed that IL‐2 signaling was required to maintain open chromatin at hundreds of gene regulatory elements, many of which control subsequent stimulus‐dependent alternative pathways of T cell differentiation.
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Mechanistically, tumor cells avidly consumed methionine and outcompeted T cells for methionine by expressing high levels of the methionine transporter SLC43A2.
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Bian, Y., Li, W., Kremer, D. M., Sajjakulnukit, P., Li, S., Crespo, J., Nwosu, Z. C., Zhang, L., Czerwonka, A., Pawłowska, A., Xia, H., Li, J., Liao, P., Yu, J., Vatan, L., Szeliga, W., Wei, S., Grove, S., Liu, J. R., … Zou, W. (2020). Cancer SLC43A2 alters T cell methionine metabolism and histone methylation. Nature, 1–6. https://doi.org/10.1038/s41586-020-2682-1 Cite
Scientists showed that 10,11-dehydrocurvularin (2–8 μM) dose-dependently inhibited the proliferation, migration and invasion of human breast cancer cell lines MDA-MB-231 and MDA-MB-468, and induced cell apoptosis.
[acta pharmacologica sinica]
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Isobologram analysis revealed that the signal transducer and activator of transcription (STAT) 5 inhibitor pimozide combined with enzalutamide had additive and synergistic inhibitory effects on cell viability in the used models.
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Erb, H. H. H., Bodenbender, J., Handle, F., Diehl, T., Donix, L., Tsaur, I., Gleave, M., Haferkamp, A., Huber, J., Fuessel, S., Juengel, E., Culig, Z., & Thomas, C. (2020). Assessment of STAT5 as a potential therapy target in enzalutamide-resistant prostate cancer. PLOS ONE, 15(8), e0237248. https://doi.org/10.1371/journal.pone.0237248 Cite
The authors analyzed 1,148 patient-derived B-cell leukemia samples, and found that individual mutations did not promote leukemogenesis unless they converged on one single oncogenic pathway that was characteristic of the differentiation stage of transformed B cells.