Scientists showed that tumor-secreted protease cathepsin C promotes breast-to-lung metastasis by regulating recruitment of neutrophils and formation of neutrophil extracellular traps.
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Xiao, Y., Cong, M., Li, J., He, D., Wu, Q., Tian, P., Wang, Y., Yang, S., Liang, C., Liang, Y., Wen, J., Liu, Y., Luo, W., Lv, X., He, Y., Cheng, D., Zhou, T., Zhao, W., Zhang, P., … Hu, G. (2021). Cathepsin C promotes breast cancer lung metastasis by modulating neutrophil infiltration and neutrophil extracellular trap formation. Cancer Cell, 0(0). https://doi.org/10.1016/j.ccell.2020.12.012 Cite
Investigators demonstrated that STING was a critical regulator of nociception through type-I interferon signaling in peripheral nociceptive sensory neurons.
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Donnelly, C. R., Jiang, C., Andriessen, A. S., Wang, K., Wang, Z., Ding, H., Zhao, J., Luo, X., Lee, M. S., Lei, Y. L., Maixner, W., Ko, M.-C., & Ji, R.-R. (2021). STING controls nociception via type I interferon signalling in sensory neurons. Nature, 1–6. https://doi.org/10.1038/s41586-020-03151-1 Cite
The authors provides a comprehensive summary of the processes regulated by tumor-associated cells that promote the immune escape of melanoma cells.
[International Journal of Molecular Sciences]
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Scientists discuss recent breakthroughs in the field and highlight different models for functional ex vivo organoid or enteroidderived culture systems.
[Current Opinion in Microbiology]
Montefiore Health System and Albert Einstein College of Medicine have received a five-year, $111 million grant from the National Cancer Institute to lead this research consortium.
Researchers showed that the non-nucleoside reverse transcriptase inhibitors, SPV122 in combination with MEK inhibitors strongly inhibited BRAF-mutant melanoma cell growth, induced apoptosis, and delayed the emergence of resistance to target therapy in vitro.
[Cell Communication and Signaling]
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Fattore, L., Malpicci, D., Milite, C., Castellano, S., Sbardella, G., Botti, G., Ascierto, P. A., Mancini, R., & Ciliberto, G. (2020). Reverse transcriptase inhibition potentiates target therapy in BRAF-mutant melanomas: effects on cell proliferation, apoptosis, DNA-damage, ROS induction and mitochondrial membrane depolarization. Cell Communication and Signaling, 18(1), 150. https://doi.org/10.1186/s12964-020-00633-7 Cite
Scientists demonstratd that sphingosine kinase 2 functioned during lymphocytic choriomeningitis virus Cl 13 infection to limit T cell immune pathology, which subsequently aided in the establishment of virus-induced immunosuppression and the resultant viral persistence.
[Journal of Clinical Investigation]
Researchers investigated whether REV-ERB activity regulates HIV-1 replication and found REV-ERB agonists inhibited HIV-1 promoter activity in cell lines, primary human CD4 T cells and macrophages, whilst antagonism or genetic disruption of REV-ERB increased promoter activity.
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Borrmann, H., Davies, R., Dickinson, M., Pedroza-Pacheco, I., Schilling, M., Vaughan-Jackson, A., Magri, A., James, W., Balfe, P., Borrow, P., McKeating, J. A., & Zhuang, X. (2020). Pharmacological activation of the circadian component REV-ERB inhibits HIV-1 replication. Scientific Reports, 10(1), 13271. https://doi.org/10.1038/s41598-020-70170-3 Cite
Scientists investigated the in vivo regulation of IFN-γ production by CD8+ T cells, DN T cells and NK cells in response to acute Toxoplasma gondii infection.
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Kupz, A., Pai, S., Giacomin, P. R., Whan, J. A., Walker, R. A., Hammoudi, P.-M., Smith, N. C., & Miller, C. M. (2020). Treatment of mice with S4B6 IL-2 complex prevents lethal toxoplasmosis via IL-12- and IL-18-dependent interferon-gamma production by non-CD4 immune cells. Scientific Reports, 10(1), 13115. https://doi.org/10.1038/s41598-020-70102-1 Cite
As large trials get underway to test the vaccines needed to stop the global coronavirus pandemic, one group has realized it is being left out and is not happy: people living with HIV.
Researchers summarize current knowledge on the role of the C-C chemokine ligand 5/C-C chemokine receptor type 5 (CCL5/CCR5) axis in cancer.
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