Recruitment of myeloid-derived suppressor cells (MDSCs) into the tumor microenvironment (TME) contributes to cancer immune evasion. Scientists compared the growth and metastasis of melanoma and breast cancer xenografts in mice exhibiting or not exhibiting targeted deletion of Cxcr2 in myeloid cells.
[Cancer Immunology Research]
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Researchers evaluated the efficacy of Withaferin A, derived from the medicinal plant Withania Somnifera, as a novel therapeutic agent for the treatment of melanoma.
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Scientists showed that acetylsalicylic acid and salicylic acid present anticancer effects against a murine model of implanted melanoma. These effects were also validated in 3D- and 2D-cultured melanoma B16F10 cells, where the drugs promoted pro-apoptotic effects.
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Ausina, P., Branco, J. R., Demaria, T. M., Esteves, A. M., Leandro, J. G. B., Ochioni, A. C., Mendonça, A. P. M., Palhano, F. L., Oliveira, M. F., Abou-Kheir, W., Sola-Penna, M., & Zancan, P. (2020). Acetylsalicylic acid and salicylic acid present anticancer properties against melanoma by promoting nitric oxide-dependent endoplasmic reticulum stress and apoptosis. Scientific Reports, 10(1), 19617. https://doi.org/10.1038/s41598-020-76824-6 Cite
Scientists determined the role of autophagy in apoptosis and the generation of immunogenic signals using murine wild-type B16-F10 melanoma cells and cells with beclin-1 gene knockout.
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Prieto, K., Lozano, M. P., Urueña, C., Alméciga-Díaz, C. J., Fiorentino, S., & Barreto, A. (2020). The delay in cell death caused by the induction of autophagy by P2Et extract is essential for the generation of immunogenic signals in melanoma cells. Apoptosis. https://doi.org/10.1007/s10495-020-01643-z Cite
The authors focused on deubiquitinating enzymes, which regulate protein stability through ubiquitin–proteasome systems, and identified 26S proteasome non-ATPase regulatory subunit 14 (PSMD14) as a molecule related to melanoma growth using siRNA library screening.
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The authors revealed that the lncRNA LHFPL3-AS1-long, generated from the polypyrimidine tract binding protein 1-mediated splicing of the LHFPL3-AS1 precursor, upregulated B-cell lymphoma-2 (BCL2) protein to contribute to tumorigenesis of melanoma stem cells.
[Cell Death & Disease]
Scientists demonstrated a general strategy to fabricate personalized nanovaccines based on a cationic fluoropolymer for post-surgical cancer immunotherapy.
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Xu, J., Lv, J., Zhuang, Q., Yang, Z., Cao, Z., Xu, L., Pei, P., Wang, C., Wu, H., Dong, Z., Chao, Y., Wang, C., Yang, K., Peng, R., Cheng, Y., & Liu, Z. (2020). A general strategy towards personalized nanovaccines based on fluoropolymers for post-surgical cancer immunotherapy. Nature Nanotechnology, 1–10. https://doi.org/10.1038/s41565-020-00781-4 Cite
Investigators developed a bone marrow-avid nanobiologic platform designed specifically to induce trained immunity. They established the potent anti-tumor capabilities of our lead candidate MTP 10-HDL in a B16F10 mouse melanoma model.
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Priem, B., Leent, M. M. T. van, Teunissen, A. J. P., Sofias, A. M., Mourits, V. P., Willemsen, L., Klein, E. D., Oosterwijk, R. S., Meerwaldt, A. E., Munitz, J., Prévot, G., Verschuur, A. V., Nauta, S. A., Leeuwen, E. M. van, Fisher, E. L., Jong, K. A. M. de, Zhao, Y., Toner, Y. C., Soultanidis, G., … Mulder, W. J. M. (2020). Trained Immunity-Promoting Nanobiologic Therapy Suppresses Tumor Growth and Potentiates Checkpoint Inhibition. Cell, 183(3), 786-801.e19. https://doi.org/10.1016/j.cell.2020.09.059 Cite
The authors focus on the major alterations affecting lipid storage organelles and lipid metabolism, discuss how glycerophospholipids, sphingolipids, sterols and eicosanoids metabolic dysregulations contribute to the phenotype plasticity of melanoma cells and/or melanoma aggressiveness, and highlight therapeutic approaches targeting lipid metabolism that could be applicable for melanoma treatment.
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Investigators describe the functional characterization of acetylcholine receptors in different tumor types, placing attention on melanoma.
Scientists demonstrated that ABL1/2 kinase activities and/or expression were potentiated in cell lines and patient samples following resistance, and ABL1/2 drove BRAF and BRAF/MEK inhibitor resistance by inducing reactivation of MEK/ERK/MYC signaling.
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Tripathi, R., Liu, Z., Jain, A., Lyon, A., Meeks, C., Richards, D., Liu, J., He, D., Wang, C., Nespi, M., Rymar, A., Wang, P., Wilson, M., & Plattner, R. (2020). Combating acquired resistance to MAPK inhibitors in melanoma by targeting Abl1/2-mediated reactivation of MEK/ERK/MYC signaling. Nature Communications, 11(1), 5463. https://doi.org/10.1038/s41467-020-19075-3 Cite