The authors focus on brain microenvironment features impacted by tumor biology. They also discuss limits of current preclinical models and how complementary models, such as humanized animals and organoids, will allow deeper mechanistic insights on cancer biology, allowing for more efficient testing of therapeutic strategies, including immunotherapy, for brain cancers.
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Researchers isolated macrophages from mice and humans, polarized them ex vivo, and examined their functional interaction with breast cancer cells in culture and in mice.
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Gómez, V., Eykyn, T. R., Mustapha, R., Flores-Borja, F., Male, V., Barber, P. R., Patsialou, A., Green, R., Panagaki, F., Li, C. W., Fruhwirth, G. O., Ros, S., Brindle, K. M., & Ng, T. (2020). Breast cancer–associated macrophages promote tumorigenesis by suppressing succinate dehydrogenase in tumor cells. Science Signaling, 13(652). https://doi.org/10.1126/scisignal.aax4585 Cite
Researchers identified the dual function cytokine IL-33 as an orchestrator of the glioblastoma microenvironment that contributed to tumorigenesis.
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Glioma-derived IL-33 orchestrates an inflammatory brain tumor microenvironment that accelerates glioma progression | Nature Communications. (n.d.). Retrieved October 5, 2020, from https://www.nature.com/articles/s41467-020-18569-4 Cite
The hybrid cell membrane nanovesicles blocked CD47-signal regulatory protein alpha signaling axis while promoting M2-to-M1 repolarization within the tumor microenvironment, significantly preventing both local recurrence and distant metastasis in malignant melanoma models.
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Rao, L., Wu, L., Liu, Z., Tian, R., Yu, G., Zhou, Z., Yang, K., Xiong, H.-G., Zhang, A., Yu, G.-T., Sun, W., Xu, H., Guo, J., Li, A., Chen, H., Sun, Z.-J., Fu, Y.-X., & Chen, X. (2020). Hybrid cellular membrane nanovesicles amplify macrophage immune responses against cancer recurrence and metastasis. Nature Communications, 11(1), 4909. https://doi.org/10.1038/s41467-020-18626-y Cite
This study displayed histological and immunohistochemical analyses of a malignant tumor model developed from cancer stem cells converted from human iPSCs in a cancer microenvironment prepared from the conditioned medium of a pancreatic cancer cell line.
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The hepatocellular carcinoma ecosystem displayed features reminiscent of fetal development, including re-emergence of fetal-associated endothelial cells and fetal-like tumor-associated macrophages.
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Sharma, A., Seow, J. J. W., Dutertre, C.-A., Pai, R., Blériot, C., Mishra, A., Wong, R. M. M., Singh, G. S. N., Sudhagar, S., Khalilnezhad, S., Erdal, S., Teo, H. M., Khalilnezhad, A., Chakarov, S., Lim, T. K. H., Fui, A. C. Y., Chieh, A. K. W., Chung, C. P., Bonney, G. K., … DasGupta, R. (2020). Onco-fetal Reprogramming of Endothelial Cells Drives Immunosuppressive Macrophages in Hepatocellular Carcinoma. Cell, 0(0). https://doi.org/10.1016/j.cell.2020.08.040 Cite
Researchers investigated whether the down-regulation of Scm-like with four mbt domains 2 (SFMBT2) regulated the infiltration of preadipocytes and tumor-associated macrophages in prostate cancer.
The tumor microenvironment (TME) is a highly complex environment that surrounds tumors. Interactions between cancer cells/non-cancerous cells and cells/non-cell components in the TME support tumor initiation, development, and metastasis. Of the cell types in the TME, tumor-associated macrophages (TAMs) have gained attention owing to their crucial roles in supporting tumors and conferring therapy resistance.
[Trends in Pharmacological Sciences]
The authors demonstrated that P2X7 was highly expressed in tumor-associated macrophages (TAMs) and that P2X7 deficiency impaired the “M2-like” polarization of TAMs via down-regulation of STAT6 and IRF4 phosphorylation both in vivo and in vitro.
[Cancer Immunology Research]
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Non-enzymatic chitinase-3 like-protein-1 (CHI3L1) binds to chitin, heparin, and hyaluronic acid, and is regulated by ECM changes, cytokines, growth factors, drugs, and stress. This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis, then posits investigational strategies for targeted therapies.
[Signal Transduction and Targeted Therapy]
Scientists showed that Epstein–Barr virus could promote the expression of p-ATR and M2-type TAMs transformation in clinical nasopharyngeal carcinoma specimens.
[Cell Death & Disease]