Scientists examined the feasibility of simultaneous ABCB1/ABCG2 inhibition with i.v. co-infusion of erlotinib and tariquidar by studying brain distribution of the model ABCB1/ABCG2 substrate [11C]erlotinib in mice and rhesus macaques with PET. Tolerability of the erlotinib/tariquidar combination was assessed in human embryonic stem cell-derived cerebral organoids.
[Journal of Cerebral Blood Flow and Metabolism]
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Tournier, N., Goutal, S., Mairinger, S., Lozano, I. H., Filip, T., Sauberer, M., Caillé, F., Breuil, L., Stanek, J., Freeman, A. F., Novarino, G., Truillet, C., Wanek, T., & Langer, O. (2020). Complete inhibition of ABCB1 and ABCG2 at the blood–brain barrier by co-infusion of erlotinib and tariquidar to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib: Journal of Cerebral Blood Flow & Metabolism. https://doi.org/10.1177/0271678X20965500 Cite
The authors describe a method to study whole-tissue extracellular matrix (ECM) effects from disease states associated with metastasis on tumor cell phenotypes and identified the individual ECM proteins and signaling pathways that were driving these effects. They showed that decellularized ECM from tumor-bearing and obese mammary glands drives TNBC cell invasion.
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Decellularized extracellular matrix scaffolds identify full-length collagen VI as a driver of breast cancer cell invasion in obesity and metastasis | Science Advances. (n.d.). Retrieved October 21, 2020, from https://advances.sciencemag.org/content/6/43/eabc3175 Cite
Researchers explored the underlying mechanisms behind treatment resistance and the lack of success with anti-EGFR therapy in the clinic. After generating a number of treatment resistant Glioblastoma cell lines they observed that resistant cell lines lacked EGFR activation and expression.
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Areeb, Z., Stuart, S. F., West, A. J., Gomez, J., Nguyen, H. P. T., Paradiso, L., Zulkifli, A., Jones, J., Kaye, A. H., Morokoff, A. P., & Luwor, R. B. (2020). Reduced EGFR and increased miR-221 is associated with increased resistance to temozolomide and radiotherapy in glioblastoma. Scientific Reports, 10(1), 17768. https://doi.org/10.1038/s41598-020-74746-x Cite
The authors identified RFPL3 as a potential import cargo for IPO13, which was found to be overexpressed in NSCLC cells and tissues.
[Cell Death & Disease]
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Zohud, B. A., Guo, P., Zohud, B. A., Li, F., Hao, J. J., Shan, X., Yu, W., Guo, W., Qin, Y., & Cai, X. (2020). Importin 13 promotes NSCLC progression by mediating RFPL3 nuclear translocation and hTERT expression upregulation. Cell Death & Disease, 11(10), 1–15. https://doi.org/10.1038/s41419-020-03101-9 Cite
Scientists used patient-derived organoids derived from a familial adenomatous polyposis patient to analyze the response to chemotherapeutic agents targeting EGFR, BRAF and MEK.
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Osumi, H., Muroi, A., Sakahara, M., Kawachi, H., Okamoto, T., Natsume, Y., Yamanaka, H., Takano, H., Kusama, D., Shinozaki, E., Ooki, A., Yamaguchi, K., Ueno, M., Takeuchi, K., Noda, T., Nagayama, S., Koshikawa, N., & Yao, R. (2020). Evaluation of the RAS signaling network in response to MEK inhibition using organoids derived from a familial adenomatous polyposis patient. Scientific Reports, 10(1), 17455. https://doi.org/10.1038/s41598-020-74530-x Cite
Scientists discuss the possibility of using various approved drugs, or drugs currently in clinical development, to treat COVID-19. They suggest to enhance STAT1 activity and/or inhibit STAT3 functions for COVID-19 treatment.
[Cell Death & Differentiation]
The authors report a physiologically relevant assay enabling quantitative analysis of metastatic capacity of tumor cells following implantation into the CAM. Engraftment of as few as 103 non-small cell lung cancer and prostate cancer cell lines was sufficient for both primary tumor and metastasis formation.
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Pawlikowska, P., Tayoun, T., Oulhen, M., Faugeroux, V., Rouffiac, V., Aberlenc, A., Pommier, A. L., Honore, A., Marty, V., Bawa, O., Lacroix, L., Scoazec, J. Y., Chauchereau, A., Laplace-Builhe, C., & Farace, F. (2020). Exploitation of the chick embryo chorioallantoic membrane (CAM) as a platform for anti-metastatic drug testing. Scientific Reports, 10(1), 16876. https://doi.org/10.1038/s41598-020-73632-w Cite
The role of S6K1 in tyrosine kinase inhibitor resistance was determined in in vitro gain-and-loss of function studies and confirmed in subcutaneous and orthotopic mouse lung cancer models.
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Shen, H., Wang, G.-C., Li, X., Ge, X., Wang, M., Shi, Z.-M., Bhardwaj, V., Wang, Z.-X., Zinner, R. G., Peiper, S. C., Aplin, A. E., Jiang, B.-H., & He, J. (2020). S6K1 blockade overcomes acquired resistance to EGFR-TKIs in non-small cell lung cancer. Oncogene, 1–15. https://doi.org/10.1038/s41388-020-01497-4 Cite
The authors identified a 23-hydroxybetulinic acid derivative, namely DPBA, as a novel epidermal growth factor receptor (EGFR) small-molecule ligand. It exerted potent in vitro and in vivo anticancer activity in both EGFR wild type and mutant non-small cell lung cancer by degrading EGFR.
[Signal Transduction and Targeted Therapy]
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Yao, N., Wang, C.-R., Liu, M.-Q., Li, Y.-J., Chen, W.-M., Li, Z.-Q., Qi, Q., Lu, J.-J., Fan, C.-L., Chen, M.-F., Qi, M., Li, X.-B., Hong, J., Zhang, D.-M., & Ye, W.-C. (2020). Discovery of a novel EGFR ligand DPBA that degrades EGFR and suppresses EGFR-positive NSCLC growth. Signal Transduction and Targeted Therapy, 5(1), 1–13. https://doi.org/10.1038/s41392-020-00251-2 Cite
Researchers investigated the potential role and mechanism of calreticulin in regulating intracellular free Ca2+ dependent acute and chronic endoplasmic reticulum stress-induced epithelial-mesenchymal transition in pancreatic camcer in vitro and vivo.
[Journal of Experimental & Clinical Cancer Research]
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Sheng, W., Wang, G., Tang, J., Shi, X., Cao, R., Sun, J., Lin, Y. H., Jia, C., Chen, C., Zhou, J., & Dong, M. (2020). Calreticulin promotes EMT in pancreatic cancer via mediating Ca2+ dependent acute and chronic endoplasmic reticulum stress. Journal of Experimental & Clinical Cancer Research, 39(1), 209. https://doi.org/10.1186/s13046-020-01702-y Cite
75% of adenocarcinomas lack targeted therapies due to scarcity of druggable drivers. The authors classified tumors based on signaling similarities and discovered subgroups within this unmet patient population.
[Clinical Cancer Research]
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Daemen, A., Cooper, J., Myrta, S., Wongchenko, M. J., Lin, E., Long, J. E., Foreman, O., Modrusan, Z., Tremayne, J. R., Cruz, C. C. de la, Merchant, M., Martin, S. E., Yan, Y., & Junttila, M. R. (2020). Transcriptional subtypes resolve tumor heterogeneity and identify vulnerabilities to MEK inhibition in lung adenocarcinoma. Clinical Cancer Research. https://doi.org/10.1158/1078-0432.CCR-20-1835 Cite