Investigators observed that Lin28B was up‐regulated in pancreatic cancer, contributing to cellular migration and proliferation. Nuclear Lin28B upregulated TET3 mRNA and protein levels by blocking the production of mature let‐7i.
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Researchers isolated epithelial cell adhesion molecule-positive biliary epithelial cells from the mouse intrahepatic bile duct, gallbladder, and extrahepatic bile duct and established organoids derived from these cells.
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Kasuga, A., Semba, T., Sato, R., Nobusue, H., Sugihara, E., Takaishi, H., Kanai, T., Saya, H., & Arima, Y. (n.d.). Oncogenic KRAS–expressing organoids with biliary epithelial stem cell properties give rise to biliary tract cancer in mice. Cancer Science, n/a(n/a). https://doi.org/10.1111/cas.14703 Cite
The authors summarize the regulatory mode of post-translational modifications on KRAS. They also highlight the recent studies targeting these modifications having exhibited potent anti-tumor activities, including in prostate cancer.
[Acta Pharmacologica Sinica]
Investigators uncovered that ERK3, a ubiquitously expressed atypical MAPK, was required for KRAS-mediated NSCLC tumors. ERK3 is highly expressed in lung cancers, and oncogenic KRAS led to the activation and stabilization of the ERK3 protein.
[Cancer Gene Therapy]
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Using a lipidomic screen, scientists found that PLCγ1 was suppressed during hypoxia in KRAS-mutant human lung adenocarcinoma cancer cell lines.
[Nature Cell Biology]
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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
Amgen announced positive topline Phase II results from the CodeBreaK 100 clinical study, evaluating sotorasib in 126 patients with KRAS G12C-mutant advanced non-small cell lung cancer, who had failed a median of two prior lines of anti-cancer therapies.
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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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The authors focus on recent pre-clinical and clinical advances in therapies targeting aberrant genes and pathways and predict the future trend of precision oncology for pancreatic ductal adenocarcinoma.
[Journal of Hematology & Oncology]
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Scientists interrogated purified sorted tumor fractions from a series of 15 tumor samples with whole-genome copy-number variant, whole-exome sequencing, and assay for transposase-accessible chromatin using sequencing analyses.
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Lenkiewicz, E., Malasi, S., Hogenson, T. L., Flores, L. F., Barham, W., Phillips, W. J., Roesler, A. S., Chambers, K. R., Rajbhandari, N., Hayashi, A., Antal, C. E., Downes, M., Grandgenett, P. M., Hollingsworth, M. A., Cridebring, D., Xiong, Y., Lee, J.-H., Ye, Z., Yan, H., … Barrett, M. T. (2020). Genomic and Epigenomic Landscaping Defines New Therapeutic Targets for Adenosquamous Carcinoma of the Pancreas. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-0078 Cite
The authors defined a mechanism by which cholesterol metabolism controls the development and differentiation of pancreatic ductal adenocarcinoma.
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Gabitova-Cornell, L., Surumbayeva, A., Peri, S., Franco-Barraza, J., Restifo, D., Weitz, N., Ogier, C., Goldman, A. R., Hartman, T. R., Francescone, R., Tan, Y., Nicolas, E., Shah, N., Handorf, E. A., Cai, K. Q., O’Reilly, A. M., Sloma, I., Chiaverelli, R., Moffitt, R. A., … Astsaturov, I. (2020). Cholesterol Pathway Inhibition Induces TGF-β Signaling to Promote Basal Differentiation in Pancreatic Cancer. Cancer Cell, 0(0). https://doi.org/10.1016/j.ccell.2020.08.015 Cite