Tag Archives: KRAS

The KRAS/Lin28B Axis Maintains Stemness of Pancreatic Cancer Cells via the Let-7i/TET3 Pathway

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.
[Molecular Oncology]
Liu, Y., Wang, D., Zhou, M., Chen, H., Wang, H., Min, J., Chen, J., Wu, S., Ni, X., Zhang, Y., Gong, A., & Xu, M. (n.d.). The KRAS/Lin28B axis maintains stemness of pancreatic cancer cells via the let-7i/TET3 pathway. Molecular Oncology, n/a(n/a). https://doi.org/10.1002/1878-0261.12836 Cite
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Oncogenic KRAS-Expressing Organoids with Biliary Epithelial Stem Cell Properties Give Rise to Biliary Tract Cancer in Mice

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.
[Cancer Science]
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
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Post-Translational Modification of KRAS: Potential Targets for Cancer Therapy

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]
Wang, W., Yuan, T., Qian, M., Yan, F., Yang, L., He, Q., Yang, B., Lu, J., & Zhu, H. (2020). Post-translational modification of KRAS: potential targets for cancer therapy. Acta Pharmacologica Sinica, 1–11. https://doi.org/10.1038/s41401-020-00542-y Cite
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ERK3/MAPK6 Is Required for KRAS-Mediated NSCLC Tumorigenesis

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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PLCγ1 Suppression Promotes the Adaptation of KRAS-Mutant Lung Adenocarcinomas to Hypoxia

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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Evaluation of the RAS Signaling Network in Response to MEK Inhibition Using Organoids Derived from a Familial Adenomatous Polyposis Patient

Scientists used patient-derived organoids derived from a familial adenomatous polyposis patient to analyze the response to chemotherapeutic agents targeting EGFR, BRAF and MEK.
[Scientific Reports]
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
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Amgen Announces Positive Topline Phase II Results For Investigational KRAS G12C Inhibitor Sotorasib In Advanced Non-Small Cell Lung Cancer

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.
[Amgen]
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Transcriptional Subtypes Resolve Tumor Heterogeneity and Identify Vulnerabilities to MEK Inhibition in Lung Adenocarcinoma

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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Molecular Alterations and Targeted Therapy in Pancreatic Ductal Adenocarcinoma

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]
Qian, Y., Gong, Y., Fan, Z., Luo, G., Huang, Q., Deng, S., Cheng, H., Jin, K., Ni, Q., Yu, X., & Liu, C. (2020). Molecular alterations and targeted therapy in pancreatic ductal adenocarcinoma. Journal of Hematology & Oncology, 13(1), 130. https://doi.org/10.1186/s13045-020-00958-3 Cite
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Genomic and Epigenomic Landscaping Defines New Therapeutic Targets for Adenosquamous Carcinoma of the Pancreas

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.
[Cancer Research]
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
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Cholesterol Pathway Inhibition Induces TGF-β Signaling to Promote Basal Differentiation in Pancreatic Cancer

The authors defined a mechanism by which cholesterol metabolism controls the development and differentiation of pancreatic ductal adenocarcinoma.
[Cancer Cell]
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
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