The roles and mechanisms of dopamine to affect the chemotherapeutic efficacy for pancreatic cancer were studied. Multi-omics results revealed that there was a tumor-promoting vicious cycle involving murine pancreatic cancer cells and tumor-associated macrophages.
[Cancer Immunology Immunotherapy]
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Liu, Q., Zhang, R., Zhang, X., Liu, J., Wu, H., Li, Y., Cui, M., Li, T., Song, H., Gao, J., Zhang, Y., Yang, S., & Liao, Q. (2021). Dopamine improves chemotherapeutic efficacy for pancreatic cancer by regulating macrophage-derived inflammations. Cancer Immunology, Immunotherapy. https://doi.org/10.1007/s00262-020-02816-0 Cite
Scientists evaluated improvements to therapeutic efficacy through combination therapy incorporating NanoKnife and M1 virus. They showed that irreversible electroporation triggered reactive oxygen species-dependent apoptosis in pancreatic cancer cells mediated by phosphatidylinositol-3-kinase/protein kinase B pathway suppression.
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Sun, S., Liu, Y., He, C., Hu, W., Liu, W., Huang, X., Wu, J., Xie, F., Chen, C., Wang, J., Lin, Y., Zhu, W., Yan, G., Cai, J., & Li, S. (2021). Combining NanoKnife with M1 oncolytic virus enhances anticancer activity in pancreatic cancer. Cancer Letters, 502, 9–24. https://doi.org/10.1016/j.canlet.2020.12.018 Cite
Scientists evaluated the efficacy of TR1801-ADC, a newly developed ADC composed of a MET antibody conjugated to the highly potent pyrrolobenzodiazepine toxin-linker Tesirine. They first evaluated MET expression and subcellular localization in pancreatic cancer cell lines, human tumors and patient derived xenografts.
[Clinical Cancer Research]
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Cazes, A., Betancourt, O., Esparza, E., Mose, E. S., Jaquish, D., Wong, E., Wascher, A. A., Tiriac, H., Gymnopoulos, M., & Lowy, A. M. (2021). A MET Targeting Antibody-Drug Conjugate Overcomes Gemcitabine Resistance in Pancreatic Cancer. Clinical Cancer Research. https://doi.org/10.1158/1078-0432.CCR-20-3210 Cite
The authors focus on TGFB1/INHBA homodimer/Nodal-SMAD2/3 signaling network in pancreatic cancer as a pivotal central node which regulates multiple key mechanisms involved in the development of chemoresistance, including enhancement of the stem cell-like properties and tumorigenicity of pancreatic cancer cells, mediating cooperative interactions between pancreatic cancer cells and the surrounding stroma as well as regulating the deposition of ECM proteins within the tumor microenvironment.
Scientists demonstrated that ZIP4 activated ZEB1 and YAP1 through distinct mechanisms. The ZIP4-miR-373-LATS2-ZEB1/YAP1-ITGA3 signaling axis has a significant impact on pancreatic cancer metastasis and EMT plasticity.
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Liu, M., Zhang, Y., Yang, J., Zhan, H., Zhou, Z., Jiang, Y., Shi, X., Fan, X., Zhang, J., Luo, W., Fung, K.-M. A., Xu, C., Bronze, M. S., Houchen, C. W., & Li, M. (2021). Zinc Dependent Regulation of ZEB1 and YAP1 Co-activation Promotes EMT Plasticity and Metastasis in Pancreatic Cancer. Gastroenterology, 0(0). https://doi.org/10.1053/j.gastro.2020.12.077 Cite
Investigators explored the circ-0050102 expression in pancreatic cancer and its impacts on tumor malignant phenotypes, and further investigated the correlations among circ-0050102, miR-1182 and NPSR1.
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Scientists report the generation of KS-58, a KRpep-2d derivative that is identified as a bicyclic peptide and possess unnatural amino acid structures. The in vitro data and molecular dynamics simulations suggested that KS-58 entered cells and blocked intracellular Ras–effector protein interactions.
The authors discuss the role of the MET/hepatocyte growth factor (HGF) axis in tumor progression and dissemination of pancreatic cancer. Therapeutic approaches that were developed targeting either the ligand or the receptor have not been shown to translate well into clinical settings.
[International Journal of Molecular Sciences]
Subcutaneous allograft tumors with overexpression or knock-down of vascular cell adhesion molecule-1 (VCAM-1), as well as VCAM-1-blocking treatment in the spontaneous mouse model of pancreatic cancer, revealed that sVCAM-1 promotes tumor growth and resistance to gemcitabine treatment in vivo but not in vitro.
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Takahashi, R., Ijichi, H., Sano, M., Miyabayashi, K., Mohri, D., Kim, J., Kimura, G., Nakatsuka, T., Fujiwara, H., Yamamoto, K., Kudo, Y., Tanaka, Y., Tateishi, K., Nakai, Y., Morishita, Y., Soma, K., Takeda, N., Moses, H. L., Isayama, H., & Koike, K. (2020). Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancreatic cancer. Scientific Reports, 10(1), 21194. https://doi.org/10.1038/s41598-020-78320-3 Cite
Scientists showed that KP372-1 sensitized NAD(P)H:quinone oxidoreductase 1-expressing pancreatic cancer cells and spared immortalized normal pancreatic duct cells, hTERT-HPNE.
Silencing HNF1α reduced the proliferative, migratory, invasive and colony forming capabilities of pancreatic cancer cells.
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Subramani, R., Medel, J., Flores, K., Perry, C., Galvez, A., Sandoval, M., Rivera, S., Pedroza, D. A., Penner, E., Chitti, M., & Lakshmanaswamy, R. (2020). Hepatocyte nuclear factor 1 alpha influences pancreatic cancer growth and metastasis. Scientific Reports, 10(1), 20225. https://doi.org/10.1038/s41598-020-77287-5 Cite