Tag Archives: pancreatic ductal adenocarcinoma

NADK Is Activated by Oncogenic Signaling to Sustain Pancreatic Ductal Adenocarcinoma

Scientists showed that oncogenic KRAS promoted protein kinase C-mediated NAD+ kinase (NADK) phosphorylation, leading to its hyperactivation, thus sustaining both NADP+ and NADPH levels in pancreatic ductal adenocarcinoma cells.
[Cell Reports]
Schild, T., McReynolds, M. R., Shea, C., Low, V., Schaffer, B. E., Asara, J. M., Piskounova, E., Dephoure, N., Rabinowitz, J. D., Gomes, A. P., & Blenis, J. (2021). NADK is activated by oncogenic signaling to sustain pancreatic ductal adenocarcinoma. Cell Reports, 35(11). https://doi.org/10.1016/j.celrep.2021.109238 Cite
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TP53 Missense Mutations in PDAC Are Associated with Enhanced Fibrosis and an Immunosuppressive Microenvironment

Researchers suggested that missense p53 mutations might contribute to worse pancreatic ductal adenocarcinoma prognosis by promoting a more vigorous fibrotic tumor microenvironment and impeding the ability of the immune system to eliminate the cancer cells.
[Proceedings of the National Academy of Sciences of the United States of America]
Maddalena, M., Mallel, G., Nataraj, N. B., Shreberk-Shaked, M., Hassin, O., Mukherjee, S., Arandkar, S., Rotkopf, R., Kapsack, A., Lambiase, G., Pellegrino, B., Ben-Isaac, E., Golani, O., Addadi, Y., Hajaj, E., Eilam, R., Straussman, R., Yarden, Y., Lotem, M., & Oren, M. (2021). TP53 missense mutations in PDAC are associated with enhanced fibrosis and an immunosuppressive microenvironment. Proceedings of the National Academy of Sciences, 118(23). https://doi.org/10.1073/pnas.2025631118 Cite
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CF33-hNIS-antiPDL1 Virus Primes Pancreatic Ductal Adenocarcinoma for Enhanced Anti-PD-L1 Therapy

Oncolytic viral chimera, CF33-hNIS-antiPDL1 genetically modified to express anti-human PD-L1 antibody and CF33-hNIS-Δ without the anti-PD-L1 gene, were used to investigate the immunogenic effects of oncolytic virus and virus-delivered anti-PD-L1 in pancreatic ductal adenocarcinoma in vitro.
[Cancer Gene Therapy]
Zhang, Z., Yang, A., Chaurasiya, S., Park, A. K., Lu, J., Kim, S.-I., Warner, S. G., Yuan, Y.-C., Liu, Z., Han, H., Von Hoff, D., Fong, Y., & Woo, Y. (2021). CF33-hNIS-antiPDL1 virus primes pancreatic ductal adenocarcinoma for enhanced anti-PD-L1 therapy. Cancer Gene Therapy, 1–12. https://doi.org/10.1038/s41417-021-00350-4 Cite
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Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ

Scientists found that EPCAM + tumors developed in the mouse pancreas store zinc that is detectable by fluorescence-activated cell sorting using N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide (TSQ), a fluorescence chelator. EPCAM + TSQ + tumor cells isolated from the mouse pancreas formed organoids in matrigel.
[Biological Trace Element Research]
Asahina, K. (2021). Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ. Biological Trace Element Research. https://doi.org/10.1007/s12011-021-02770-7 Cite
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The Biological Underpinnings of Therapeutic Resistance in Pancreatic Cancer

The authors discuss recent advances in the understanding of the biological underpinnings of pancreatic ductal adenocarcinoma and their implications as targetable vulnerabilities in this highly lethal disease.
[Genes & Development]
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Induction of Cell Death in Pancreatic Tumors by Zinc and Its Florescence Chelator TSQ

Upon treatment with N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine, a zinc chelator, organoids degenerated and its negative effect was rescued by co-treatment with zinc, indicating that zinc is necessary for the growth and survival of tumor organoids.
[Biological Trace Element Research]
Asahina, K. (2021). Induction of Cell Death in Pancreatic Tumors by Zinc and Its Fluorescence Chelator TSQ. Biological Trace Element Research. https://doi.org/10.1007/s12011-021-02770-7 Cite
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Complement Factor B Regulates Cellular Senescence and Is Associated with Poor Prognosis in Pancreatic Cancer

Scientists performed secretome analyses of culture media of mouse pancreatic intraepithelial neoplasia and PDAC cells using Stable Isotope Labeling by Amino acid in Cell culture with click chemistry and liquid chromatography-mass spectrometry.
[Cellular Oncology]
Shimazaki, R., Takano, S., Satoh, M., Takada, M., Miyahara, Y., Sasaki, K., Yoshitomi, H., Kagawa, S., Furukawa, K., Takayashiki, T., Kuboki, S., Sogawa, K., Motohashi, S., Nomura, F., Miyazaki, M., & Ohtsuka, M. (2021). Complement factor B regulates cellular senescence and is associated with poor prognosis in pancreatic cancer. Cellular Oncology. https://doi.org/10.1007/s13402-021-00614-z Cite
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miR-194-5p Down-Regulates Tumor Cell PD-L1 Expression and Promotes Anti-tumor Immunity in Pancreatic Cancer

Investigators found that high expression of miR-194-5p in human pancreatic cancer patients is associated with a better survival rate, while increased expression of programmed cell death ligand 1 in human pancreatic cancer patients is associated with a worse survival rate.
[International Immunopharmacology]
miR-194-5p down-regulates tumor cell PD-L1 expression and promotes anti-tumor immunity in pancreatic cancer. (2021). International Immunopharmacology, 97, 107822. https://doi.org/10.1016/j.intimp.2021.107822 Cite
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Tumor Suppressive Role of miR-33a-5p in Pancreatic Ductal Adenocarcinoma Cells by Directly Targeting RAP2A

Researchers observed for the first time that miR-33a-5p expression level was significantly decreased in pancreatic ductal adenocarcinoma tissues and cell lines.
[Cellular & Molecular Biology Letters]
Lian, Y., Jiang, D., & Sun, J. (2021). Tumor suppressive role of miR-33a-5p in pancreatic ductal adenocarcinoma cells by directly targeting RAP2A. Cellular & Molecular Biology Letters, 26(1), 24. https://doi.org/10.1186/s11658-021-00265-w Cite
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TP53 Missense Mutations in PDAC Are Associated with Enhanced Fibrosis and an Immunosuppressive Microenvironment

Analysis of human pancreatic ductal adenocarcinoma (PDAC) patient data from The Cancer Genome Atlas revealed a negative association between the presence of missense mutp53 and infiltration of CD8+ T cells into the tumor.
[Proceedings of the National Academy of Sciences of the United States of America]
Maddalena, M., Mallel, G., Nataraj, N. B., Shreberk-Shaked, M., Hassin, O., Mukherjee, S., Arandkar, S., Rotkopf, R., Kapsack, A., Lambiase, G., Pellegrino, B., Ben-Isaac, E., Golani, O., Addadi, Y., Hajaj, E., Eilam, R., Straussman, R., Yarden, Y., Lotem, M., & Oren, M. (2021). TP53 missense mutations in PDAC are associated with enhanced fibrosis and an immunosuppressive microenvironment. Proceedings of the National Academy of Sciences, 118(23). https://doi.org/10.1073/pnas.2025631118 Cite
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Exploring the Complementarity of Pancreatic Ductal Adenocarcinoma Preclinical Models

Three paired pancreatic ductal adenocarcinoma preclinical models-patient-derived xenografts , xenograft-derived pancreatic organoids and xenograft-derived primary cell cultures-were derived from 20 patients and analyzed at the transcriptomic and chemosensitivity level.
[Cancers]
Hoare, O., Fraunhoffer, N., Elkaoutari, A., Gayet, O., Bigonnet, M., Roques, J., Nicolle, R., McGuckin, C., Forraz, N., Sohier, E., Tonon, L., Wajda, P., Boyault, S., Attignon, V., Tabone-Eglinger, S., Barbier, S., Mignard, C., Duchamp, O., Iovanna, J., & Dusetti, N. J. (2021). Exploring the Complementarity of Pancreatic Ductal Adenocarcinoma Preclinical Models. Cancers, 13(10), 2473. https://doi.org/10.3390/cancers13102473 Cite
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