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Your search keyword '"Lotze, Michael T"' showing total 16 results
Start Over Author "Lotze, Michael T" Journal cancer research
16 results on '"Lotze, Michael T"'

1. Parkin Deficiency Suppresses Antigen Presentation to Promote Tumor Immune Evasion and Immunotherapy Resistance

Author

Perales-Linares, Renzo, primary, Leli, Nektaria Maria, additional, Mohei, Hesham, additional, Beghi, Silvia, additional, Rivera, Osvaldo D., additional, Kostopoulos, Nektarios, additional, Giglio, Andrea, additional, George, Subin S., additional, Uribe-Herranz, Mireia, additional, Costabile, Francesca, additional, Pierini, Stefano, additional, Pustylnikov, Sergei, additional, Skoufos, Giorgos, additional, Barash, Yoseph, additional, Hatzigeorgiou, Artemis G., additional, Koumenis, Constantinos, additional, Maity, Amit, additional, Lotze, Michael T., additional, and Facciabene, Andrea, additional

Published
2023
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3. Prolactin Promotes Fibrosis and Pancreatic Cancer Progression

Author

Tandon, Manuj, primary, Coudriet, Gina M., additional, Criscimanna, Angela, additional, Socorro, Mairobys, additional, Eliliwi, Mouhanned, additional, Singhi, Aatur D., additional, Cruz-Monserrate, Zobeida, additional, Bailey, Peter, additional, Lotze, Michael T., additional, Zeh, Herbert, additional, Hu, Jing, additional, Goffin, Vincent, additional, Gittes, George K., additional, Biankin, Andrew V., additional, and Esni, Farzad, additional

Published
2019
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10. p53/HMGB1 Complexes Regulate Autophagy and Apoptosis

Author

Livesey, Kristen M., primary, Kang, Rui, additional, Vernon, Philip, additional, Buchser, William, additional, Loughran, Patricia, additional, Watkins, Simon C., additional, Zhang, Lin, additional, Manfredi, James J., additional, Zeh, Herbert J., additional, Li, Luyuan, additional, Lotze, Michael T., additional, and Tang, Daolin, additional

Published
2012
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14. The Enhanced Tumor Selectivity of an Oncolytic Vaccinia Lacking the Host Range and Antiapoptosis Genes SPI-1 and SPI-2

Author

Guo, Z. Sheng, primary, Naik, Arpana, additional, O'Malley, Mark E., additional, Popovic, Petar, additional, Demarco, Richard, additional, Hu, Yun, additional, Yin, Xiaoyu, additional, Yang, Shuting, additional, Zeh, Herbert J., additional, Moss, Bernard, additional, Lotze, Michael T., additional, and Bartlett, David L., additional

Published
2005
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15. High-Mobility Group Box 1 Promotes Hepatocellular Carcinoma Progression through miR-21-Mediated Matrix Metalloproteinase Activity.

Author

Man Chen, Yao Liu, Varley, Patrick, Ying Chang, Xing-xing He, Hai Huang, Daolin Tang, Lotze, Michael T., Jusheng Lin, and Tsung, Allan

Subjects
*LIVER cancer, *FIBROLAMELLAR hepatocellular carcinoma, *LIVER metastasis, *MATRIX metalloproteinases, *ENDOPEPTIDASES
Abstract

Liver inflammation plays a critical role in hepatocellular carcinoma (HCC) etiology. Damage-associated molecular patterns (DAMP), such as high-mobility group box 1 (HMGB1), and dysregulated miRNAs involved in inflammatory disease states, such as miR-21, may participate in the link between inflammation and cancer. We sought to determine the role of HMGB1 signaling in HCC tumor progression. We first document the concordant expression increase of HMGB1 and miR-21 in HCC cell lines and primary HCC tumor samples and subsequently show that HMGB1 stimulation results in overexpression of miR-21. These changes were found to be dependent on the IL6/STAT3 signaling axis. Invasion and migration of HCC cells in vitro were inhibited by both STAT3 and miR-21 antagonists, suggesting a role for this pathway in HCC tumor progression. We verified that HMGB1-induced expression of miR-21 in HCC provides a post-transcriptional repression of the matrix metalloproteinase (MMP) inhibitors RECK and TIMP3, which are known to impact HCC progression and metastases. Finally, we found that inhibition of miR-21 in murine HMGB1-overexpressing HCCxenografts led to reduced tumor MMP activity through released repression of the miR-21 targets RECK and TIMP3, which ultimately impeded tumor progression. The prototypical DAMP, HMGB1, is released during liver inflammation and provides a favorable environment for HCC growth. HMGB1 signaling increases miR-21 expression to mediate the enhanced activity of MMPs through RECK and TIMP3. These findings provide a novel mechanism for HMGB1-mediated HCC progression through the IL6/Stat3-miR-21 axis. [ABSTRACT FROM AUTHOR]

Published
2015
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16. Inhibiting Systemic Autophagy during Interleukin 2 Immunotherapy Promotes Long-term Tumor Regression.

Author

Xiaoyan Liang, De Vera, Michael E., Buchser, William J., de Vivar Chavez, Antonio Romo, Loughran, Patricia, Stolz, Donna Beer, Basse, Per, Tao Wang, Van Houten, Bennett, Zeh III, Herbert J., and Lotze, Michael T.

Subjects
*INTERLEUKINS, *MELANOMA, *RENAL cancer, *CANCER cells, *IMMUNOTHERAPY
Abstract

Administration of high-dose interleukin-2 (HDIL-2) has durable antitumor effects in 5% to 10% of patients with melanoma and renal cell carcinoma. However, treatment is often limited by side effects, including reversible, multiorgan dysfunction characterized by a cytokine-induced systemic autophagic syndrome. Here, we hypothesized that the autophagy inhibitor chloroquine would enhance IL-2 immunotherapeutic efficacy and limit toxicity. In an advanced murine metastatic liver tumor model, IL-2 inhibited tumor growth in a dose-dependent fashion. These antitumor effects were significantly enhanced upon addition of chloroquine. The combination of IL-2 with chloroquine increased long-term survival, decreased toxicity associated with vascular leakage, and enhanced immune cell proliferation and infiltration in the liver and spleen. HDIL-2 alone increased serum levels of HMGB1, IFN-g, IL-6, and IL-18 and also induced autophagy within the liver and translocation of HMGB1 from the nucleus to the cytosol in hepatocytes, effects that were inhibited by combined administration with chloroquine. In tumor cells, chloroquine increased autophagic vacuoles and LC3-II levels inhibited oxidative phosphorylation and ATP production and promoted apoptosis, which was associated with increased Annexin-V+/propidium iodide (PI)- cells, cleaved PARP, cleaved caspase-3, and cytochrome c release from mitochondria. Taken together, our findings provide a novel clinical strategy to enhance the efficacy of HDIL-2 immunotherapy for patients with cancer. [ABSTRACT FROM AUTHOR]

Published
2012
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