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Your search keyword '"Kurie, Jonathan M"' showing total 7 results
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7 results on '"Kurie, Jonathan M"'

1. A Novel Small-Molecule Inhibitor Targeting CREB-CBP Complex Possesses Anti-Cancer Effects along with Cell Cycle Regulation, Autophagy Suppression and Endoplasmic Reticulum Stress

Author

Lee, Jong Woo, primary, Park, Hee Sun, additional, Park, Sin-Aye, additional, Ryu, Seung-Hee, additional, Meng, Wuyi, additional, Jürgensmeier, Juliane M., additional, Kurie, Jonathan M., additional, Hong, Waun Ki, additional, Boyer, Julie L., additional, Herbst, Roy S., additional, and Koo, Ja Seok, additional

Published
2015
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2. Fibulin-2 Is a Driver of Malignant Progression in Lung Adenocarcinoma

Author

Baird, Brandi N., primary, Schliekelman, Mark J., additional, Ahn, Young-Ho, additional, Chen, Yulong, additional, Roybal, Jonathon D., additional, Gill, Bartley J., additional, Mishra, Dhruva K., additional, Erez, Baruch, additional, O’Reilly, Michael, additional, Yang, Yanan, additional, Patel, Mayuri, additional, Liu, Xin, additional, Thilaganathan, Nishan, additional, Larina, Irina V., additional, Dickinson, Mary E., additional, West, Jennifer L., additional, Gibbons, Don L., additional, Liu, Diane D., additional, Kim, Min P., additional, Hicks, John M., additional, Wistuba, Ignacio I., additional, Hanash, Samir M., additional, and Kurie, Jonathan M., additional

Published
2013
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5. Phosphatidylinositol 3-Kinase Mediates Bronchioalveolar Stem Cell Expansion in Mouse Models of Oncogenic K-ras-Induced Lung Cancer

Author

Yang, Yanan, primary, Iwanaga, Kentaro, additional, Raso, Maria Gabriela, additional, Wislez, Marie, additional, Hanna, Amy E., additional, Wieder, Eric D., additional, Molldrem, Jeffrey J., additional, Wistuba, Ignacio I., additional, Powis, Garth, additional, Demayo, Francesco J., additional, Kim, Carla F., additional, and Kurie, Jonathan M., additional

Published
2008
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7. Phosphatidylinositol 3-Kinase Mediates Bronchioalveolar Stem Cell Expansion in Mouse Models of Oncogenic Kras-Induced Lung Cancer.

Author

Yang, Yanan, Iwanaga, Kentaro, Raso, Maria Gabriela, Wislez, Marie, Hanna, Amy E., Wieder, Eric D., Molldrem, Jeffrey J., Wistuba, Ignacio I., Powis, Garth, Demayo, Francesco J., Kim, Carla F., and Kurie, Jonathan M.

Subjects
LUNG cancer complications, BIOCHEMISTRY, STEM cells, CELL populations, PHOSPHOINOSITIDES, TUMOR growth, MOLECULES, PHOSPHATASES, CHROMOSOMES, RATS as carriers of disease
Abstract

Background: Non-small cell lung cancer (NSCLC) is the most common cause of cancer-related death in Western countries. Developing more effective NSCLC therapeutics will require the elucidation of the genetic and biochemical bases for this disease. Bronchioalveolar stem cells (BASCs) are a putative cancer stem cell population in mouse models of oncogenic K-rasinduced lung adenocarcinoma, an histologic subtype of NSCLC. The signals activated by oncogenic K-ras that mediate BASC expansion have not been fully defined. Methodology/Principal Findings: We used genetic and pharmacologic approaches to modulate the activity of phosphatidylinositol 3-kinase (PI3K), a key mediator of oncogenic K-ras, in two genetic mouse models of lung adenocarcinoma. Oncogenic K-ras-induced BASC accumulation and tumor growth were blocked by treatment with a small molecule PI3K inhibitor and enhanced by inactivation of phosphatase and tensin homologue deleted from chromosome 10, a negative regulator of PI3K. Conclusions/Significance: We conclude that PI3K is a critical regulator of BASC expansion, supporting treatment strategies to target PI3K in NSCLC patients. [ABSTRACT FROM AUTHOR]

Published
2008
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