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Cancer: Ovarian Cancer
Drug: Inderal

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Total 4 results found since Jan 2013.

043 Mechanism of action of propranolol in Infantile Hemangioma: New insights from a xenograft model
8 years after propranolol was found efficacious in infantile hemangioma (IH), therapeutic mechanisms remain elusive. It has been shown, in an ovarian cancer model, that ADRB2 signaling is key for chronic stress induced tumor growth. In this model, tumor promotion is abolished by propranolol or ADRB2 siRNA but not by ADRB1 siRNA. In IH patients, after oral administration of 3 mg/kg/day of propranolol, plasma Cmax is below 1 μM, whereas propranolol has been used in vitro at 100 μM and up to 50 mg/kg in mouse models.
Source: Journal of Investigative Dermatology - August 16, 2016 Category: Dermatology Authors: F. Moisan, J. Nissen, P. Kaulanjan-Checkmodine, S. Prey, P. Dufourcq, T. Couffinhal, H. Rezvani, A. Taieb Tags: Clinical Outcomes Source Type: research

Abstract 3368: Sustained adrenergic signaling activates pro-inflammatory prostaglandin network in ovarian carcinoma
Conclusion Increased adrenergic stimulation results in a pro-inflammatory milieu mediated by prostaglandins that drives tumor progression and metastasis in ovarian cancer.Citation Format: Archana S. Nagaraja, Piotr Dorniak, Nouara Sadaoui, Guillermo Armaiz-Pena, Behrouz Zand, Sherry Y. Wu, Julie K. Allen, Rajesha Rupaimoole, Cristian Rodriguez-Aguayo, Sunila Pradeep, Lin Tan, Rebecca A. Previs, Jean M. Hansen, Peiying Yang, Garbiel Lopez-Berestein, Susan K. Lutgendorf, Steve Cole, Anil K. Sood. Sustained adrenergic signaling activates pro-inflammatory prostaglandin network in ovarian carcinoma. [abstract]. In: Proceedings ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Nagaraja, A. S., Dorniak, P., Sadaoui, N., Armaiz-Pena, G., Zand, B., Wu, S. Y., Allen, J. K., Rupaimoole, R., Rodriguez-Aguayo, C., Pradeep, S., Tan, L., Previs, R. A., Hansen, J. M., Yang, P., Lopez-Berestein, G., Lutgendorf, S. K., Cole, S., Sood, A. K Tags: Tumor Biology Source Type: research

Abstract 2359: Adrenergic regulation of MCP-1 leads to enhanced macrophage recruitment and ovarian carcinoma growth
Increased adrenergic signaling is known to promote tumor progression, but the underlying mechanisms remain poorly understood. Tumor associated macrophages (TAMs) are key components of the tumor microenvironment that contribute to pro-inflammatory processes and tumor growth. Recently, it has been reported that patients with higher levels of adrenergic signaling have higher counts of MMP-9-producing TAMs. Here, we examined factors responsible for stress-mediated effects on monocyte/macrophage recruitment into the tumor microenvironment and the resultant effects on tumor growth. Conditioned media from norepinephrine- or epine...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Armaiz-Pena, G. N., Gonzalez-Villasana, V., Nagaraja, A. S., Rodriguez-Aguayo, C., Dorniak, P., Previs, R., Sadaoui, N., Stone, R., Matsuo, K., Dalton, H. J., Lutgendorf, S. K., Sood, A. K., Lopez-Berestein, G. Tags: Tumor Biology Source Type: research

Abstract 158: Sustained adrenergic signaling activates pro-inflammatory networks in ovarian carcinoma
Conclusion Increased adrenergic stimulation results in a pro-inflammatory milieu that drives tumor progression and metastasis. Citation Format: Archana S. Nagaraja, Guillermo Armaiz-Pena, Julie Allen, Nouara C. Sadaoui, Behrouz Zand, Peiying Yang, Lin Tan, Steve Cole, Susan Lutgendorf, Anil K. Sood. Sustained adrenergic signaling activates pro-inflammatory networks in ovarian carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 158. doi:10.1158/1538-7445.AM2014-158
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Nagaraja, A. S., Armaiz-Pena, G., Allen, J., Sadaoui, N. C., Zand, B., Yang, P., Tan, L., Cole, S., Lutgendorf, S., Sood, A. K. Tags: Tumor Biology Source Type: research