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Ivan, Cristina

https://orcid.org/0000-0002-4848-0168

Mayo Clinic

The University of Texas MD Anderson Cancer Center

Citations 2

Dynamin 2 along with microRNA-199a reciprocally regulate hypoxia-inducible factors and ovarian cancer metastasis
Joshi, Hemant , Subramanian, Indira V., Schnettler, Erica, Rupaimoole, Rajesha , Evans, Colleen, Saluja, Manju, Jing, Yawu, Ivan, Cristina , Shah, Vijay H. , Ramakrishnan, Sundaram , Ghosh, Goutam , Roy, Sabita , Zeng, Yan , Sood, Anil K.

Proceedings of the National Academy of Sciences | March 25, 2014 | Volume: 111 | Issue: 14 | Pages: 5331-5336

10.1073/pnas.1317242111 Get It

Significance Tumor cells adapt to hypoxia by modulating energy production and utilization. Endocytosis is an energy-consuming process that is suppressed during hypoxia. Our studies show that Dynamin 2 (DNM2), a key component of endocytic machinery, is transcriptionally suppressed by HIF-1. Genetic and pharmacological inactivation of DNM2 stabilized HIF-1α and HIF-2α. Furthermore, miR-199a, which is encoded from the opposite strand of DNM2 , exerts reciprocal negative regulation upon HIF-1α and HIF-2α. Overexpression of miR-199a decreased HIF-1α and HIF-2α, cell migration, and metastasis. These findings establish a regulatory loop between endocytic pathway and hypoxic response in tumor cells.
Prognostic value of miR-155 in individuals with monoclonal B-cell lymphocytosis and patients with B chronic lymphocytic leukemia
Ivan, Cristina , Shimizu, Masayoshi , Rabe, Kari G. , Nouraee, Nazila , Ikuo, Mariko, Ghosh, Asish K. , Rassenti, Laura Z., Xiao, Lianchun , Hu, Jianhua , Reuben, James M. , Calin, Steliana , You, M. James , Manning, John T. , Wierda, William G. , Keating, Michael J. , Călin, George A. , Calin, George A. , Ferrajoli, Alessandra , Shanafelt, Tait D. , Lerner, Susan A. , Wierda, William G. , Estrov, Zeev E. , O’Brien, Susan , Kipps, Thomas J. , Kay, Neil E. , Chaffee, Kari G.

Blood | July 3, 2013 | Volume: 122 | Issue: 11 | Pages: 1891-1899

10.1182/blood-2013-01-478222 Get It

Key Points miR-155 levels are significantly and increasingly overexpressed as normal B cells progress to MBL and to CLL. Plasma levels of miR-155 before treatment were significantly lower in patients with CLL who experienced complete response than in all others.