Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab


  • Hyunsuk Shim
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_3681-2



2-Methoxyestradiol (2ME2) is a naturally occurring substance that is produced when the hormone estradiol is processed (metabolized) in the body. 2ME2 prevents both tumor growth (antiproliferative) and the formation of new blood vessels that tumors require to grow (antiangiogenic). Although 2ME2 is derived from estradiol, it binds poorly to estrogen receptors. On the contrary, it binds directly to a protein called tubulin, which is involved in cell division. This binding not only interferes with cell division (cell growth) but also inhibits hypoxia inducible factor-1 (HIF-1), an important factor for tumor cell survival. Additionally, 2ME2 has been reported to preferentially kill tumor cells, sparing normal cells, by causing reactive oxygen species (ROS) accumulation in cancer cells.

2ME2 under the trademark Panzem® (EntreMed Inc., Rockville, MD) is currently in Phase I/II clinical studies to investigate its safety and efficacy...


Vascular Endothelial Growth Factor Arsenic Trioxide Vascular Endothelial Growth Factor Secretion Microtubule Disruption Colchicine Binding Site 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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  1. Kang SH, Cho HT, Devi S et al (2006) Antitumor effect of 2-methoxyestradiol in a rat orthotopic brain tumor model. Cancer Res 66:11991–11997CrossRefPubMedGoogle Scholar
  2. LaVallee TM, Zhan XH, Johnson MS et al (2003) 2-methoxyestradiol up-regulates death receptor 5 and induces apoptosis through activation of the extrinsic pathway. Cancer Res 63:468–475PubMedGoogle Scholar
  3. Mabjeesh NJ, Escuin D, LaVallee TM et al (2003) 2ME2 inhibits tumor growth and angiogenesis by disrupting microtubules and dysregulating HIF. Cancer Cell 3:363–375CrossRefPubMedGoogle Scholar
  4. Pelicano H, Feng L, Zhou Y et al (2003) Inhibition of mitochondrial respiration: a novel strategy to enhance drug-induced apoptosis in human leukemia cells by a reactive oxygen species-mediated mechanism. J Biol Chem 278:37832–37839CrossRefPubMedGoogle Scholar
  5. Seegers JC, Aveling ML, Van Aswegen CH et al (1989) The cytotoxic effects of estradiol-17 beta, catecholestradiols and methoxyestradiols on dividing MCF-7 and HeLa cells. J Steroid Biochem 32:797–809CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Department of Hematology/OncologyWinship Cancer Institute, Emory UniversityAtlantaUSA