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Brooks C.L.,Stemline Therapeutics | Gu W.,Columbia University
Cell Research | Year: 2010

The tumor suppressor p53 is a multifunctional, highly regulated, and promoter-specific transcriptional factor that is uniquely sensitive to DNA damage and cellular stress signaling. The mechanisms by which p53 directs a damaged cell down either a cell growth arrest or an apoptotic pathway remain poorly understood. Evidence suggests that the in vivo functions of p53 seem to balance the cell-fate choice with the type and severity of damage that occurs. The concept of antirepression, or inhibition of factors that normally keep p53 at bay, may help explain the physiological mechanisms for p53 activation. These factors also provide novel chemotherapeutic targets for the reactivation of p53 in tumors harboring a wild-type copy of the gene. © 2010 IBCB, SIBS, CAS.

Brooks C.L.,Stemline Therapeutics | Gu W.,Columbia University
FEBS Letters | Year: 2011

The ubiquitination pathway is a highly dynamic and coordinated process that regulates degradation as well as numerous processes of proteins within a cell. The p53 tumor suppressor and several factors in the pathway are regulated by ubiquitin as well as ubiquitin-like proteins. These modifications are critical for the function of p53 and control both the degradation of the protein as well as localization and activity. Importantly, more recent studies have identified deubiquitination enzymes that can specifically remove ubiquitin moieties from p53 or other factors in the pathway, and the reversible nature of this process adds yet another layer of regulatory control of p53. This review highlights the recent advances in our knowledge of ubiquitin and the p53 pathway. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Stemline Therapeutics | Date: 2014-10-02

Provided are methods for treating cancer in a patient, comprising administration of a therapeutically effective regimen of cantharidin or cantharidin analog of formula of formula I, II or III wherein R

Stemline Therapeutics | Date: 2015-02-26

The present invention provides antibodies that bind to the IL-3 receptor alpha subunit alpha (Il3R) chain, and compositions comprising such antibodies. The present invention provides methods for inhibiting or reducing an IL3R-expressing cell population, the methods comprising contacting a population of IL3R-expressing cells (e.g., cancer cells and/or cancer stem cells) with an antibody that binds to IL3R. The present invention also provides antibody conjugates comprising an antibody that binds to an IL3R chain linked to a cytotoxic agent or anticellular agent and compositions comprising such conjugates. The present invention also provides methods for preventing, treating and/or managing a disorder associated with IL3R-expressing cells (e.g., a hematological cancer), the methods comprising administering to a subject in need thereof an antibody that binds to IL3R.

Stemline Therapeutics | Date: 2013-03-19

Provided herein are methods for treating cancer in a subject comprising administering to the subject a therapeutically effective amount of a peptide derived from the EphA2 protein and/or the IL-13R2 protein and monitoring the amount of cancer stem cells in said subject. Also provided herein are methods for monitoring the efficacy of an EphA2 peptide-based cancer treatment or an IL-13R2 peptide-based cancer treatment in a patient with cancer, comprising monitoring the amount of cancer stem cells in said subject prior to, during, and/or following cancer treatment of a patient.

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