Viewing Study NCT02006550


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Study NCT ID: NCT02006550
Status: TERMINATED
Last Update Posted: 2019-04-01
First Post: 2013-12-04
Is NOT Gene Therapy: True
Has Adverse Events: False

Brief Title: Interrogation of Wnt, Notch and Hedgehog Activity in Primary Tumor Samples
Sponsor: University of Miami
Organization:

Study Overview

Official Title: Interrogation of Wnt, Notch and Hedgehog Activity in Primary Tumor Samples
Status: TERMINATED
Status Verified Date: 2019-03
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Lack of Resources and Personnel
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: Cancer results when undifferentiated cells grow in an uncontrolled manner, crowding out normal cells, causing morbidity and ultimately mortality. The cancer stem cell theory suggests that most tumors undergo a process of differentiation through which a relatively rare cancer stem or progenitor cell (CSC) gives rise to more differentiated populations of cells (including transiently amplifying cells) comprising the bulk of the tumor. As a result of this cellular diversity, one or more cells within the tumor are likely to be resistant to therapy. Among cells resistant to a given therapy, only CSCs can repopulate the tumor. A key feature of this resistant subset of CSCs is that they repopulate a tumor resistant to the original intervention. The cellular programs driving the uncontrolled proliferation of many solid tumors result from aberrant activity of Wnt, Shh, and/or Notch signaling pathways in CSC. Thus, therapies that down-regulate the activity of these fundamental pathways in CSCs will be effective in the treatment of cancer. The investigators' research program focuses on the elucidation of signaling mechanisms, control of cellular processes and discovery of small molecules that selectively target Wnt, Shh, and Notch signaling pathways that are fundamental to CSCs. Our preliminary results identified a novel Notch associated protein NACK that functions as a transcriptional co-activator of Notch. Moreover, Nack is expressed in human solid tumors and is required for cell survival and tumor growth in notch -dependent tumor cells. The investigators' aim is to further interrogate the link between Notch and Nack.
Detailed Description: None

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: False
Is a FDA Regulated Device?: False
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: