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Identification of DNA Polymerase Theta Inactivation Mechanism
Case ID:
C15287
Report of Invention:
4/23/2018
Web Published:
5/25/2023
Unmet Need
Loss of DNA repair is an early and frequent event in the growth of tumors, occurring in 40 to 50% of breast, lung and ovarian cancer patients. The inability to repair damaged DNA provides a selective growth advantage to tumor cells as this results in genetic instability and enhanced mutation rates, which can drive tumor growth. These DNA repair–deficient cancers often become dependent on backup DNA repair pathways, which can be exploited to eliminate cancer cells. The development of inhibitors that target DNA repair in tumors has recently gained interest as a new focus in advancing cancer treatments. DNA Polymerase theta (Pol Φ) is a repair enzyme specifically expressed in tumors and associated with poor clinical outcomes. Importantly, disruption of Pol Φ sensitizes cancer cells to radiotherapy and has been shown to be lethal in animal models of BRCA-deficient cancer. Therefore, the development of methods to identify and develop inhibitors to Pol Φ could be medically and economically important.
Technology Overview
Hopkins inventors have identified a mutation in the active site of Pol Φ that has reduced its activity more than 3,000-fold. Using patented technology developed previously at Johns Hopkins, the inventors plan to screen libraries of molecules as potential irreversible inhibitors of Pol Φ.
Stage of Development
Conceptual
Publications
Laverty, DJ, et al. ACS Chemical Biology 12(6), 1584-1592, 2017
Patent Information:
Title
App Type
Country
Serial No.
Patent No.
File Date
Issued Date
Expire Date
Patent Status
Identification of DNA Polymerase Theta Inactivation Mechanism
PCT: Patent Cooperation Treaty
United States
17/259,032
1/8/2021
Pending
Direct Link:
https://jhu.technologypublisher.com/technology/51177
Inventors:
Category(s):
Technology Classifications > Therapeutic Modalities > Gene Therapies, Technology Classifications > Therapeutic Modalities > Cell Therapies,
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For Information, Contact:
Mohit Ganguly
mgangul1@jh.edu
410-614-0300
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