Title Information
Title
Antagonistic effect of aspartate-β-hydroxylase on chemotherapeutics in cholangiocarcinoma
Type of Resource
text
Name: Personal
Name Part
Cao, Kevin
Role
Role Term: Text
creator
Name: Personal
Name Part
Wands, Jack
Role
Role Term: Text
Advisor
Name: Personal
Name Part
Huang, Chiung-Kuei
Role
Role Term: Text
Reader
Name: Personal
Name Part
Li, Ji Su
Role
Role Term: Text
Reader
Name: Corporate
Name Part
Brown University. Department of Molecular Pharmacology, Physiology and Biotechnology
Role
Role Term: Text
sponsor
Origin Information
Copyright Date
2019
Physical Description
Extent
, 37 p.
digitalOrigin
born digital
Note: thesis
Thesis (Sc. M.)--Brown University, 2019
Genre (aat)
theses
Abstract
Bile duct cancer, known as cholangiocarcinoma (CCA), is a rare but highly aggressive cancer with a 3% incident in all gastrointestinal cancers. The only known curative treatment for CCA is surgical resection at an early stage, however, CCA is usually asymptomatic until advanced local or metastatic stages where surgical resection may not be considered curative or possible therapy. Aspartate-β-hydroxylase (ASPH) is a type 2 transmembrane protein that is frequently found to be upregulated in a number of cancers including CCA. The expression of ASPH has been associated with a poorer prognosis and a worse response to chemotherapy. Here, we examine the role of ASPH in chemotherapy and how it influences the DNA damage response.
Subject (fast) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00886581")
Topic
DNA damage
Subject (fast) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00831700")
Topic
Bile ducts--Cancer
Subject
Topic
ASPH
Language
Language Term (ISO639-2B)
English
Record Information
Record Content Source (marcorg)
RPB
Record Creation Date (encoding="iso8601")
20190603
Identifier: DOI
10.26300/e9nv-a670
Access Condition: rights statement (href="http://rightsstatements.org/vocab/InC/1.0/")
In Copyright
Access Condition: restriction on access
Collection is open for research.