Exploiting RhoA Mutations in Diffuse Gastric Adenocarcinoma and Targeting Intertwined RhoA and Yap1 Pathways for Therapeutic Advantage

reportActive / Technical Report | Accession Number: AD1046138 | Open PDF

Abstract:

Our IDEA is on the right track. We have successfully inserted a fluorescent marker mOrange into MITs Dr. Zhangs pLenti-Crispr-v2, making transfection into mammalian cells easier and visible under fluorescent microscope, it the same time, those cells under Crispr editing are also selectable with puromycin. We have successfully knocked-out RhoA expression in cell lines of AGS and GT5.With RhoA knockout in cell line GT5, Yap1 is also significantly downregulated. Reintroducing mutant RhoA-Y42C is in progress.

Author(s):
Ajani, Jaffer
Author Organization(s):
The University of Texas MD Anderson Cancer Center Houston United States
Descriptive Note:
Technical Report,15 Sep 2016,14 Sep 2017
Pagination:
0034

Security Markings

DOCUMENT & CONTEXTUAL SUMMARY

Distribution:
Approved For Public Release
Distribution Statement:
Approved For Public Release;

RECORD

Collection: TR
Subject Terms
Joint Capability Areas:
JCA_5_Command and Control; JCA_5.3_Planning; JCA_1.2.1_Training; JCA_1.2.5_Lessons Learned; JCA_1.2.3_Educating
Communities of Interest:
No COI(s) Identified
Descriptor(s):
PLASMIDS, cell line, CARCINOMA, mutations
Field(s)/Group(s):
Medicine and Medical Research, Genetic Engineering and Molecular Biology
Keyword(s):
RHOA, YAP1, mouse model, CRISPR CAS9, dgac (diffuse gac), gac (gastric adenocarcinoma)
Report Date:
2017 Oct 01
Creation Date:
2018 Feb 13