University of Groningen
CRISPR/Cas9 and targeted cancer therapy Liu, Bin
DOI:
10.33612/diss.99103461
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date: 2019
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
Liu, B. (2019). CRISPR/Cas9 and targeted cancer therapy. University of Groningen. https://doi.org/10.33612/diss.99103461
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum.
Propositions
Belonging to the thesis
CRISPR/Cas9 and targeted cancer therapy by Bin Liu
1. CRISPR/Cas9 is a powerful tool not only for cancer research but also for cancer treatment.
2. EGFR targeting mediated by CRISPR/Cas9 is a promising strategy for treatment of non-small cell lung cancer.
3. CXCR7 contributes to survival and resistance of KRAS-mutant non-small cell lung cancer upon EGFR targeting.
4. Cyclin D1 inhibition resensitizes erlotinib-resistant (ER) cells to erlotinib. Cyclin D1 may be a potential therapeutic target for patients with EGFR inhibitors resistant NSCLC.
5. Regulation of chromatin compaction by inhibiting HAT and/or HDAC activity can modulate CRISPR/Cas9-based gene editing
6. EGFR knockout is not equivalent to EGFR inhibition. Tumor cells can develop resistance to inhibitors as well as to CRISPR/Cas9-mediated EGFR knockout, but resistance mechanisms do not have to be the same. Understanding those mechanisms would be helpful for cancer therapy.
7. Things are the hardest right before they get better; this is the truth for life, for science, and particularly for life sciences