91ÉçÇø

Sidong Huang

Academic title(s): 

Associate Professor, Department of Biochemistry

Scientific Director, 91ÉçÇø Platform for Cellular Perturbation (MPCP)

Sidong Huang
Contact Information
Address: 

McIntyre Medical Sciences Building
3655 promenade Sir-William-Osler
Office: Room 800C; Lab: 800
Montreal, Quebec H3G 1Y6

Email address: 
sidong.huang [at] mcgill.ca
Phone: 
Office: 514-398-4447
Lab: 514-398-5446
Department: 
Biochemistry
Goodman Cancer Institute
Area(s): 
Bioinformatics and Genomics
Cancer
Degree(s): 

2003 – PhD,  University of California, San Francisco

Current research: 

Functional Genomics to Guide Cancer Therapy

Our laboratory uses functional genomic tools to study cancer-relevant pathways and to guide cancer therapy. We aim to identify novel genes and networks that modulate response to cancer drugs, and to uncover genetic dependencies of cancer-relevant pathways that can be exploited therapeutically.

Overcoming drug resistance to cancer therapeutics

Drug resistance remains a major clinical challenge for cancer therapy. Not all patients respond to the same treatments and many patients who initially respond to the therapies develop drug resistance. Thus, a better understanding of resistance mechanisms is essential to enable the rational development of effective treatments. Using unbiased functional genetic screens, we aim to uncover novel genes and network interactions that modulate response to cancer therapeutics. Furthermore, we will reveal the mechanism of action to help devise treatment strategies to overcome drug resistance.

Targeting hard-to-treat cancer driver mutations

Genotype-directed cancer therapeutics often target gain-of-function oncogenic mutations in cancer cells and thus have less side effects in normal tissue. However, some cancer driver mutations such as inactivation of tumour suppressors are not directly actionable. In this context, we use customized druggable gene-family shRNA/CRISPR libraries and compound collections to identify alternative targets, whose inhibition is synthetic lethal with these cancer driver mutations. We aim to uncover vulnerabilities of hard-to-treat cancers that can be exploited therapeutically.

Selected publications: 

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