Here are the things that keep me up at night:
Myung Chang Lee (Noah Lee)
SF Bay Area, CA, US
Representative article
• Led large-scale multi-modal analyses
• Performed
• Served as the lead computational analyst for
• Contributed
• Drove
Representative article
• Researched genetic and cellular determinants of SCLC initiation and progression at the laboratory of Dr. Julien Sage at Stanford Medicine (Departments of Pediatrics and Genetics)
• Scaled available datasets for SCLC genomics 20x,
• Generated a novel
• Developed CRISPR/Cas9 screening-compatible viral vectors and mouse models of lung cancer to
• Drove experimental design and analysis for in vitro and in vivo studies, authoring SOPs to standardize work procedures and improve reproducibility of
• Performed
Representative article
• Examined glioblastoma (GBM) stem cell maintenance and self-renewal under hypoxia and possible treatments at the laboratories of Dr. Mark Israel (until June 2017) and Dr. Matthew Havrda, with Dr. Damian Almiron-Bonnin serving as the mentor.
• Analyzed paired glioma transcriptomes in R and IPA (n=9; 18 samples) to identify genes and pathways associated with
• Authored an honors thesis, utilizing
We conduct transcriptomic analyses and non-negative matrix factorization on 271 pre-treatment patient tumor samples from IMpower133 and identify four subsets. The NE tumors with low tumor-associated macrophage (TAM) but high T-effector signals demonstrate longer overall survival with PD-L1 blockade and CE versus CE alone than non-NE tumors with high TAM and high T-effector signal. Our study offers a clinically relevant approach to discriminate SCLC patients likely benefitting most from immunotherapies and highlights the complex mechanisms underlying immunotherapy responses.
Here, we develop a quantitative multiplexed approach on the basis of lentiviral barcoding with somatic CRISPR-Cas9-mediated genome editing to functionally investigate candidate regulators of tumor initiation and growth in genetically engineered mouse models of SCLC. Candidate drivers of SCLC identified from a meta-analysis across multiple human SCLC genomic datasets were tested using this approach, which defines both positive and detrimental impacts of inactivating 40 genes across candidate pathways on SCLC development. This analysis and subsequent validation in human SCLC cells establish TSC1 in the PI3K-AKT-mTOR pathway as a robust tumor suppressor in SCLC.
The authors found that the gene expression patterns characterizing fluorescent and nonfluorescent GBM surgical specimens were profoundly different and were associated with distinct cellular functions and different biological pathways. Nonfluorescent tumor tissue tended to resemble the neural subtype of GBM; meanwhile, fluorescent tumor tissue did not exhibit a prominent pattern corresponding to known subtypes of GBM. Consistent with this observation, neural GBM samples from The Cancer Genome Atlas database exhibited a significantly lower fluorescence score than nonneural GBM samples as determined by a fluorescence gene signature developed by the authors.
Mentors: Dr. Barzin Nabet and Dr. Robert Johnston
Thesis: Investigating Genetic and
Cellular Determinants of Small Cell Lung Cancer Initiation and Progression
Thesis Advisor: Dr. Julien Sage
Thesis Committee: Dr. Monte Winslow, Dr. Erinn Rankin, Dr. Paul Khavari
Same as above
Thesis: Benztropine
sensitizes glioma cells to temozolomide
Honors Thesis Advisors: Dr. Damian Almiron-Bonnin, Dr. Matthew Havrda, and Dr. Mark Israel
