Bio

Honors & Awards


  • NSF GRFP Fellow, National Science Foundation (2017-2020)
  • Stanford Graduate Fellowship, Vice Provost for Graduate Education, Stanford University (2016-2019)
  • Rhodes Finalist, Rhodes Trust (2015)
  • Thomas J. Bardos Science Education Award, American Association for Cancer Research (2014-2015)

Professional Affiliations and Activities


  • Logistics Head, Biomedical Computation At Stanford (BCATS) Symposium (2017 - Present)

Membership Organizations


Education & Certifications


  • B.S., Michigan State University, Genomics and Molecular Genetics (2016)

Stanford Advisors


Research & Scholarship

Lab Affiliations


Publications

All Publications


  • Exosomes in the tumor microenvironment as mediators of cancer therapy resistance. Molecular cancer Li, I., Nabet, B. Y. 2019; 18 (1): 32

    Abstract

    Exosomes are small extracellular vesicles that contain genetic material, proteins, and lipids. They function as potent signaling molecules between cancer cells and the surrounding cells that comprise the tumor microenvironment (TME). Exosomes derived from both tumor and stromal cells have been implicated in all stages of cancer progression and play an important role in therapy resistance. Moreover, due to their nature as mediators of cell-cell communication, they are integral to TME-dependent therapy resistance. In this review, we discuss current exosome isolation and profiling techniques and their role in TME interactions and therapy resistance. We also explore emerging clinical applications of both exosomes as biomarkers, direct therapeutic targets, and engineered nanocarriers. In order to fully understand the TME, careful interrogation of exosomes and their cargo is critical. This understanding is a promising avenue for the development of effective clinical applications.

    View details for DOI 10.1186/s12943-019-0975-5

    View details for PubMedID 30823926

  • GR-RNF43 Regulation In Colorectal Cancer Journal of Proteomics and Genomics Research Dalgic, E., Li, I., Nath, A., Chan, C. 2016
  • Elevated free fatty acid uptake via CD36 promotes epithelial-mesenchymal transition in hepatocellular carcinoma SCIENTIFIC REPORTS Nath, A., Li, I., Roberts, L. R., Chan, C. 2015; 5

    Abstract

    Hepatocellular carcinoma (HCC) is the second-leading cause of cancer-related death worldwide, and the factors influencing HCC progression are poorly understood. Here we reveal that HCC progression via induction of epithelial-mesenchymal transition (EMT) is closely associated with the expression of CD36/fatty acid translocase and elevated free fatty acid (FFA) levels. Although obesity is manifested as elevated FFA levels, the degree of EMT was not associated with the body mass index of the patients, highlighting the specific roles of CD36 and FFA uptake. Treatment of human liver cancer cell lines with FFAs exacerbated the EMT phenotype, whereas chemical inhibition of CD36 mitigated these effects. Furthermore, the Wnt and TGF-β signaling pathways were activated upon FFA treatment, potentially acting as upstream activators of the EMT program. These results provide the first direct evidence associating CD36 and elevated FFAs with HCC progression.

    View details for DOI 10.1038/srep14752

    View details for Web of Science ID 000362096300002

    View details for PubMedID 26424075

    View details for PubMedCentralID PMC4589791