With a background in Biomedical science, I’ve been interested in opportunities where I can utilize and enhance my research skills, learn about human disease mechanisms with clinical manifestations and become proficient as an independent thinker, mentor and researcher.
Current Role at Stanford
Affiliated with research projects in cell biology and cancer biology with prior experience with immunostaining and tissue sectioning, flow cytometry, related data analysis, and knowledge of human immune cell populations. In the lab, I perform primarily immunohistochemistry on FFPE human tissues/ liquid samples, microtome FFPE sectioning, antibody conjugation, molecular biology techniques such as SDS-PAGE electrophoresis with evaluation. I'm also involved in lab management and general maintenance.
Education & Certifications
Master of Biomedical Science, The University of Melbourne, Cancer Biology (2016)
Bachelor of Biomedicine, The University of Melbourne, Neuroscience (2013)
Service, Volunteer and Community Work
Patient Experience Volunteer, Stanford Healthcare
Matter of Balance Coach, Stanford Healthcare
Skills and Expertise
Single-cell spatial proteomic imaging for human neuropathology.
Acta neuropathologica communications
2022; 10 (1): 158
Neurodegenerative disorders are characterized by phenotypic changes and hallmark proteopathies. Quantifying these in archival human brain tissues remains indispensable for validating animal models and understanding disease mechanisms. We present a framework for nanometer-scale, spatial proteomics with multiplex ion beam imaging (MIBI) for capturing neuropathological features. MIBI facilitated simultaneous, quantitative imaging of 36 proteins on archival human hippocampus from individuals spanning cognitively normal to dementia. Customized analysis strategies identified cell types and proteopathies in the hippocampus across stages of Alzheimer's disease (AD) neuropathologic change. We show microglia-pathologic tau interactions in hippocampal CA1 subfield in AD dementia. Data driven, sample independent creation of spatial proteomic regions identified persistent neurons in pathologic tau neighborhoods expressing mitochondrial protein MFN2, regardless of cognitive status, suggesting a survival advantage. Our study revealed unique insights from multiplexed imaging and data-driven approaches for neuropathologic analysis and serves broadly as a methodology for spatial proteomic analysis of archival human neuropathology. TEASER: Multiplex Ion beam Imaging enables deep spatial phenotyping of human neuropathology-associated cellular and disease features.
View details for DOI 10.1186/s40478-022-01465-x
View details for PubMedID 36333818
Transition to invasive breast cancer is associated with progressive changes in the structure and composition of tumor stroma.
2022; 185 (2): 299-310.e18
Ductal carcinoma in situ (DCIS) is a pre-invasive lesion that is thought to be a precursor to invasive breast cancer (IBC). To understand the changes in the tumor microenvironment (TME) accompanying transition to IBC, we used multiplexed ion beam imaging by time of flight (MIBI-TOF) and a 37-plex antibody staining panel to interrogate 79 clinically annotated surgical resections using machine learning tools for cell segmentation, pixel-based clustering, and object morphometrics. Comparison of normal breast with patient-matched DCIS and IBC revealed coordinated transitions between four TME states that were delineated based on the location and function of myoepithelium, fibroblasts, and immune cells. Surprisingly, myoepithelial disruption was more advanced in DCIS patients that did not develop IBC, suggesting this process could be protective against recurrence. Taken together, this HTAN Breast PreCancer Atlas study offers insight into drivers of IBC relapse and emphasizes the importance of the TME in regulating these processes.
View details for DOI 10.1016/j.cell.2021.12.023
View details for PubMedID 35063072
- Key Players and Potential Therapies in the Development of Breast Cancer Metastasis to the Spine Key Players and Potential Therapies in the Development of Breast Cancer Metastasis to the Spine 2022; 10 (1)
Multiplexed Single-cell Metabolic Profiles Organize the Spectrum of Cytotoxic Human T Cells
View details for DOI 10.1101/2020.01.17.909796
Spatio-temporal coordination at the maternal-fetal interface promotes trophoblast invasion and vascular remodeling in the first half of human pregnancy
View details for DOI 10.1101/2021.09.08.459490
- In-depth characterization of immune cells in preeclampsia using Multiplexed Ion Beam Imaging by Time-of-Flight (MIBI-TOF) MOSBY-ELSEVIER. 2020: S156–S157
Single-cell metabolic profiling of human cytotoxic T cells.
Cellular metabolism regulates immune cell activation, differentiation and effector functions, but current metabolic approaches lack single-cell resolution and simultaneous characterization of cellular phenotype. In this study, we developed an approach to characterize the metabolic regulome of single cells together with their phenotypic identity. The method, termed single-cell metabolic regulome profiling (scMEP), quantifies proteins that regulate metabolic pathway activity using high-dimensional antibody-based technologies. We employed mass cytometry (cytometry by time of flight, CyTOF) to benchmark scMEP against bulk metabolic assays by reconstructing the metabolic remodeling of in vitro-activated naive and memory CD8+ T cells. We applied the approach to clinical samples and identified tissue-restricted, metabolically repressed cytotoxic T cells in human colorectal carcinoma. Combining our method with multiplexed ion beam imaging by time of flight (MIBI-TOF), we uncovered the spatial organization of metabolic programs in human tissues, which indicated exclusion of metabolically repressed immune cells from the tumor-immune boundary. Overall, our approach enables robust approximation of metabolic and functional states in individual cells.
View details for DOI 10.1038/s41587-020-0651-8
View details for PubMedID 32868913
TRAIL-induced variation of cell signaling states provides nonheritable resistance to apoptosis.
Life science alliance
2019; 2 (6)
TNFalpha-related apoptosis-inducing ligand (TRAIL), specifically initiates programmed cell death, but often fails to eradicate all cells, making it an ineffective therapy for cancer. This fractional killing is linked to cellular variation that bulk assays cannot capture. Here, we quantify the diversity in cellular signaling responses to TRAIL, linking it to apoptotic frequency across numerous cell systems with single-cell mass cytometry (CyTOF). Although all cells respond to TRAIL, a variable fraction persists without apoptotic progression. This cell-specific behavior is nonheritable where both the TRAIL-induced signaling responses and frequency of apoptotic resistance remain unaffected by prior exposure. The diversity of signaling states upon exposure is correlated to TRAIL resistance. Concomitantly, constricting the variation in signaling response with kinase inhibitors proportionally decreases TRAIL resistance. Simultaneously, TRAIL-induced de novo translation in resistant cells, when blocked by cycloheximide, abrogated all TRAIL resistance. This work highlights how cell signaling diversity, and subsequent translation response, relates to nonheritable fractional escape from TRAIL-induced apoptosis. This refined view of TRAIL resistance provides new avenues to study death ligands in general.
View details for DOI 10.26508/lsa.201900554
View details for PubMedID 31704709