NCI Division of Cancer Biology Junior Investigators Meeting (Abstract)

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# Created User IP address First Name Middle Initial Last Name Degree(s) Position/Title/Career Status Organization Organization Address Email Abstract Category Abstract Keywords Abstract Title Abstract Operations
4 Thu, 08/13/2026 - 11:08 Anonymous 10.208.28.62 Jeffrey Hsu B.S. M.S. University of Virginia Charlottesville uem3ed@virginia.edu Use my abstract for team formation only (do not consider it for a presentation) HER2 locally modulates the hormone receptor-negative DCIS microenvironment Ductal carcinoma in situ (DCIS) breast premalignancies account for ≥20% of all new diagnoses yet they do not align with standard invasive breast cancer subtypes. In DCIS, amplification of the HER2 receptor tyrosine kinase is two times more common than in invasive breast cancer, suggesting distinct roles in premalignancy. Using highly multiplexed imaging and biocomputational statistics to profile HER2-associated DCIS microenvironments, we asked whether HER2 expression coincides with different cellular constituents around DCIS lesions that are hormone receptor (HR)–negative and immune infiltrated. HER2 protein expression was variable across and within patient samples and was associated with the largest change in stromal cellularity relative to other profiled DCIS cell states (KRT5, γH2AX, Ki67). Compared to DCIS lesions with low or absent HER2 (HER2-low), lesions with high HER2 expression (HER2-high) had significantly fewer fibroblasts, CD8+ T cells, and macrophages. Interestingly, co-variation analysis of cell-type pairs revealed increased associations between cancer-associated fibroblast (CAF)/myofibroblastic CAF (myCAF) densities and resting fibroblast/myofibroblast densities, suggesting tighter coupling among fibroblast states in HER2-high regions. Separately, we compared HER2-positive and HER2-negative HR–negative DCIS patient cases from the Human Tumor Atlas Network by differential expression analysis of secretome genes, identifying a depletion in the matrisome-associated gene, lysyl oxidase (LOX), in HER2-positive cases. In vivo studies suggested that periductal CAF and myCAF densities were depleted following HER2 overexpression, whereas LOX overexpression produced a reciprocal increase in these populations. Collectively, these results suggest that HER2 locally shifts fibroblast-state coordination and dilutes immune presence in the DCIS microenvironment through LOX.
3 Mon, 08/10/2026 - 17:11 Anonymous 10.208.28.62 Isha Bhorkar M.S. Graduate Student University of Michigan Ann Arbor, MI ibhorkar@umich.edu Consider my abstract for a Methodology/Technology presentation Mechanobiology, Shear stress, Microfluidics, Organoids Multiscale Approaches for Studying Fluid Shear Stress and Mechanoadaptation in Human Fallopian Tube Epithelium The fallopian tube (FT) epithelium is the tissue of origin for most high-grade serous ovarian carcinoma (HGSOC). FT epithelial cells are continuously exposed to fluid shear from follicular fluid release, peristaltic contractions, and ciliary beating, yet how this mechanical environment shapes epithelial behavior and early transformation risk remains poorly understood. My research addresses this gap by combining computational modeling of luminal fluid mechanics with experimental mechanosensing studies in patient-derived microfluidic models.
To characterize the physical environment, I use NanoCT imaging and a custom Python pipeline (skeletonization, perpendicular plane resampling, hydraulic diameter calculation) to reconstruct patient-specific FT luminal geometry and estimate physiological wall shear stress, capturing how mucosal folding shapes the flow environment. These geometric models also feed into computational simulations to generate patient-informed shear estimates.
To link this biomechanical context to cellular response, cells from patient FT organoids are exposed to calibrated, physiological shear stress in microfluidic devices, alongside immortalized comparator lines that provide a transformed counterpart to normal FT epithelium. Cellular responses are characterized through RNA sequencing, live calcium imaging with pharmacological modulation of mechanosensitive channels, and immunofluorescence-based quantification of cytoskeletal organization and epithelial morphology. A perfused, membrane-based device extends this workflow to resolve mechanosensing across ciliated and secretory cell populations.
This work has given me hands-on expertise in patient-derived organoid culture, microfluidic device design and fabrication, quantitative image analysis, and the integration of structural, computational, and transcriptomic data. This biophysical and quantitative perspective could contribute to collaborative projects that connect tissue mechanics, tissue architecture, and mechanosensing to early cancer risk, detection, or progression across tissue types.
2 Mon, 08/10/2026 - 14:07 Anonymous 10.208.28.62 Sydney Quijano B.S Graduate Student Purdue University West Lafayette Indiana squijano@purdue.edu Consider my abstract for a Methodology/Technology presentation Loss of SPINK5 mediates the outgrowth of disseminated breast cancer Following establishment and treatment of primary disease, systemically disseminated breast cancer cells can remain dormant for years only to evolve into therapy-resistant metastases. Specific environmental influences that contribute to the transition from dormant to metastatic disease remain poorly characterized. Herein, we utilized mouse models to evaluate the influence of alcohol consumption on emergence from pulmonary dormancy. Consistent with prior reports, we found that animals consuming alcohol demonstrated decreased adaptive immune presence and increased extracellular matrix deposition in their lungs compared to non-drinking counterparts. Seeding the D2.OR model of pulmonary dormancy cells followed by alcohol consumption caused outgrowth of macroscopic lesions. Isolation and culture of these tumors produced an independent subline (D2.OR-EtOH) capable of pulmonary outgrowth upon reinjection into immunocompetent, alcohol naïve animals. Gene expression analysis of D2.OR-EtOH indicated downregulation of the serine peptidase inhibitor Kazal type 5 (SPINK5) compared to parental cells. Genetic depletion of SPINK5 from parental D2.OR cells was sufficient to allow pulmonary outgrowth in vivo. Evaluation of the immune infiltrate into alcohol-induced pulmonary lesions demonstrated high numbers of neutrophils and the formation of neutrophil extracellular traps (NETs), structures associated with breakage of pulmonary dormancy. D2.OR-EtOH subline and SPINK5-depleted D2.OR cells more readily induced NET formation when cocultured with neutrophils. Overall, our studies demonstrate that alcohol consumption can break pulmonary dormancy by altering the interaction of tumor cells with innate immune cells. Furthermore, our work identifies SPINK5 as an important contributor to metastatic progression in breast cancer through its regulation of interacting neutrophils.
1 Mon, 08/10/2026 - 10:54 Anonymous 10.208.24.93 Heber L. Rocha Ph.D. in Computational Modeling Assistant Scientist Indiana University Bloomington hlimadar@iu.edu Consider my abstract for a Methodology/Technology presentation agent-based modeling, uncertainty quantification, PhysiCell, model calibration, Bayesian inference, tumor microenvironment, computational oncology, open-source software UQ-PhysiCell: Uncertainty Quantification and Calibration for Agent-Based Models of Cancer My research in computational and mathematical oncology centers on multiscale agent-based models (ABMs) of cancer, in which individual cells are autonomous agents governed by rules for proliferation, migration, death, and signaling, coupled to continuum descriptions of oxygen, nutrients, and cytokines. As one of the developers of PhysiCell, an open-source framework for physics-based multicellular simulation, I have built ABMs of tumor growth, immune-tumor interactions, and treatment response that reproduce experimentally observed behaviors. However, the high-dimensional parameter spaces, stochasticity, and computational cost of ABMs pose major challenges for calibration, uncertainty quantification (UQ), and systematic comparison of competing mechanistic hypotheses, capabilities that are essential for predictive, data-grounded modeling. The next stage of my research addresses this gap. I lead development of UQ-PhysiCell, an extensible open-source Python framework that enables uncertainty quantification, calibration, and model selection for PhysiCell models. UQ-PhysiCell manages simulation inputs and outputs (parameters, initial conditions, cell behavior rules) and orchestrates large simulation ensembles with multiple levels of parallelism, integrating directly with established Python libraries for sensitivity analysis, optimization, Bayesian inference, and surrogate modeling. By decoupling model execution from statistical analysis, it lowers the barrier to rigorous, reproducible uncertainty-aware analysis and moves ABMs beyond single best-fit simulations toward interpretable predictions with quantified confidence. In collaborative cancer research projects, I contribute end-to-end modeling support: formalizing mechanistic hypotheses, building and calibrating tumor microenvironment ABMs against imaging and spatial omics data, and quantifying uncertainty in model-based predictions to guide experimental design.