A5036152877- Esophageal Cancer Research and Treatment
- Colorectal Cancer Screening and Detection
- Pancreatic and Hepatic Oncology Research
- RNA modifications and cancer
- CRISPR and Genetic Engineering
- Cancer Genomics and Diagnostics
- Helicobacter pylori-related gastroenterology studies
- Cancer Cells and Metastasis
- 3D Printing in Biomedical Research
- Digestive system and related health
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- Microfluidic and Bio-sensing Technologies
- Pancreatic function and diabetes
- Single-cell and spatial transcriptomics
- CAR-T cell therapy research
- Cholangiocarcinoma and Gallbladder Cancer Studies
- RNA regulation and disease
- Innovative Microfluidic and Catalytic Techniques Innovation
- interferon and immune responses
- AI in cancer detection
- Mathematical Biology Tumor Growth
- Ubiquitin and proteasome pathways
- Microbial Inactivation Methods
- Cancer-related Molecular Pathways
The University of Texas MD Anderson Cancer Center
2019-2024
Cornell University
2013-2022
New York State College of Agriculture & Life Sciences
2016
Ithaca College
2014
Optimization of pancreatic CTC immunocapture and phenotyping in a microfluidic device.
Intraductal papillary mucinous neoplasms (IPMN) of the pancreas are bona fide precursor lesions pancreatic ductal adenocarcinoma (PDAC). The most common subtype IPMNs harbors a gastric foveolar-type epithelium, and these low-grade harbingers with high-grade dysplasia cancer. molecular underpinning differentiation in is unknown, although identifying drivers this indolent phenotype might enable opportunities for intercepting progression to IPMN We conducted spatial transcriptomics on cohort...
We used automated electrorotation to measure the cytoplasmic permittivity, conductivity, and specific membrane capacitance of pancreatic cancer cells under environmental perturbation evaluate effects serum starvation, epithelial-to-mesenchymal transition, evolution chemotherapy resistance which may be associated with development dissemination cancer. First, we compared gemcitabine-resistant BxPC3 subclones gemcitabine-naive parental cells. Second, serum-starved PANC-1 them untreated...
Abstract Advances in rare cell capture technology have made possible the interrogation of circulating tumor cells (CTCs) captured from whole patient blood. However, locating device by manual counting bottlenecks data processing being tedious (hours per sample) and compromises results inconsistent prone to user bias. Some recent work has been done automate location classification process address these problems, employing image machine learning (ML) algorithms locate classify fluorescent...
Conventional genetically engineered mouse models (GEMM) are time-consuming, laborious, and offer limited spatiotemporal control. Here, we describe the development of a streamlined platform for in vivo gene activation using CRISPR (CRISPRa) technology. Unlike conventional GEMMs, this model system allows flexible, sustained, timed one or more target genes single pooled lentiviral guides. Myc Yap1 were used as oncogenes to demonstrate primary pancreatic organoid cultures vitro enhanced...
The development of diverse spatial profiling technologies has provided an unprecedented insight into molecular mechanisms driving cancer pathogenesis. Here, we conducted the first integrated cross-species assessment transcriptomics and metabolomics alterations associated with progression intraductal papillary mucinous neoplasms (IPMN), bona fide cystic precursors pancreatic ductal adenocarcinoma (PDAC).Matrix Assisted Laster Desorption/Ionization (MALDI) mass spectrometry (MS)-based imaging...
Abstract Background: While the genetic landscapes of pancreatic ductal adenocarcinoma (PDAC) and non-small cell lung cancer (NSCLC) are well described, contribution individual genes transcriptomic programs to tumor initiation, progression metastasis remain incompletely understood. To quantify oncogenic potential identify that drive metastasis, we have developed a platform for in vivo CRISPR activation (CRISPRa) screening allows us delineate tissue-specific oncogene selection. Material...
Abstract Oncogenic “hotspot” mutations of KRAS and GNAS are two major driver alterations in Intraductal Papillary Mucinous Neoplasms (IPMNs), which bona fide precursor lesions pancreatic ductal adenocarcinoma (PDAC). We previously reported that pancreas-specific KrasG12D GnasR201C expression caused IPMN development, with subsequent progression to PDAC p48-Cre; LSL-KrasG12D; Rosa26R-LSL-rtTA-TetO-GnasR201C mice (referred as “Kras;Gnas” mice). This study aimed clarify the functional roles...
ABSTRACT Objective Oncogenic “hotspot” mutations of KRAS and GNAS are two major driver alterations in Intraductal Papillary Mucinous Neoplasms (IPMNs), which bona fide precursors to pancreatic ductal adenocarcinoma. We previously reported that pancreas-specific Kras G12D Gnas R201C co-expression p48 Cre ; LSL-G12D Rosa26 LSL-rtTA Tg (TetO- ) mice (“ Kras;Gnas ” mice) caused development cystic lesions recapitulating IPMNs. Here, we aim unveil the consequences mutant expression on phenotype,...
Abstract Purpose: To define the metabolic alterations associated with malignant progression of intraductal papillary mucinous neoplasm (IPMN). Experimental Procedures: Matrix-assisted laser desorption/ionization (MALDI)-mass spectrometry (MS) was conducted for spatial characterization lipid profiles on frozen tissue sections from resected human IPMN patients. The specimen set consisted either low-grade dysplasia (LG) (n=15), high-grade (HG) (n=4), or an pancreatic ductal adenocarcinoma...
Abstract The existence of asymptomatic precursor lesions that are known to predate invasive pancreatic ductal adenocarcinoma (PDAC) by years provides a compelling rationale for cancer interception efforts. One such is intraductal papillary mucinous neoplasm (IPMN). Using Matrix-Assisted Laser Desorption/Ionization Mass Spectrometry (MALDI-MS) imaging metabolites in tissue sections from resected patient IPMN cases (N=23) and KrasG12D/GnasR201C mouse model IPMN, we have made discovery long...
Abstract Background: To date, targeted therapies have largely failed in eliciting sustained responses advanced pancreatic ductal adenocarcinoma (PDAC). KRAS-targeted the potential to drastically transform clinical management. Emerging data indicate that only a subset of patients respond, and acquired resistance is common. Here, we used combination vivo CRISPR activation (CRISPRa) screening vitro/preclinical models identify synergistic combinations with KRAS inhibition (KRASi) lung cancer....
Background Oncogenic ‘hotspot’ mutations of KRAS and GNAS are two major driver alterations in intraductal papillary mucinous neoplasms (IPMNs), which bona fide precursors to pancreatic ductal adenocarcinoma. We previously reported that pancreas-specific Kras G12D Gnas R201C co-expression p48 Cre ; LSL-G12D Rosa26 LSL-rtTA Tg (TetO-Gnas ) mice ( ‘Kras;Gnas ’ mice) caused development cystic lesions recapitulating IPMNs. Objective aim unveil the consequences mutant expression on phenotype,...
<p>Differentially expressed genes between LG, HG, and PDAC samples per region.</p>
<p>Comparisons in cell type proportions predicted by RCTD between LG and HGPDAC epilesional, jutxalesional, perilesional spots.</p>
<p>Comparisons in cell type proportions predicted by RCTD between LG and HGPDAC epilesional, jutxalesional, perilesional spots.</p>
<p>Patient and clinical information for the IPMN samples included in COMET cohort.</p>
<p>Patient and clinical information for the IPMN samples included in COMET cohort.</p>
<p>Predicted NKX6-2 targets and transcription factors associated with expression evaluated by GENIE3.</p>
<p>Overlap between genes differentially expressed in the NKX6-2 overexpressing and control Kras;Gnas cell line Nkx6-2 positive negative spots from ST epithelial spots.</p>
<p>Predicted NKX6-2 targets and transcription factors associated with expression evaluated by GENIE3.</p>
<p>Differentially expressed genes between NKX6-2 overexpressing and control KPC cell lines.</p>