Current Scholars

Current Scholars



Winston Yun-Han Chang
Winston Yun-Han Chang
Lab: Hanash

Project: Investigating interferon gamma-mediated epithelial regeneration as a pathologic mechanism of colorectal cancer

My research focuses on interferon gamma and its ability to induce intestinal stem cell proliferation. I am investigating this mechanism’s contribution to intestinal epithelial regeneration in response to tissue damage during bacterial infection, and how this mechanism is commandeered to support colorectal cancer growth. These studies will be insightful towards understanding bacterial infection as a risk factor for colorectal cancer development and strategies by which colorectal cancer can resist anti-tumor immunity. 

Pablo Guasp Baratech
Pablo Guasp Baratech
Lab: Balachandran

Project: Identification of Mal as a novel immune suppressor in pancreatic cancer

By studying an extraordinary cohort of long-term survivors of pancreatic cancer we identified the myelin and lymphocyte protein (MAL) as a potential novel molecule that inhibits immune responses. This project will study how MAL suppresses immune responses in pancreatic cancer, to potentially target MAL in new immunotherapies.

Katrina Mar
Katrina Mar
Lab: Hohl

Project: Murine coronavirus infection exacerbates pulmonary fungal disease

The COVID-19 pandemic has highlighted the infectious morbidity and mortality associated with co-infections with coronaviruses and invasive molds, even in apparently immune competent individuals. These observations suggest that the induction of an antiviral immune response occurs at the cost of an effective antifungal response. To investigate how mounting a distinct immune response to a secondary pathogen infection can be deleterious to the host, I have established a co-infection model that facilitates a deep mechanistic dissection of antifungal immunity in the context of pulmonary infection with a murine coronavirus.

Alexander Settle
Alexander Settle
Lab: Huse

Project: Exploring the importance of mechanosensing in antibody-dependent cellular phagocytosis

Phagocytosis, the process by which immune cells engulf and destroy pathogens and cancer, is sensitive to the mechanical properties of the target. Specifically, macrophages efficiently engulf rigid cargo but are less effective at engulfing soft material such as cancer cells. My work focuses on the mechanism by which macrophages preferentially destroy rigid targets to understand how to engineer macrophages to enhance phagocytosis of soft cancer cells.

Yan-Ting Chen
Yan-Ting Chen
Lab: Vardhana

Project: Exploring translational dysregulation as a driver of T-cell exhaustion.

T-cells, which are immune cells that play an essential role in anti-tumor defense, exhibit decreased production of anti-tumor molecules within tumors over time. In this proposal, I hypothesize that the imbalance of nutrient supply and demand underlies as a roadblock for T-cell anti-tumor activity. The results of this proposal will provide insights on the synergy between establishing nutrient balance and immunotherapy to improve T-cell activity against cancer.

Olga Lyudovyk
Olga Lyudovyk
Lab: Greenbaum

Project: Deep Learning model of T-Cell recognition of antigens and its applications in cancer to inform immunotherapy design and predict response

Olga’s research applies modern computational methods and leverages large public datasets to tackle the unsolved problem of T-cell specificity: which T-cells recognize which antigens. The model elucidated antigen-specific recognition motifs in T-cell receptor (TCR) sequences for SARS-CoV2 Spike antigens, enabled tracking clinically relevant TCRs in patient repertoires during COVID-19 infection, and is evaluated for predicting vaccine-specific TCRs in responders to the pancreatic ductal adenocarcinoma vaccine. Model predictions can be applied in the cancer setting to inform T-cell selection for adoptive cell therapies, predict and track T-cell response to cancer immunotherapy and vaccines.

Ron Baik
Lab: Sfeir

Project: Investigating the Impact of Mitochondrial DNA Mutations on Hematopoietic Stem and Progenitor Cells

Mutations in mtDNA alter mitochondrial function and have been implicated in hematological disorders including myelodysplastic syndrome, Pearson’s syndrome, and clonal hematopoiesis, which can lead to blood cancers. My research goal is to investigate the impact of mtDNA mutations on the expansion and differentiation of CD34+ hematopoietic stem and progenitor cells (HSPCs) and explore how mtDNA aberrations contribute to premature hematopoietic aging and other malignancies. 

Miklos Lengyel
Lab: Niethammer 

Project: Deciphering the role of oxo-eicosanoid signaling in intestinal inflammation and bowel cancer

Environmental factors leading to chronic inflammation of the gastrointestinal tract such as a high-fat diet are well-known risk factors for tumor development in the intestines. Arachidonic acid is a fatty acid found in the human diet. Chemical derivatives of arachidonic acid play important roles in in inflammation. 5-oxo-eicosatetraenoic acid (5-oxo-ETE) is one of these molecules. This molecule is almost completely unstudied because rodents do not have OXER1, the receptor of 5-oxo-ETE. I have found that loss of OXER1 in zebrafish leads to chronic intestinal inflammation due to increased gut barrier damage.  My research will use zebrafish and human tissue models to understand this new protective effect of OXER1, with the goal of developing new strategies to increase the resilience of the intestinal barrier.

Korbinian Kropp
Lab: Klebanoff

Project: Defining the molecular mechanisms of enhanced tumor cell killing by CD4+ T cells through targeting of the RNA binding protein PCBP2

A major reason that CD8+ T cell-based tumor immunotherapies are ineffective – either initially or after a period of treatment – is due to tumor mutations that result in CD8+ T cells being incapable of directly recognizing and killing cancer cells. However, a significant proportion of solid tumors express HLA-II which enables tumors to be recognized and eliminated by an alternative lymphocyte subset called CD4+ T cells. In this project, we seek to investigate why disruption of the RNA binding protein PCBP2 results in enhanced CD4+ T cell elimination of tumor cells that have become resistant to CD8+ T cells.

Yuzuka Kanno
Lab: Gitlin 

Project: Regulation of anti-cancer innate immunity through the non-canonical IKK axis

Designing next-generation cancer immunotherapies requires a deeper understanding of how to sensitize tumors to immune attack. The kinases TBK1 and IKK-epsilon (known as the non-canonical IKKs) have emerged as attractive immunotherapy targets, but the underlying mechanisms remain poorly understood. This project will investigate novel mechanistic aspects of non-canonical IKK biology and their implications for cancer immunotherapy.

Kathleen Luckett
Lab: Ganesh 

Project: Elucidating the Functional Consequence of Mutations in ZFP36L2 on the Tumor Immune Microenvironment in Colorectal Cancer

The tumor microenvironment of microsatellite stable/mismatch repair proficient (MSS/MMRp) colorectal cancer, which accounts for 85% of primary colorectal cancer and over 95% of metastatic colorectal cancer, is immunologically “cold”, and consequently these patients respond poorly to checkpoint immunotherapy. My research is focused on characterizing tumor intrinsic mechanisms that suppress inflammatory gene expression, thereby maintaining immune evasion both within the tumor microenvironment and throughout the metastatic cascade. The ultimate goal of my work is to identify novel targets and biomarkers of response to immunotherapy in colorectal cancer.

Hexiao Wang
Lab: Petrini 

Project: Chronic Interferon Stimulated Gene Transcription Promotes Breast Cancer Development

The MRE11 complex is integral to the maintenance of genome stability. Mre11 hypomorphism leads to increased Interferon Stimulated Gene (ISG) transcription and associated chromatin changes. My project is to investigate how these epithelia derived ISGs affect the microenvironment and promote oncogene-induced breast cancer development.