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ChristianaCare and The Wistar Institute advance partnership with new cancer research strategies

Mar 16, 2022

4 min

ChristianaCare’s Helen F. Graham Cancer Center & Research Institute is advancing its historic partnership with the Ellen and Ronald Caplan Cancer Center of The Wistar Institute in Philadelphia with three new research projects under way.


The new research projects consist of a population health study targeting triple negative breast cancer. Other projects focus on a new therapeutic target for epithelial ovarian cancer, the most lethal gynecologic cancer in the developed world, and the development of “mini organs” derived from stem cells.


Targeting triple negative breast cancer

Delaware has one of the highest incidence rates of triple-negative breast cancer in the United States. This highly aggressive cancer has few treatment options, because the cells test negative for three known treatment targets – estrogen, progesterone and HER2 protein receptors.


Working with patient data from the Graham Cancer Center, researchers are investigating potential contributing factors such as diet, alcohol use and genetic variants among women, and the effects of these on cancer metabolism. The team will also examine spatial relationships between cancer “hot spots”—geographic areas with a higher-than-expected prevalence—and modifiable risk factors.


Key resources for the study are blood and tissue samples from the Graham Cancer Center’s Tissue Procurement Center and its statewide High-Risk Family Cancer Registry.


The research team will be led by Director of Population Health Research at ChristianaCare Scott Siegel, Ph.D., and Lead Research Scientist Jennifer Sims Mourtada, Ph.D., at the Graham Cancer Center’s Cawley Center for Translational Cancer Research (CTCR). They will join Zachary Schug, Ph.D., at Wistar’s Molecular and Cellular Oncogenesis Program.


Researching novel therapy for ovarian cancer

The latest study supported by the Graham Cancer Center’s Tissue Procurement Program targets KAT6A expression as a novel therapy for ovarian cancer caused by a specific genetic mutation, called PP2R1A.


Epithelial ovarian cancer is the most common form of ovarian cancer and the leading cause of gynecologic cancer deaths in the United States. Chemoresistance to currently available platinum-based drugs like cisplatin represents a major treatment challenge, as more than 50 percent of affected women ultimately relapse and die from this disease.


Wistar’s Rugang Zhang, Ph.D., leader of the Immunology, Microenvironment and Metastases Program, is focused on developing novel therapeutics for subtypes of ovarian cancer that currently have no effective therapies and on improving the current standard of care. Dr. Zhang’s previous work suggests that KAT6A signaling plays a critical role in ovarian cancer progression. Targeting this signaling pathway could be an effective strategy for treating ovarian cancer.


Working with Dr. Zhang on this project are Graham Cancer Center gynecologic oncologists Mark Cadungog, M.D., director of Robotic Surgery, and Sudeshna Chatterjee-Paer, M.D., and Cawley CTCR’s Stephanie Jean, M.D., director of Gynecologic Oncology Research. Also collaborating with the team is Wistar’s Alessandro Gardini, Ph.D., assistant professor in the Gene Expression & Regulation Program.


‘Mini organs’ offer hope for therapeutics

Dr. Sims-Mourtada at the Cawley CTCR will lead a new program to culture organ-specific tissue from stem cells that could change the way diseases are studied and treated.


These so called “mini organs” or “organoids” are three-dimensional tissue cultures grown in the lab that replicate the complexity and functions of a specific tissue or organ found in the body. Organoids offer scientists a better model for how drugs and other therapeutics might interact with a patient’s particular type of tumor, opening new avenues for precision medicine.


“The ability to grow each patient’s tumor in a three-dimensional organoid along with our capability to create patient-derived xenograft or animal models as part of our PDX core, will allow us to fully capture the effects of genetic as well as gene altering behavioral and environmental influences that are lacking in current research models,” said Dr. Sims-Mourtada. “Our collaboration with Wistar to build these programs raises our clinical platform to the next level for studying new cancer biomarkers and treatments.”


Advancing a Pioneering Partnership

The Graham Cancer Center made history when it signed a first-of-its-kind agreement in 2011 with The Wistar Institute, pairing a National Cancer Institute, NCI-designated basic research institution with a community cancer center that is also an NCI Community Oncology Research Program (NCORP).


“Our partnership with Wistar has attracted national recognition as a model of collaboration that leverages cutting-edge research to benefit cancer prevention and therapy statewide,” says Nicholas J. Petrelli, M.D., Bank of America endowed medical director of ChristianaCare’s Helen F. Graham Cancer Center and Research Institute. “With Wistar, our productive collaborations over the last decade continue to drive discovery research toward clinical trials to benefit patients here at the Graham Cancer Center and in communities everywhere.”


“The Graham Center has been an ideal partner in our mission,” said Dario C. Altieri, M.D., Wistar president and CEO and director of the Ellen and Ronald Caplan Cancer Center. “Our scientists at Wistar have access to clinically-annotated primary patient specimens of the highest quality. As the majority of patients at the Graham Cancer Center are treatment naïve, this collaboration affords an opportunity to conduct unique, high impact mechanistic and correlative studies that will ultimately advance important scientific discoveries that hopefully will lead to better cancer therapies.”

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ChristianaCare Launches Organoid Core to Personalize Cancer Treatment

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In a major step forward for cancer care, researchers at ChristianaCare’s Gene Editing Institute have shown that disabling the NRF2 gene with CRISPR technology can reverse chemotherapy resistance in lung cancer. The approach restores drug sensitivity and slows tumor growth. The findings were published Nov. 13, 2025 in the online edition of Molecular Therapy Oncology. This breakthrough stems from more than a decade of research by the Gene Editing Institute into the NRF2 gene, a known driver of treatment resistance. The results were consistent across multiple in vitro studies using human lung cancer cell lines and in vivo animal models. “We’ve seen compelling evidence at every stage of research,” said Kelly Banas, Ph.D., lead author of the study and associate director of research at the Gene Editing Institute. “It’s a strong foundation for taking the next step toward clinical trials.” Potential Beyond Lung Cancer The study focused on lung squamous cell carcinoma, an aggressive and common form of non-small cell lung cancer (NSCLC) that accounts for 20% to 30% of all lung cancer cases, according to the American Cancer Society. It’s estimated that over 190,000 people in the U.S. will be diagnosed in 2025. While the research centered on this cancer type, the implications are broader. Overactive NRF2 contributes to chemotherapy resistance in several solid tumors, including liver, esophageal and head and neck cancers. The results suggest a CRISPR-based strategy targeting NRF2 could help resensitize a wide range of treatment-resistant tumors to standard chemotherapy. “This is a significant step toward overcoming one of the biggest challenges in cancer therapy — drug resistance,” Banas said. “By targeting a key transcription factor that drives resistance, we’ve shown that gene editing can re-sensitize tumors to standard treatment. We’re hopeful that in clinical trials and beyond, this is what will allow chemotherapy to improve outcomes for patients and could enable them to remain healthier during the entirety of their treatment regimen.” Targeting a Master Switch for Resistance The research zeroed in on a tumor-specific mutation, R34G, in the NRF2 gene, which acts as a master regulator of cellular stress responses. When overactive, NRF2 helps cancer cells withstand chemotherapy. Using CRISPR/Cas9, the team engineered lung cancer cells with the R34G mutation and successfully knocked out NRF2. This restored sensitivity to chemotherapy drugs such as carboplatin and paclitaxel. In animal models, tumors directly treated with CRISPR to knockout NRF2 grew more slowly and responded better to treatment. “This work brings transformational change to how we think about treating resistant cancers,” said Eric Kmiec, Ph.D., senior author of the study and executive director of the Gene Editing Institute. “Instead of developing entirely new drugs, we are using gene editing to make existing ones effective again.” Editing Reaches Threshold Levels One of the most promising discoveries was that disrupting NRF2 in just 20% to 40% of tumor cells, was enough to improve the response to chemotherapy and shrink tumors. This insight is particularly relevant for clinical use, where editing every cancer cell may not be feasible. To test therapy in mice, the researchers used lipid nanoparticles (LNPs), a non-viral method with high efficiency and low risk of unintended, off-target effects. Sequencing confirmed that the edits were highly specific to the mutated NRF2 gene, with minimal unintended changes elsewhere in the genome. “The power of this CRISPR therapy lies in its precision. It’s like an arrow that hits only the bullseye,” said Banas. “This level of specificity with minimal unanticipated genomic side effects offers real hope for the cancer patients who could one day receive this treatment.”

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