Featured Post from ChristianaCare

ChristianaCare and JPMorgan Chase & Co. Partner to Build Health Care Career Opportunities for Delaware Teens

Sep 1, 2023

2 min

ChristianaCare has received a $100,000 grant from JPMorgan Chase & Co. to launch a youth employment program to build a more diverse and inclusive health care workforce.



“At ChristianaCare, we embrace diversity and show respect to everyone,” said Dia Williams Adams, MPA, vice president of philanthropy at ChristianaCare. “Providing exposure to health care careers at an early age and building pipelines to employment are key components to building strong and healthy communities. We are deeply grateful to JPMorgan Chase for its generosity and commitment to inclusion and diversity.”


The program, Health Impacts, is a year-long pilot program designed to connect youth ages 16 to 18 from low-to-moderate income households within the Greater Wilmington area to career opportunities in health care. Health Impacts will include an intensive training program, during which the teens will learn from ChristianaCare health professionals about workforce development skills and the characteristics essential for career success. The training program will be followed by a nine-month paid internship that culminates with employment opportunities at ChristianaCare.


During the internship the teens will receive additional career coaching and participate in work-based learning assignments to help them develop skills, such as effective interviewing, relationship building and a strong work ethic.


“There are fantastic opportunities in health care today that can match up with a wide variety of interests and provide young people with a career path that offers financial stability and growth – plus the personal rewards of doing work that helps others,” said Kamela Smith, M.Ed., manager of Community Education and Engagement at ChristianaCare. “This program is an exciting opportunity to expand our local health care workforce while inspiring young people in our community to be the next generation of caregivers.”


JPMorgan Chase’s support of Health Impacts is part of a $30 billion Racial Equity Commitment by the global financial services provider to help close the racial wealth gap and advance economic inclusion among communities that are underserved in the United States.


“As one of Delaware’s largest employers, we are incredibly focused on creating a more equitable and inclusive economy for more residents across the region,” said Jac Rivers, Vice President, Global Philanthropy Program Officer Eastern Region, JPMorgan Chase. “Building a skilled workforce and ensuring that all people, regardless of background, have access to the support they need is critical to these efforts. Together with a dynamic community partner like ChristianaCare, and the launch of their new Summer Youth Employment Program (SYEP) in Wilmington, we can truly help unlock opportunity for more Delaware residents to access meaningful jobs and lasting economic growth.”


To learn more about ways to give to ChristianaCare, visit https://www.christianacare.org/donors.


Powered by

You might also like...

Check out some other posts from ChristianaCare

3 min

Gene Editing Breakthrough Offers New Hope for Head and Neck Cancer Patients

Researchers at the ChristianaCare Gene Editing Institute have made an important advance in treating head and neck cancers. By using CRISPR gene editing, the team found a way to restore how well chemotherapy works in tumors that have stopped responding to treatment. Their results, now published in Molecular Therapy Oncology, could change how doctors treat these aggressive cancers and give new hope to many patients who face limited options. Head and neck cancer is the seventh most common cancer worldwide, and cases are expected to rise by 30 percent every year by 2030. Even with progress in surgery, chemotherapy and immunotherapy, many patients still reach a point where treatment no longer works. The ChristianaCare team aimed to solve this challenge at its source. Targeting the Heart of Drug Resistance The researchers focused on a gene called NRF2. This gene acts like a master switch that helps cancer cells survive stress and resist chemotherapy. Because NRF2 plays such a central role in tumor growth, the team chose to develop a genetic therapy that disables the gene itself rather than targeting a single protein, which is common in traditional drug development. Since NRF2 is a transcription factor, shutting it down in a lasting way is more likely to succeed through CRISPR gene editing. Their major advance was showing that CRISPR can successfully disrupt NRF2 in head and neck cancer cells and in esophageal cancer cells. This work builds on earlier studies in lung cancer, where blocking NRF2 made tumors more sensitive to chemotherapy and improved survival in animal models. “Our goal was to break through the wall of drug resistance that so many patients face,” said Natalia Rivera Torres, Ph.D., the study’s lead author. “By precisely editing the NRF2 gene, we can make cancer cells vulnerable again to standard treatments. This could improve outcomes and quality of life.” Precision Matters: The Power of Target Choice The study also showed that the location of the CRISPR cut within the NRF2 gene makes a big difference. The strongest results came from targeting exon 4, a part of the gene that controls a key section of the NRF2 protein. Editing this region reduced NRF2 levels by 90 percent and made cancer cells much more sensitive to chemotherapy. In comparison, editing exon 2 was less effective even though it still caused high levels of gene disruption. The team also found that a process called exon skipping, where sections of genetic code are rearranged, can affect the outcome of gene editing. This discovery highlights how important careful design and testing are when building gene editing therapies. A Platform for Broader Impact ChristianaCare researchers saw the same results in both head and neck cancer cells and esophageal cancer cells. This suggests the strategy could help treat many solid tumors that have high levels of NRF2 and are known for strong drug resistance. “This is more than just a single experiment,” said Eric Kmiec, Ph.D., director of the Gene Editing Institute and senior author of the study. “We are building a platform that can be adapted to different cancers. Our earlier work in lung cancer showed the promise of this approach, and now we see it working in other hard to treat tumors. It is an exciting step toward making gene editing a meaningful part of cancer treatment.” Looking Ahead: Toward Clinical Application With these strong results, the team is now focused on finding the safest and most effective way to deliver the gene editing tools directly to tumors. Their goal is to reduce how much standard treatment a patient needs in order to get the best result with fewer side effects. “Drug resistance is one of the biggest challenges in cancer care,” Rivera Torres said. “If we can overcome it with gene editing, we could give patients more time, better quality of life and a renewed sense of hope.” Kmiec added, “We are committed to moving this technology forward quickly while always keeping the patient in mind. The future of cancer treatment is personal, precise and, we believe, within reach.”

4 min

Researchers Reveal How a Common Gene Mutation Disrupts Colon Tissue Renewal and Sparks Early Tumor Growth

A team of researchers from ChristianaCare and the University of Delaware has uncovered a key early step in how colorectal cancer begins. Their new study shows that a common genetic mutation in colorectal cancer disrupts the colon’s normal tissue renewal process, causing immature cells to build up, tissue structure to break down and early tumors to form. Their findings were published in the journal Cancers. “This finding changes how we think about the very first steps of colon cancer,” said Bruce Boman, M.D., Ph.D., senior author of the study and a senior researcher at the Cawley Center for Translational Cancer Research at ChristianaCare’s Helen F. Graham Cancer Center & Research Institute. “Instead of cancer starting because cells grow too fast, we found that it may start because the normal tissue renewal process slows down, creating a backup of cells that should have moved on. That backup sets the stage for tumors to grow.” The study was led by a multidisciplinary team of engineers, mathematicians, pathologists and tumor biologists from four research institutions. Colorectal cancer is one of the most common and deadly cancers worldwide. According to the World Health Organization, more than 1.9 million people are diagnosed each year, and about 930,000 people die from the disease annually. How healthy colon tissue renews itself The lining of the colon is constantly renewing itself. Every day, billions of cells are shed and replaced to keep the tissue healthy and working properly. This process depends on a steady cycle. New cells form at the base of tiny pockets called crypts, mature as they move upward, and are eventually shed. The new study shows how this natural process breaks down when a mutation occurs in a gene called APC, which is altered in about 90 percent of colorectal cancers. Rather than speeding up cell growth, the APC mutation creates a slowdown, or bottleneck, in the colon tissue’s renewal cycle. According to Boman, this slowdown causes dividing cells to pile up instead of moving through the system as they should. The result is a kind of tumor cell “traffic jam” that leads to distorted tissue and the formation of adenomas, early growths that can become cancerous. What APC-mutant tissue looks like To see these changes up close, the team compared healthy colon tissue with tissue from patients who have familial adenomatous polyposis, or FAP, an inherited condition caused by APC mutations. The differences were clear: APC-mutant crypts contained more immature, rapidly dividing cells. Fewer cells matured into specialized cells needed for healthy tissue. The zone where cells divide extended higher than normal. The overall renewal cycle took longer. “These findings are significant because they show how cancer-driving mutations change tissues that normally renew themselves nonstop,” Boman said. Pairing patient tissue with computer modeling To see how these changes happen over time, the researchers studied patient tissue and used a computer model that shows how colon cells normally grow and renew. When they slowed this renewal process in the model, it matched what they saw in tissue with the APC mutation. Cells became crowded, the structures lost their normal shape, and early tumor-like growths, known as adenomas, began to form. This confirmed that delayed renewal alone can trigger the earliest changes linked to colon cancer, even before cells appear abnormal under a microscope. “Our findings show that APC mutation does more than turn on growth signals,” Boman said. “It changes the timing of renewal. Once that timing is off, the tissue becomes vulnerable to structural damage and early tumor growth.” Building on earlier research This study builds on earlier work by the same team that mapped how healthy colon tissue renews itself. In prior studies, the researchers identified five basic biological rules that guide how colon cells grow, move and replace one another in a steady, organized way. The new findings show what happens when that system breaks down. A common mutation called APC slows the normal renewal process. Young, stem-like cells begin to build up before they can mature. Over time, that imbalance creates the conditions for early tumor growth. To pinpoint how these changes unfold, researchers Gilberto Schleiniger, Ph.D., and Christopher Raymond, Ph.D., from the University of Delaware’s Department of Mathematical Sciences paired mathematical models with real patient tissue data. Their work shows that even small delays in cell renewal can push healthy tissue toward cancer. “This gives us a clearer picture of how cancer can start long before a tumor is visible,” said Schleiniger. “By understanding the rules that keep healthy tissue in balance, we can see where and how things begin to go off track.” A possible path toward future treatments The findings also point toward a potential new approach to treatment. The researchers found evidence that the disrupted renewal process may trigger a chain reaction that allows pre-cancerous cells to keep copying themselves and fueling tumor growth. By targeting this process, it may be possible to restore normal renewal timing and healthier tissue structure before cancer becomes established. “This study shows that cancer isn’t just about rogue cells, but about a system that’s fallen out of rhythm,” said Bruce Boman, M.D., Ph.D. “If we can reset that renewal process, we may be able to prevent or slow early tumor growth before it gains momentum.”

3 min

CorriXR Launches Bold Collaboration to Create First Inhaled CRISPR Therapy for Lung Cancer

CorriXR Therapeutics, ChristianaCare’s first commercial biotherapeutics spinout, has launched a major collaboration with InhaTarget Therapeutics and Merxin Ltd to develop an inhaled genetic therapy for lung cancer. The goal is to deliver a CRISPR-based treatment straight to tumors in the lungs to improve effectiveness and cut harmful side effects. A New Way to Treat Lung Cancer Lung cancer remains one of the deadliest cancers worldwide. Squamous cell lung carcinoma, an aggressive form of non-small cell lung cancer, accounts for up to 30% of cases. More than 380,000 people are diagnosed each year, yet the five-year survival rate stays under 15%. Standard chemotherapy and immunotherapy often become less effective, and many patients develop resistance that leaves them with few options and rising toxicity. CorriXR is taking aim at this problem. Its CRISPR gene editing system targets NRF2, a key driver of treatment resistance. By switching off NRF2, the therapy has the potential to make tumors sensitive to chemotherapy again and give patients a chance at better outcomes. As reported in a recent paper in Molecular Therapy Oncology, researchers at ChristianaCare’s Gene Editing Institute showed in preclinical lung cancer models that disabling NRF2 can resensitize tumors to chemotherapy with minimal off-target effects. “This partnership is about more than science. It’s about hope for patients,” said Eric Kmiec, Ph.D., founder and CEO of CorriXR Therapeutics and chief scientific officer at ChristianaCare’s Gene Editing Institute. “Lung cancer patients deserve therapies that work and improve quality of life. By combining our CRISPR-based technology with inhaled delivery, we can target tumors directly and reduce systemic toxicity. Our goal is to make treatment simpler, more effective and less invasive.” How the Inhaled Delivery System Works The treatment will be given through inhalation using InhaTarget’s lipid nanoparticle formulation delivered by Merxin Ltd’s advanced inhaler platform. The goal is a non-invasive therapy that patients could use at home. “Combining our pulmonary drug delivery LNP platform with CorriXR’s groundbreaking science and Merxin Ltd’s device technology has the potential to reshape the landscape of lung cancer treatment. We are eager to advance work on this novel combination,” said Frédéric De Coninck, Ph.D., co-founder and CEO of InhaTarget Therapeutics. Merxin Ltd’s technology is central to the approach. Its inhalers are built to deliver precise, consistent doses straight to the lungs. For this collaboration, Merxin Ltd is adapting its device to handle lipid nanoparticle formulations for the first time in a cancer treatment. “Our advanced inhaler technology is designed to ensure non-invasive, precise, consistent delivery of novel therapeutics,” said Philippe Rogueda, Ph.D., co-founder and chief business officer of Merxin Ltd. “We are excited to contribute to this vital effort and help bring innovative solutions to patients with lung cancer.” Why This Matters Patients with squamous cell lung carcinoma often face a fast-moving disease and few treatment choices. A therapy that can reach tumors directly, reduce toxicity and avoid resistance would mark a major shift. “This collaboration underscores the power of combining innovative science with practical delivery solutions,” said Kmiec. “Our CRISPR-based approach is designed to overcome one of the toughest challenges in oncology: treatment resistance. By partnering with experts in inhalation technology, we are moving closer to a therapy that is not only effective but accessible.” Studies will begin soon, with a substantial set of results on effectiveness and impact expected by spring 2026.

View all posts
Powered by