This Is a Critical Moment: Delaware Must Not Go Backward in Health Equity

May 2, 2024

5 min

LeRoi Hicks, M.D., MPH, MACP

The proposed Delaware House Bill 350 is well-intended but would have terrible consequences for Delaware’s most vulnerable populations. There is a better way.


By LeRoi S. Hicks, M.D., MPH, FACP


As a Black physician who has dedicated his 25-year career to understanding and addressing health equity, I am deeply concerned about Delaware’s proposed House Bill 350, which aims to address rising health care costs by establishing a body of political appointees that would oversee the budgets of Delaware’s nonprofit hospitals.


While the goal of bending the cost curve in health care may be well-intentioned, this bill will have horrific consequences for Delaware’s most vulnerable populations, including Black people, Hispanic people and other groups that have been traditionally underserved in health care. We can and must work together to solve this problem and provide the right care, in the right place, at the right time.


A tale of two cities


To borrow a phrase from Charles Dickens, Delaware, like much of America, is a tale of two cities. The experience of life—including a healthy, safe environment and access to good-quality health care—is vastly different depending on where you live and your demographic background. In the city of Wilmington, for example, ZIP codes that are just a few miles apart represent more than 20 years difference in life expectancy. This is not OK—it’s a sign that we have serious structural problems in our communities that are causing harm to people and making their lives shorter.


Importantly, chopping $360 million out of Delaware’s hospital budgets, as House Bill 350 would do in year one, is not going to help this problem—it’s going to make it worse. And in doing so, it would ultimately make health care in Delaware more expensive—not less expensive.


The key to lowering health care costs is to improve quality, access and equity

Data show that about 5% of patients in the United States account for more than 50% of all health care costs. These are primarily patients who have complex and poorly managed chronic conditions that cause them to end up in the most expensive care settings—hospitals, operating rooms, emergency departments.


The key to driving down health care costs is to improve quality and equity so that everyone is supported in achieving their best health, and these high users of the most expensive kinds of care are better supported in managing their health conditions such as diabetes or heart failure in the appropriate way. In doing so, they prevent the need for costly emergency or “rescue” care.


Let’s do more—not less—of what we already know works


Health care is not a one-size-fits-all industry. The delivery of care for patients across a diverse population requires multiple interventions at the same time. These interventions are designed not only to improve the quality of care but also to close the gap in terms of health care disparities. That’s important, because when we improve care and outcomes for the most vulnerable populations, we tend to get things right for everyone.


One type of intervention is about doing exactly the right things for a patient based on the evidence of what will help—and doing nothing extra that will cause harm or generate additional costs without providing additional benefit. An example of this might be ensuring that every patient who has a heart attack gets a certain drug called a beta blocker right after their heart attack, and they receive clear guidance and support on the actions they must take to reduce their risk of a second heart attack, such as regular exercise and good nutrition.


The second type of intervention is for the highest-risk populations. These are patients who live in poor communities where there are no gyms and no grocery stores, and people commonly have challenges with transportation and lack of access to resources that makes it difficult—sometimes impossible—to follow their plan for follow-up care. They lack access to high-nutrient food that reduces their risk of a second heart attack. They also live in areas where there are fewer health care providers compared to more affluent areas.


These interventions tend to be very intensive and do not generate income for health systems; in fact, they require significant non-reimbursed investment, but they are necessary to keep our most vulnerable patients healthy.


The medical community has developed interventions for these populations that are proven to work. A local example is the Delaware Food Pharmacy program, which connects at-risk patients with healthy food and supports their ability to prepare it. The program helps patients improve their overall health and effectively manage their chronic conditions so they can prevent an adverse event that would put them back in the hospital or emergency department.


When we work together, we succeed


We’ve seen incredible examples of how this work can be successful right here in Delaware. Delaware was the first state in the country to eliminate a racial disparity in colorectal cancer, and we did this by expanding cancer services, including making it easy for vulnerable people to get preventive cancer care and screenings. This is an incredible success story that continues to this day, and it was the result of thoughtful, detail-oriented partnerships among the state and the health care community. The work continues as we collaborate to reduce the impact and mortality of breast cancer in our state.


Unfortunately, these kinds of interventions are the first thing to go when health care budgets get slashed, because they don’t generate revenue and are not self-sustaining. These kinds of activities need to be funded—either through grants or an external funder, or by the hospitals and health care systems.


By narrowly focusing on cost, we risk losing the progress we have made


Delaware House Bill 350, as it’s proposed, would cause harm in two ways:


  1. First, it would compromise our ability to invest in these kinds of interventions that work.
  2. Second, it increases the risk that higher-cost health services and programs that are disproportionately needed by people in vulnerable communities could become no longer available in Delaware.


In states where the government has intervened in the name of cutting costs, like Vermont and Massachusetts, we see the consequences–less quality and reduced equitable access to much-needed services. House Bill 350 will widen the gap between those who have means and those who are more vulnerable.


These changes will lead to increased disease burden on these populations. They will end up in the emergency room more and hospitalized more, which is by far the most expensive kind of care. That’s not what anyone wants—and it’s the opposite of what this bill was intended to accomplish.


At this moment, in Delaware, we have an opportunity to put our state on a sustainable path to better health for all Delawareans. House Bill 350 is not that path. However, the discussion that House Bill 350 has started is something that we can build on by bringing together the stakeholders we need to collaborate with to solve these complicated problems. That includes Delaware’s government and legislators, the hospitals and health centers, the insurance, pharmacy and medical device industries, and most importantly, patients and the doctors who care for them.


LeRoi Hicks, M.D., is the campus executive director for ChristianaCare, Wilmington Campus.

Connect with:
LeRoi Hicks, M.D., MPH, MACP

LeRoi Hicks, M.D., MPH, MACP

President, ChristianaCare, Wilmington campus

Dr. Hicks is the recipient of numerous clinical and research awards and is nationally known for his research on health care disparities.

Social Determinants of Health/Health DisparitiesMedicineChronic DiseaseInternal MedicineHealth Equity
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