Dr. DelNero is an assistant professor with the Division of Community Health and Research in the Department of Internal Medicine at the University of Arkansas for Medical Sciences (UAMS). His research involves implementation science, community engagement and biomedical engineering.

DelNero studies the connection between the Cancer Institute and the catchment area. The ‘catchment area’ refers to the geographic area that UAMS serves in its research, treatment and outreach. The catchment area provides a geographic scope to monitor cancer trends, identify pronounced disparities and enact cancer control strategies. Information about the catchment area can improve the implementation of evidence-based programs to reduce the burden of cancer. A better understanding of the catchment area ensures that all segments of the population benefit from advances in cancer prevention, early detection, treatment and survivorship care.

DelNero also studies the relationship between blood vessels and cancer metabolism. He developed “tumor-on-a-chip” devices to investigate tissue perfusion and cell energy status. His research contributed to new strategies to predict whether patients are likely to benefit from drugs that target specific metabolic pathways.

DelNero completed a postdoc with the Implementation Science team in the Division of Cancer Control and Population Sciences at the National Cancer Institute. He earned a bachelor’s degree in chemical engineering at Vanderbilt, a Master’s in Public Health at Harvard and a Ph.D. in biomedical engineering at Cornell. His articles appeared in CEBP, Nature Protocols, Science Translational Medicine, Advanced Drug Delivery Reviews and Biomaterials.

DelNero is originally from Kansas. Outside of lab, he enjoys spending time with friends and family. His hobbies include baking and running. Last month, he hiked the Ozark Highland Trail and fell in love with the Arkansas mountains. He is excited to join the team at UAMS!

pdelnero@uams.edu
(501) 526-4340
CI-10166

Presented annually since 2009, the Winthrop P. Rockefeller Cancer Institute Seeds of Science Awards assist cancer researchers in collecting data and developing projects that have the potential to result in significant research findings.

This year we had a record number of applicants and have supported a record number of investigators. These efforts directly support our mission to achieve NCI designation. 

The following four Cancer Institute members will receive $50,000 individual pilot awards: 

Katie Ryan, Ph.D.

Assistant Professor, Department of Biochemistry & Molecular Biology.

A proteomics approach to determining how driver mutations effect the metastatic potential of lung cancer.

Mohammad Alinoor Rahman, Ph.D.

Assistant Professor, Department of Biochemistry & Molecular Biology.

Understanding and Targeting Aberrant Splicing in MDS-RS.

Michael Bauer, Ph.D.

Assistant Professor, Department of Biomedical Informatics

Mechanism of the novel NEK2 signaling pathways in myeloma progression.

Yong-Chen “William” Lu, Ph.D.

Assistant Professor, Department of Pathology

Detecting mitochondrial DNA mutations at the single-cell level.

In addition to supporting novel ideas from individual Cancer Institute members, we also support team science by funding groups of laboratories that join forces to address challenging cancer research questions. The following research teams will receive $100,000 each to support their work. 

$100,000 Team Awards 

Sayem Miah, Ph.D., Mohammad Rahman, Ph.D., and Stephanie Byrum, Ph.D., assistant professors in the Department of Biochemistry and Molecular Biology. Loss of FAM60A promotes HBB induced mammary gland tumorigenesis.

Bolni “Marius” Nagalo, Ph.D., assistant professor in the Department of Pathology, Martin Cannon, Ph.D., professor in the Department of Microbiology and Immunology and Alexei Basnakian, M.D., Ph.D., professor in the Department of Pharmacology & Toxicology. Immunotherapy of hepatocellular carcinoma by live attenuated vaccine vectors.

Samantha Kendrick, Ph.D., assistant professor in the Department of Biochemistry & Molecular Biology and Brendan Frett, Ph.D., assistant professor in the Department of Pharmaceutical Sciences. NEK2 kinase as a new oncogenic vulnerability in lymphoma.

Justin Leung, Ph.D., assistant professor in the Department of Radiation Oncology and Brian Koss, Ph.D., assistant professor in the Department of Biochemistry & Molecular Biology. Functional ORFeome atlas. 

Adam Wolfe, M.D., Ph.D., assistant professor in the Department of Radiation Oncology, Isabelle Racine Miousse, Ph.D., assistant professor in the Department of Biochemistry & Molecular Biology and Nukhet Aykin-Burns, Ph.D., associate professor in the Department of Pharmaceutical Sciences. Synergizing methionine restriction with radiation therapy in KRAS mutant rectal cancer.

Kevin Raney, Ph.D., professor, Eric Enemark, Ph.D., associate professor, Robert Eoff, Ph.D., professor – all in the Department of Biochemistry & Molecular Biology – and Karl Boehme, Ph.D., associate professor in the Department of Microbiology & Immunology. Helicases, Non-Canonical DNA and Their Links to Cancer through Innate Immunity.

Hong-yu Li, Ph.D., professor in the Department of Pharmaceutical Sciences and Zhiqiang Qin, M.D., Ph.D., associate professor in the Department of Pathology. Development of Potent Dual HDACs/BRD4 Inhibitors for the Treatment of Virus-associated Lymphomas.

Assistant Professor
Pediatric Hematology and Oncology
Department of Pediatrics, UAMS College of Medicine
Arkansas Children’s Research Institute

What is your relationship to cancer?

As described by Dr. Siddhartha Mukherjee in his Pulitzer Prize winning monograph, cancer is and continues to be “The Emperor of All Maladies”. Being diagnosed with cancer is always scary for obvious reasons. Not only it is difficult to diagnose, treat and experience, it is also difficult to describe. Cancer is not one disease, but a collective name for what can happen when our body’s chemical instruction manual goes wrong.

I have my training and experience in biological engineering and had no concrete plan to pursue cancer research. During my training at the Cancer Institute, I first came in close contact with cancer patients, while sharing the elevators or getting foods at the cafeteria. I was deeply saddened to see the painful faces, their struggle to walk freely like a healthy individual, and a silent fear in the eyes of their family. This gradually changed my perception and motivated me to steer my interest to cancer research where my efforts and skillset could ultimately have an important impact in the lives of cancer patients and their families.

What do you hope to contribute as a member of the Winthrop P. Rockefeller Cancer Institute?

Arkansas Children’s Research Institute and UAMS provided me with a unique opportunity to invest my interest in pediatric leukemia research, which also allows for broadening the scope for cancer research in Arkansas. Dynamic collaborative efforts between the institutes are also supportive of the goal of the Winthrop P. Rockefeller Cancer Institute in achieving National Cancer Institute designation. I would like to contribute to the institutional goal and vision by publishing our innovative research, strengthening collaborative efforts and obtaining competitive research fundings. I am also highly motivated to host trainees at the undergraduate, graduate or advanced level in our laboratory and have them acquire critical assets, including knowledge, skills, and interest in cancer research.

Tell us about your current research?

Our laboratory presently focuses on a deadliest subtype of pediatric acute myeloid leukemia (AML). Although AML impacts all ages, AML with the ETO2-GLIS2 fusion oncoprotein is a unique entity of early childhood (< 3 years). Infants and young children with this type of AML have among the worst outcomes of all pediatric AML subtypes. The fusion between ETO2 and GLIS2 occurs due to an inversion event at chromosome16, which is not detected by routine cytogenetics and thus must be specifically sought by fluorescent in-situ hybridization technique or molecular studies, likely explaining its late and recent discovery. Whole genome sequencing studies have failed to identify additional second hit coding gene mutations in these cases and the overall mutational burden is among the lowest of all human cancers.

In contrast, laboratory stem-cell models show that introduction of the fusion alone is sufficient for malignant transformation. Thus, ETO2-GLIS2 AML is suspected to be critically supported by epigenetic mechanisms, however these have not been adequately investigated. Previous literature suggests that ETO2-GLIS2 induce havoc changes in chromatin architecture and preferentially activates H3K27ac marked chromatin at atypical (neo) gene loci, which are defined as super-enhancers (SE) that are supportive of sustenance of leukemic gene expression.

Based on previous literature and our preliminary data, we identified that mediator (MED) 12 like (MED12L) protein is epigenetically enhanced and overexpressed in ETO2-GLIS2 positive AML subgroup, and co-upregulated with CDK8 of the MED-kinase module. Given ETO2-GLIS2 and MED12L mutually occupies the neo-SE element, and MED proteins aid in formation and sustenance of SE activities in cancer, we aim to investigate the (1) MED12L interactions with ETO2-GLIS2 bound or unbound to SE associated proteins and determine (2) whether epigenetic perturbations of MED12L can impair aberrant transcriptional machinery and overall leukemic growth. Our studies are expected to develop novel insights into changes in chromatin architecture and mediator-enhancer mechanisms, favoring leukemic growth, which may be relevant to other AML subtypes and hematological malignancies.    

A native of Calcutta, India, Dr. Choudhury earned bachelor’s and master’s degrees from the University of Calcutta. He received a Ph.D. in biotechnology from the Indian Statistical Institute, during which time he received multiple senior research fellowship awards and a postdoctoral fellowship in nano science and technology.  In 2013, he was awarded a three-year postdoctoral fellowship from the W.M KECK Foundation at Purdue University to study in the laboratory of Professor Joseph Irudayaraj. He joined the UAMS Myeloma Center as a research associate in 2013 and was promoted to assistant professor in the Department of Pediatrics in 2020. He is a member of the Cancer Institute’s Cancer Biology Research Group. He received a 2020-2021 UAMS Seeds of Science Award. His work is widely published in such journals as Blood Cancer Journal, Cancers, Cancer Research Cells, Journal of Hematology & Oncology, Scientifics Reports, and Oncotarget.

Assistant Professor, Department of Pathology, UAMS College of Medicine; Cancer Biology Research Group, Winthrop P. Rockefeller Cancer Institute

What is your relationship to cancer?

Prior to joining the Winthrop P. Rockefeller Cancer Institute and UAMS, I worked at the National Institutes of Health (NIH) Clinical Center for 11 years. I had the unique experience to meet many cancer patients who joined our clinical trial programs. Experimental treatments provided by us were likely the last hope for them, and I admired their courage and generosity with all my heart. Because of this, I saw many patients fighting for their lives in the intensive care units, and most of them passed away soon after the experimental treatments failed. This experience completely changed my view of life and death. On the bright side, I witnessed firsthand the development of a breakthrough in cancer treatment called cancer immunotherapy. Several cancer patients were saved from certain death and are now cancer-free, in part because of my research at the NIH.

Tell us about your current research?

Cancer immunotherapy is a new type of cancer treatment and uses a patients’ own immune system to attack cancer. T-cells play a major role in cancer immunotherapy, and several types

of T cell-based cancer immunotherapy have shown strong clinical responses for cancer patients. However, most previous studies have been focused on therapies suitable for the Caucasian population. As a result, cancer patients within the underserved populations, including African American and Hispanic populations, are less likely to qualify for these new treatments

in the near future. To address this, I focus on the development of new T cell-based cancer immunotherapies for underserved populations. I feel very grateful that the Cancer

Institute and Translational Research Institute at UAMS support this type of research.

What do you hope to contribute to cancer research and to the Winthrop P. Rockefeller Cancer Institute?

As a team member at the Cancer Institute, I plan to establish a robust research program based

on my previous experience at the National Cancer Institute (NCI), NIH. Since I joined the UAMS, I appreciate the research environment, shared resources and funding provided by the Cancer Institute. I also feel grateful for the help and advice from my mentors through the mentorship program and KL2 program. More importantly, the leadership at the Cancer Institute, Department of Pathology and UAMS has led us to make significant progress in order to elevate the status of this institution. Therefore, I feel very proud to be part of this dream team, with the goal of becoming one of the NCI-designated cancer centers in the near future.

About Dr. Lu

Dr. Lu is a co-investigator with Mayumi Nakagawa, M.D., Ph.D., for an NCI R01 grant studying the T-cell responses to high-risk HPV. He is the recipient of the 2021 UAMS Translational Research Institute KL2 Award. A native of Taiwan, he received his Ph.D. training at Princess Margaret Cancer Centre, University of Toronto, Canada. After finishing his Ph.D. training, he became a postdoctoral visiting fellow at Surgery Branch, NCI, NIH. Lu was promoted to a staff scientist position, prior to joining the UAMS in early 2021. 

Cancer Biology Research Group
Assistant Professor, Department of Pathology, College of Medicine

What is your relationship to cancer?

My journey to become a cancer researcher began after completing my undergraduate training at the University of Ouagadougou in Burkina Faso. I was privileged to join the unique graduate program in infectious diseases there and received my Ph.D. summa cum laude in 2012. Soon, I began to learn about hepatocellular carcinoma (HCC) while drawing blood from cancer patients during clinical rotations at the Military Medical Centre Lamizana in Ouagadougou.

I was struck by the high incidence of hepatitis B (HBV)-induced HCC among young patients, the majority who succumbed from their diseases within a few weeks of the diagnosis. Worst still, there was no warning of cancer risk and no preventive treatment.

Marius Bolni Nagalo, Ph.D.

However, like most other young aspiring biomedical researchers who preceded me, an acute and profound realization of the lack of resources and trained personnel to achieve clinically beneficial outcomes for these patients quickly served to temper, but by no means eliminate my inherent and requisite optimism and tenacity to care for these patients. I decided to further my training in drug development with a focus on the use of viral vectors to treat human cancers.

What do you hope to contribute to the Cancer Institute?

The current goal of the Cancer Institute is to obtain an NCI designation. Although it is a tremendous task, I have witnessed during my interview the commitment of Dr. Birrer to achieving this milestone. The Cancer Institute has four programs with the specific mission to develop innovative approaches that can be translated into patients and attract extramural funding to benefit the health and well-being of the people of Arkansas.  My expertise in engineering and applying viral vectors in cancer gene therapy and oncolytic viral therapy could improve the outcomes for cancer patients with limited therapeutic options and contribute to our goal of obtaining NCI designation.

Tell us about your current research?

I am an assistant professor of Pathology in the Division of Experimental Pathology at UAMS. My research program focuses on developing tumor-specific viral vectors for oncolytic viral therapy and gene therapy in human cancers, especially hepatobiliary and pancreatic cancers. With my collaborators at UAMS, we are delineating strategies to use live-attenuated vaccine vectors as affordable cancer immunotherapies. I firmly believe that this research endeavor will help address health disparities in access to cancer care, particularly in economically disadvantaged areas of the United States. 

To learn more, view Dr. Nagalo’s research profile

Questions? Email bmnagalo@uams.edu

Fenghuang Zhan, M.D., is executive director of Myeloma Center Basic Research and the Morrison Family Endowed Chair at UAMS. He serves as a professor in the Department of Internal Medicine and is leader of the Genetics, Genomics and Proteomics faculty. His research is funded by competitive grants of over $3 million. He is a recipient of a $1.8 million grant from the Riney Foundation.

“The most important part of my contribution is to translate my research results into clinic usage to help improve myeloma care,” says Zhan.

View Research Profile

Tells about your current research

I’m researching drug resistance and immune therapy in multiple myeloma (MM). The extreme variability in survival among patients with MM suggests that specific genetic lesions, possibly reflected in altered gene expression profile patterns in tumor cells, may account for the divergent clinical outcomes. My laboratory is interested in understanding how the genetic alterations in cancer cells contribute to tumor progression, alter treatment response, and create vulnerabilities that may be targeted therapeutically. Our previous work demonstrates that High NEK2 drives myeloma drug resistance and poor prognosis. Monotherapy with PD-1/PD-L1 inhibitors has shown disappointing results in MM, even though targeting immune checkpoints represents a new and very promising approach for the treatment of many solid tumors and certain types of hematologic malignancies. Is there any relationship between NEK2 and the disappointing results of targeting immune checkpoints in MM? To facilitate our research, we are combining genetic and genomic tools that enable us to explore various aspects of cancer biology in a comprehensive way. Current efforts strive to identify new components of NEK2 networks and characterize their impact on immune checkpoints blockade response. In addition, we are defining new biomarkers for targeting immune checkpoint therapy and developing new strategies for high risk (PR/relapsed) MM patients. 

Another research focus is on tumor-initiating cells (TICs) in MM. Although a universally accepted TIC phenotype has not yet been identified, the establishment of a TIC phenotype is critical if we want to fully understand the biology of these cells. Many studies indicate that CD24 has been recognized as a legitimate cancer stem cell marker in multiple cancers. Our studies demonstrated that CD24⁺ MM cells maintain the features of self-renewal and drug resistance in MM, providing a biomarker for myeloma genesis and targeted therapy. Myeloma tumor-initiating cells (MM-TICs), characterized by increased drug resistance and self-renewal capacity, are very likely responsible for our failure to cure myeloma in the majority of patients. Our goal is (1) To determine how the CD24⁺ primary MM cells (CD38⁺CD45^–) contribute to drug resistance; (2) To define TIC features; and (3) To develop MM TIC-targeted therapies in vitro and in vivo in a pre-clinical mouse model.  

Multiple Myeloma is virtually always preceded by a monoclonal gammopathy of undetermined significance (MGUS) or smoldering myeloma (SMM), which are pre-malignant conditions and more prevalent in the elderly population. MGUS patients are not routinely screened since there is currently no treatment that has demonstrated efficacy in reducing the risk of progression of MGUS to MM. Taking advantage of our expertise in MGUS and MM biology and the area of genomics, with relevant mouse models in hand and availability of exceptional human MGUS resources, we are uniquely positioned to discover the key factors that are associated with MGUS progression. Then we are able to develop novel therapies based on a modulation of MGUS risk factors.