Maged Zeineldin

Maged Zeineldin
  • Assistant Professor (Starting Fall 2024)

Contact Info


I completed my medical education at the Faculty of Medicine, Alexandria University, Egypt, where I pursued clinical and laboratory genetics following my medical internship. During this phase, I earned a master's degree in human genetics, focusing on the molecular diagnosis of Fragile-X syndrome carriers. My research extended to exploring the impact of genetic polymorphisms on prevalent conditions such as preeclampsia and diabetes mellitus. I also obtained a postgraduate diploma in information technology with a specialization in bioinformatics from Alexandria University. In my thesis, I designed a new alignment tool. Then I received a 3-years scholarship from Ford Foundation to pursue my Ph.D. studies at the University of Kansas, in Kristi Neufeld's laboratory. During my doctoral research, I studied the tumor suppressor gene APC in colon cancer and Familial Adenomatous Polyposis (FAP). After finishing my PhD, I joined Dr. Mike Dyer's group at St. Jude Children's Research Hospital, focusing on the role of Alpha Thalassemia Retardation X-linked (ATRX) gene mutations in neuroblastoma, utilizing next-generation sequencing (NGS). This theme persisted as I transitioned to the T. Larman lab at Johns Hopkins University School of Medicine, where my current research explores how the epigenome, metabolome, and microenvironment collectively influence genetic mutations during neoplastic transformation.


Postdoctoral Training, St. Jude Children’s Research Hospital, Memphis, TN
Ph.D. in Molecular, Cellular and Developmental Biology, University of Kansas, Lawrence, KS
Post-graduate Diploma Information Technology, Alexandria University, Egypt
M.S. in Genetics, Alexandria University, Egypt
MBBCh (MD), Alexandria University, Egypt


The interaction between genetic, epigenetic, and metabolic landscapes in development to target tumors.

The connection between differentiation and oncogenesis is particularly prevalent in cancer especially pediatric tumors. Many childhood cancers are not found in adults because they arise during a particular stage of development and differentiation. Also, the genomic landscape of pediatric cancer is less complex than that of adult tumors. Accumulated data suggest that differentiation arrest in the appropriate developmental milieu underlies many pediatric tumors. One of the best examples of this concept is neuroblastoma, a tumor of the developing sympathoadrenal lineage. High risk neuroblastoma is a leading cause of cancer-related death in children. Despite advancements in the treatment of pediatric cancers in recent times, the 5-year survival rate for neuroblastoma remains lagging at approximately 50%.

Oncogenic and developmental pathways are often integrated because proliferation and differentiation must be precisely coordinated during development. For example, MYCN is an important transcription factor during the differentiation of the sympathetic ganglia and MYCN amplification is the most common oncogenic mutation in neuroblastoma6.

Similarly, mutations in epigenetic regulators are highly prevalent and thought to further contribute to disruptions in cellular differentiation required for tumorigenesis. Among these, mutations of the chromatin remodeler ATRX are the most common and are associated with high-risk neuroblastoma. Notably, ATRX is crucial for the development of the nervous system, and germline mutations of ATRX cause developmental defects and neuronal cell death. This coupling of differentiation/oncogenesis suggests that certain epigenetic states can limit or permit specific oncogenic mutations. Indeed, we found that MYCN-induced epigenetic and metabolic reprograming are not compatible with the epigenetic landscape associated with ATRX mutations in neuroblastoma. 

In Zeineldin lab, we study the interaction between genetic, epigenetic and metabolomic landscapes in differentiation and tumor formation and will exploit the synthetic lethality between MYCN amplification and ATRX mutations to uncover new therapeutic targets. The combination of these two directions allows us to contribute to both the basic understanding of cell and developmental biology of the peripheral nervous system and to translate the finding to novel therapeutic strategies. We have two main projects in the lab:

  1. Project 1: Understanding the epigenetic and metabolic consequences of ATRX mutations on developing sympathetic neurons and neuroblastoma.
  2. project 2: Testing novel epigenetic and metabolic vulnerabilities for to treat high-risk neuroblastoma

Selected Publications