Discover how St. Jude researchers uncovered how regional differences in the developing brain shape diffuse midline glioma formation.

Discover how St. Jude researchers uncovered how regional differences in the developing brain shape diffuse midline glioma formation.

Explore how St. Jude researchers helped usher in the era of sequencing into diagnostics for pediatric cancers, overcoming previous challenges and limitations.

Learn how St. Jude scientists use epigenetics research to uncover vulnerabilities that can be used to treat neurologic disease, cancer, and blood disorders.

See how St. Jude researchers are using epigenetics to better understand how to diagnose and treat pediatric brain tumors.

Nature Reviews Cancer, Published online: 10 April 2026; doi:10.1038/s41568-026-00930-2In a recent study, Gudenas et al. map pineoblastoma subgroups to pinealocyte progenitors and identify a shared photoreceptor-like transcriptional network across pineoblastoma, retinoblastoma and group 3 medulloblastoma, revealing a developmental vulnerability with therapeutic potential.

Nature, Published online: 25 March 2026; doi:10.1038/s41586-026-10270-8 Single-nucleus chromatin and RNA sequencing identifies epigenetic chromatin domains that confer vulnerability to paediatric brain tumours such as ependymomas, providing insight into the development of such tumours despite ‘quiet’ genomes.

Single-nucleus chromatin and RNA sequencing identifies epigenetic chromatin domains that confer vulnerability to paediatric brain tumours such as ependymomas, providing insight into the development of...

In this issue of Cancer Cell, Gudenas et al. reveal that Group 3 medulloblastoma, pineoblastoma, and retinoblastoma converge on a shared tumor-associated photoreceptor signature rooted in transient developmental progenitors. This work reframes these malignancies as diseases of common developmental vulnerability and identifies shared transcriptional dependencies with potential therapeutic relevance.

Pineoblastoma is an aggressive childhood brain cancer. Using single-cell transcriptomics of patient tumors, developing pineal gland, and engineered models, Gudenas et al. identify pinealocyte progenit...

Smith et al. present M-PACT, a deep neural network leveraging low-input cell-free DNA methylation profiles to achieve robust classification of pediatric brain tumors and enable cellular deconvolution ...

See how M-PACT, an AI-powered algorithm can sift through ctDNA in cerebrospinal fluid and molecularly classify tumors based on their DNA methylation pattern

Find how St. Jude researchers discovered a new way to group patients with medulloblastoma, which could lead to major reduction in treatment-related toxicity.

Arabzade, Shirnekhi, Varadharajan, Ippagunta and colleagues show that the zinc finger translocation-associated (ZFTA) fusion oncoproteins gain intrinsically disordered regions, inducing nuclear conden...

Discover research showing that small disordered regions of a fusion protein creates droplets called condensates that are essential to ependymoma development.

Nature, Published online: 09 July 2025; doi:10.1038/s41586-025-09247-w Lack of evidence for the transitional cerebellar progenitor

Find out how B7-H3-targted chimeric antigen receptor (CAR) T cells successfully killed ependymoma tumors in some models but still faced resistance in others.

Nature - Lack of evidence for the transitional cerebellar progenitor

Abstract. Purpose: Targeted treatments are desperately needed for ependymomas (EPNs). Chimeric antigen receptor (CAR) T-cells have immense potential to transform patient outcomes. However, CAR T-cell ...

Dang et al. report that group-3 medulloblastomas (MBs) show c-MYC-driven high DLAT expression. In these tumors, wild-type IDH1 epigenetically regulates c-MYC, and inhibiting IDH1 lowers c-MYC and DLAT expression. Further, DLAT sensitizes group-3 MBs to cuproptosis. Notably, the copper ionophore elesclomol is toxic to multiple group-3 MB models, underscoring its therapeutic potential.

Elp1 heterozygous LOF mutations in Sonic hedgehog medulloblastoma (MB) elevate transformation risk in granule neuron precursors through stalled differentiation, DNA replication stress, genomic instability, and accelerated cell cycle. Pharmacological restoration of p53 signaling in ELP1-deficient tumor cells suppresses tumor growth and represents a potential therapeutic opportunity.

Uncover how ELP1 gene defects drive pediatric brain cancer—and learn how that revealed MDM2 inhibition as a targeted therapy to restore tumor suppressor p53.