2026 Research Grant Recipients
The ABTA Research Program oversees the competitive, peer-reviewed grant process to ensure funding goes to the most promising brain tumor research. Once awarded, we track each project’s progress and long-term outcomes to measure impact and advance discoveries in the field.
2025 ABTA-Funded Research Projects
The ABTA awarded more than $1.3 million towards 31 grants
The 2025 funded projects span multiple tumor types
- Glioblastoma
- Medulloblastoma
- Metastatic Brain Tumors
- Malignant Glioma
- Diffuse Midline Gliomas
Research areas of focus
- Immunology/Immunotherapy
- Drug Therapies/Experimental Therapeutics
- Epigenetics
- Biomarkers
- Radiation Therapy
- Proteomics
Flexible Research Fund
The ABTA Flexible Research Fund is a flexible approach to target research funding to key gaps in the brain tumor funding landscape. Through these projects the ABTA intends to drive progress in under-recognized areas of research to improve our understanding and the treatment of brain tumors and improve outcomes for patients.
Isabella Glitza, MD, PhD
Institution: The University of Texas MD Anderson Cancer Center
Among solid tumors, metastatic melanoma (MM) has one of the highest risks of spreading to the cerebrospinal fluid (CSF) and lining surrounding the brain, known as leptomeningeal disease (LMD). Patients with LMD face a median overall survival (OS) of only ~4 months. Treatment options are very limited, which must urgently change.
We have shown that delivering Nivolumab (nivo) immunotherapy directly into the CSF (intrathecal injection; IT) can double survival for MM and lung cancer patients with LMD. Further, in melanoma patients without brain or LMD involvement, combining two immunotherapy drugs – nivo and relatlimab (rela) – led to better results than nivo alone. Building on this, we conducted a first-in-human trial testing combined IT/intravenous (IV) nivo/rela in MM patients with LMD.
We also discovered unique gut and oral bacterial patterns (microbiome) linked to clinical outcome in brain metastasis and showed that changing these bacterial patterns affects immune activity in the brain. Our proposal will examine the immune cells in CSF and blood, along with gut and oral microbiome patterns, to assess how they relate to treatment efficacy in our LMD trial. We have successfully enrolled all planned participants and are finalizing sample collection, including blood, CSF, gut and oral microbiome, for our proposed analyses. We are confident that this research will advance our understanding of LMD and could lead to novel treatments for patients facing this devastating complication.
Basic Research Fellowship
The Basic Research Fellowship is a two-year, $100,000 grant, awarded to post-doctoral fellows who are mentored by established and nationally-recognized experts in the neuro-oncology field.
Ahmed Gad, PhD
Institution: Baylor College of Medicine
Mentor: Nabil Ahmed, MD
Tribute: In memory of Kaitlyn Berg
Chimeric antigen receptor T cell (CAR-T) therapy is an innovative treatment that engineers a patient’s own immune cells to find and destroy cancer. While this approach has succeeded in some blood cancers, brain tumor trials have shown only limited tumor control, along with significant side effects.
One major challenge in brain tumors is that drug targets vary widely across tumor types. For instance, the expression levels of HER2, a common target in solid tumors, in glioblastoma are often too low for CAR-T to detect, while in ependymoma and breast cancer brain metastases, they can be so high that they overstimulate and exhaust CAR-T. Many targets, including HER2, are also found at low levels in vital organs like the lungs, raising the risk of toxicity.
Unlike chemical drugs that can be dosed precisely, CAR-T are living drugs whose activity is difficult to adjust once infused. This project aims to develop a “remote control” (RC) system that can fine tune CAR-T activity after infusion in brain cancer patients. Our RC system repurposes two FDA-approved drugs: danoprevir, to boost CAR-T activity when tumors are hard to detect, and grazoprevir, to reduce or completely halt CAR-T activity when overactivation or attacks on healthy tissues occur.
By enabling precise and remote tuning of CAR-T activity, this approach could improve both the efficacy and safety of treating brain cancers.
Michael Kilian, PhD
Institution: Brigham and Women’s Hospital
Mentor: Francisco Quintana, PhD
Tribute: Co-funded by StacheStrong
Glioblastoma (GBM) is an aggressive primary tumor of the central nervous system, with limited available treatment options due to the heterogeneity of tumor cells and their ability to evade the immune response. The meninges are the membrane layers that cover and protect the brain. The dura, the outermost of the three meningeal membranes, has recently been identified as important site for immune cell activation in the setting of neuroinflammation like multiple sclerosis. However, the contribution of the dura in the immune response against brain tumors, like GBM, is still unknown. This project aims at identifying anti-tumor immunity-promoting or inhibiting cell-cell interactions in recently identified immune cell clusters in the dura using a novel technology called RABID-Seq a barcoding method that allows to study cell communication in vivo, spatial sequencing technologies to study cells in a spatial context as well as functional studies and human GBM tissue. We hypothesize that the dura is a unique priming location for tumor-reactive T cells augmenting anti-tumor functions. The basic understanding of meningeal driven anti-tumor immune responses can potentially lead to novel treatment approaches like tissue-specific delivery of immunostimulatory factors or the genetic modifications of cellular tumor-targeting products like CAR-T cells.
Kavita Rawat, PhD
Institution: University of Pennsylvania
Mentor: Dolores Hambardzumyan, PhD
Tribute: In honor of Joel A. Gingras Jr.
Glioblastoma is the most common and aggressive type of brain cancer in adults. Glioblastoma is particularly hard difficult to treat, which leads to poor prognosis. For instance, with standard of care treatment, the median survival of glioblastoma patients is only 14.6 months. The immune system, which protects the body from infections and diseases, might also play a role in helping tumors grow as tumors are known to hijack the immune system for their own benefit. One of the key cells in the immune system is neutrophils, which are the body’s first line of defense against infections, helping to fight off bacteria and other harmful invaders. However, recent research shows that the aberrant activation of these cells might also support the growth and spread of cancer, including glioblastoma. In our study, we are investigating how neutrophils contribute to glioblastoma development and whether targeting these cells could help slow down or stop the glioblastoma progression. By understanding the relationship between neutrophils and glioblastoma, we hope to discover new ways to treat this challenging cancer and improve patient outcomes.
Amy Wisdom, MD, PhD
Institution: Massachusetts General Hospital
Mentor: Stefani Spranger, PhD
Tribute: Fully supported by Tap Cancer Out
Glioblastoma is the most aggressive type of brain cancer, with limited treatment options and poor survival rates. Unlike other cancers that respond to immunotherapy, glioblastomas suppress the immune system, making it difficult for the body to fight the tumor. My research focuses on understanding how glioblastomas evade immune detection by disrupting the function of key immune cells called dendritic cells, which are responsible for activating tumor-fighting T cells. I will use advanced mouse models to determine where and how these immune cells interact with glioblastomas, and how treatments like radiation and chemotherapy influence this process. By identifying the mechanisms that prevent the immune system from attacking glioblastoma, this study could reveal new ways to enhance immune-based therapies. Ultimately, this research aims to improve treatment strategies and offer new hope for patients battling this devastating disease.
Ningning Liang, PhD
Institution: University of Michigan
Mentor: Daniel Richard Wahl, MD, PhD
Tribute: In memory of Stephanie Lee Kramer
Glioblastoma (GBM) is the most prevalent and aggressive brain tumor in adults, with fewer than 10% of patients surviving beyond five years. Radiation therapy (RT) provides initial benefits, but GBM almost always comes back. Our team, tracing GBM patients with 13C6-glucose, a traceable form of glucose by Mass Spectrum, found that GBMs increase absorption of serine, an important amino acid, from their surroundings. Serine is crucial for synthesizing proteins, lipids, and nucleic acids, and provide one-carbon units. Limiting serine uptake was found to slow down glioma growth. The sources of environmental serine in GBM and how it contributes to tumor growth, however, remain unclear.
Our combined RNA sequencing and isotope tracing modeling indicated that astrocytes, which are normal brain cells, are the primary source of serine in human brain. We also analyzed the cell culture media and found serine was the most abundant metabolites secreted by astrocytes but consumed by GBM cells. We further established that astrocyte-conditioned media enhances RT resistance in GBM cells and reversed when we inhibit serine secretion in astrocytes. Reducing dietary serine also decreases GBM PDX growth in mice models. These findings indicate that serine uptake is vital for GBM growth and treatment resistance.
We will further explore how serine promotes the RT resistance in GBM with traceable 13C3-serine and RNA sequencing in cells and in mice. We will infuse 13C3-serine into GBM patients and analyze the flux difference among various cell types. Our work aims to unveil new potential therapeutic targets for the treatment of GBM.
Akshaya Ravishkumar Lakshmi, PhD
Institution: University of California, San Francisco
Mentor: Joanna J Phillips, MD, PhD
Tribute: Fully supported by the Karl Schmidt Oligodendroglioma Research Fund
The tumor-associated immune response is strikingly different across subtypes of brain tumors. By studying what makes these responses so different we can learn how the anti-tumor immune response is regulated. Taking this approach, we have identified a factor that is associated with an immune-enriched subset of human glioma and we have demonstrated that this factor can promote an anti-tumor immune response and prolong overall survival in a mouse model for glioblastoma. In this proposal I will investigate how this factor can reprogram the tumor-immune microenvironment and promote an anti-tumor response. These studies will provide valuable insights on the regulation of anti-tumor immunity in the brain. They will also lay the groundwork for developing innovative immunotherapeutic strategies to help the patient’s own immune system fight the tumor.
Discovery Grants
A Discovery Grant is a one-year, $50,000 grant to support cutting-edge, innovative approaches that have the potential to change current diagnostic or treatment standards of care for either adult or pediatric brain tumors.
Nandini Acharya, PhD
Institution: The Ohio State University
Mentor: Monica Venere, PhD
Tribute: In honor of Charles “Chip” McKinley Greenlee
Glioblastoma (GBM) is the most aggressive brain cancer and has a median survival of only 12–15 months despite the standard of care. While immunotherapy has revolutionized cancer treatment, GBM remains highly resistant; thus, overcoming this resistance is crucial for improved patient outcomes.
Our research investigates an overlooked regulator of immune responses in GBM: nociceptors, the pain-sensing neurons. Though nociceptors have been shown to modulate immunity outside the central nervous system, their role in GBM remains unexplored. Our preliminary data show that nociceptors in GBM bearing mice are activated, and these tumor-activated nociceptors actively foster an immunosuppressive tumor microenvironment. Chemically disrupting nociceptors improve survival in GBM-bearing mice and enhance their response to immunotherapy. In this proposal, we will use single-nucleus RNA sequencing to map molecular changes in nociceptors and integrate this data with our previously generated single-cell RNA sequencing of immune cells from the meninges and tumor tissue of GBM-bearing mice. This will help reveal how GBM manipulates neuro-immune interactions to evade immune attacks.
These insights could lead to new treatment strategies, such as repurposing FDA-approved nociceptor-targeting drugs or identifying novel therapeutic targets to enhance immunotherapy. By disrupting the ability of GBM to hijack the nervous system, we aim to reshape the immune landscape, improve immunotherapy efficacy, and provide new hope for patients with GBM.
Mariella Filbin, MD, PhD
Institution: Dana-Farber Cancer Institute
Tribute: Co-funded by the Yuvaan Tiwari Foundation
Pediatric diffuse midline gliomas (DMG) are incurable brain cancers with a median survival of 9-12 months and no long-term survivors. To date, focal radiation remains the standard of care but improves survival by only a few months. Unfortunately, rapid radiation resistance ultimately arises in all DMG, resulting in lethal tumor recurrence in 100% of patients. Despite intense research efforts over the past four decades, there is still a lack of mechanistic understanding of the biology underlying DMG radiation resistance. While there is ample evidence that direct communication between normal brain cells (neurons) and cancer cells is critical to fuel growth of pediatric brain tumors; whether these important interactions contribute to treatment failure in DMG is currently not known. The innovative work outlined in this proposal will enable us to discover the biochemical mechanisms through which DMG cells exploit interactions with surrounding normal neurons to survive radiation-induced cell killing. If successful, these experiments have the potential to (i) completely transform our understanding of how resistance to radiation develops in DMG as well as other deadly brain tumors, and (ii) lead to the development of new therapeutic approaches to make radiation treatment more effective. Hence, this proposal addresses a critical need to understand the mechanisms underlying DMG radiation resistance and improve the efficacy of treatment for children diagnosed with DMG.
Luciano Garofano, PhD
Institution: University of Miami
Mentor: Antonio Iavarone, MD
Tribute: In memory of Brian Bouts
Glioblastoma (GBM) is an uncurable form of primary brain tumor with extremely poor prognosis. Despite current state-of-the-art therapy that includes surgery, irradiation and chemotherapy, all patients experience tumor progression, unfortunately. Numerous efforts have been made in the scientific community to design more appropriate therapeutic strategies. Some of these studies include computational approaches to sort tumor patients into subgroups of GBM, to understand the specific biological functions activated within these tumors and identify therapeutic targets. Single cell data allowed to discriminate tumor cells from the non-malignant cell components, and study how distinct tumor cell states interact within the tumor microenvironment. Moreover, proteomics analysis allowed for the discovery of kinases, proteins that specifically regulate tumor signaling, important for tumor growth and to repurpose current drugs for cancer therapy. Here, this study will examine the composition of the GBM ecosystem, dissect the biological mechanisms of GBM tumorigenesis and aggressiveness, and identify novel therapeutic opportunities for GBM. The development of innovative computational tools to understand the role of kinases in the reprogramming of GBM tumor-TME ecosystems is necessary to elucidate the mechanisms of therapeutic resistance.
Robyn Gartrell, MD
Institution: Johns Hopkins University School of Medicine
Tribute: Co-funded by StacheStrong
Atypical teratoid/rhabdoid tumors (AT/RT) are very tough brain tumors to treat. They’re aggressive and don’t respond well to chemotherapy, even at high doses. These treatments can make patients very sick and often they have to stay in the hospital. While radiation therapy can be used to target this tumor, patients with AT/RT are typically infants or toddlers under 3 years old and standard radiation at this age can cause delayed development. A new kind of radiation called FLASH has been shown to be safer for the brain than the usual type in tests on adult animals and even young healthy mice. FLASH has not yet been studied in very young mice in their first week of life. Since AT/RT mostly affects infants, it is essential to know how FLASH would affect this age group. Our study proposes to investigate how FLASH radiation therapy influences brain function and tumor control in AT/RT, aiming to shed light on a potential treatment approach for these challenging tumors while also preventing serious brain toxicity.
Filipe Pereira, PhD
Institution: Lund University
Tribute: Fully supported by an Anonymous Family Foundation
Cancer heterogeneity and the formation of an immunosuppressive tumor microenvironment (TME) are among the causes of failure of immunotherapy. Glioblastoma (GBM) is a highly heterogeneous tumor type, characterized by intra-tumoral and systemic immunosuppression.
Cellular reprogramming is emerging as a tumor-agnostic and immunosuppression-independent immunotherapy. My group has previously reprogrammed cancer cells into antigen-presenting conventional dendritic cells type 1 (cDC1). cDC1 are rare in tumor tissue but, even at low numbers, are sufficient to induce cancer cell death by the immune system. The current proposal aims to evaluate cDC1 reprogramming as a GBM immunotherapy. First, we will assess the feasibility of reprogramming GBM cells within the brain and characterize the immune mechanisms launched by cDC1-like cells in mouse models with different TME and immunogenicity profiles. Then, we will evaluate cDC1 reprogramming and associated immunogenicity in human patient-derived GBM organotypic cultures with an established immunosuppressive TME. Lastly, we will demonstrate the efficacy and safety of the cDC1 reprogramming approach in syngeneic models, validating it as a gene therapy for GBM. By connecting cellular reprogramming and immunotherapy in a novel gene therapy, our strategy has the potential to provide a personalized and effective treatment for GBM patients.
John Prensner, MD, PhD
Institution: University of Michigan
Mentor: Sriram Venneti, MD, PhD
Tribute: Co-funded by StacheStrong
Children diagnosed with diffuse midline glioma (DMG), including diffuse midline pontine glioma (DIPG), are faced with a dismal prognosis: over 90% of patients will die from disease within two years. Removal of these tumors by surgery is not possible, and so current treatment focuses on radiation therapy, which is not curative for patients. Our research has worked to unveil a new potential avenue for therapy for these children through investigation of the ‘dark’ proteome. This term refers to the thousands of small proteins generated by DMG/DIPG cells that have not been previously studied. We have pioneered cutting-edge methods to identify key cancer drivers from the dark proteome of medulloblastoma and other cancers. In this American Brain Tumor Association award, we will employ multiple patient-derived models of DMG/DIPG to define the dark proteome of associated with cancer gene mutations that cause DMG/DIPG in children. In addition, we will identify how radiation treatment – the standard therapy for children with DMG/DIPG – creates new opportunities for therapies based on the dark proteome. Overall, we expect this project to catalyze a new direction of research in DMG/DIPG by demonstrating the extent and relevance of the dark proteome, which may be used as a platform for future therapeutic developments.
Xueqin Sun, PhD
Institution: Sanford Burnham Prebys Medical Discovery Institute
Mentor: Charles Spruck, PhD
Tribute: Fully supported by an Anonymous Family Foundation
Glioblastoma (GBM) remains the most common and deadly type of primary brain cancer, leading to death of approximately half of all patients within just one year from the time of diagnosis and 95% within five years. We have discovered BRD8 protein as a novel and promising therapeutic candidate that, when targeted, could extend survival in about 71% of GBM cases—specifically those that still retain the tumor-suppressing protein p53. We further find that BRD8—the culprit for GBM aggressiveness, is kept at high levels by its partner protein, MRGBP. MRGBP shields BRD8 from being broken down by the proteasome—a machine that breaks down unneeded or erroneous proteins in the cell. This project aims to understand whether and how BRD8 is protected by MRGBP to block our body’s natural anti-tumor defense. We seek to answer this question using comprehensive methods from two aspects: 1) Is BRD8 protected by MRGBP from degradation; 2) Does BRD8 degradation restore the body’s natural anti-tumor ability? Successful completion of this innovative and timely project will provide insights into eradicating BRD8 using the proteasome; thereby, unleashes the intrinsic tumor suppression activity of p53 to halt GBM, paving the way for developing more effective therapies for people afflicted with this devastating malignancy.
Dong Wang, PhD
Institution: University of Colorado Denver
Mentor: Rajeev Vibhakar, MD, PhD
Tribute: Fully supported by an Anonymous Family Foundation
Medulloblastoma is the most common malignant brain tumor in children, and tumors driven by the MYC oncogene are particularly aggressive and resistant to standard treatments. We hypothesize that MYC, along with another key driver gene, OTX2, promotes tumor growth by increasing protein production, which relies on ribosomes—the structures in cells that build proteins. Our research has shown that a gene called CDK8 is essential for maintaining MYC and OTX2 activity and supporting ribosome production in these tumors. We will investigate whether blocking CDK8—either alone or in combination with other inhibitors that also regulate ribosome biogenesis—can slow tumor growth and improve treatment options for children with MYC-driven medulloblastoma. If successful, this work could lay the foundation for developing new therapies that may advance toward clinical trials.
Murat Yildirim, PhD
Institution: Cleveland Clinic
Mentor: Justin Lathia, PhD
Tribute: In memory of Kaitlyn Berg
Glioblastoma (GBM) is the deadliest form of brain cancer, with most patients surviving only about a year after diagnosis. In addition to rapid tumor growth, GBM disrupts brain function, causing memory loss, movement problems, and seizures. These symptoms often appear late in the disease, making early detection and intervention critical. Our project will explore how GBM affects brain activity and behavior from its earliest stages, with the goal of developing better diagnostic tools and treatment strategies. In Aim 1, we will use advanced brain imaging techniques to track real-time brain activity and chemical signaling in mice before and after tumor formation. By monitoring pupil size, facial movements, and walking patterns, we will train artificial intelligence models to recognize early warning signs of GBM-related brain dysfunction. In Aim 2, we will test whether light-based therapies (optogenetics) can restore brain function in mice with GBM. By stimulating inhibitory brain circuits, we aim to correct the harmful changes GBM causes in brain networks. If successful, this approach could pave the way for new, targeted therapies to improve brain function in GBM patients. By combining early detection strategies with innovative treatments, this research aims to slow disease progression and improve patient outcomes, offering hope for a more effective fight against GBM.
Andrew Dhawan, MD, DPhil
Institution: Cleveland Clinic
Mentor: Justin Lathia, PhD
Tribute: Fully supported by an Anonymous Family Foundation
Glioblastoma (GBM), the most aggressive and common form of brain cancer, presents a significant treatment challenge due to the frequent development of resistance to temozolomide (TMZ), the standard chemotherapy drug, particularly after radiation therapy. Our research is focused on understanding the interplay between the tumor cells and the normal brain cells that surround them within the tumor microenvironment. We hypothesize that these normal brain cells actively contribute to making GBM cells resistant to TMZ following radiation. To investigate this, we will use laboratory models called co-cultures, where we can precisely control a mixture of GBM cells and different types of normal brain cells, called astrocytes, neurons, and microglia, mimicking the environment within a patient’s tumor. By exposing these models to radiation and then TMZ, we can carefully observe how drug resistance emerges under various conditions and identify the specific roles of different normal brain cell types. We will also be looking closely at specific molecular signals, that we suspect are involved in this process of resistance. Ultimately, our goal is to uncover the mechanisms by which normal brain cells help GBM cells evade the effects of TMZ after radiation. This knowledge could lead to the development of new and more effective therapies that target these interactions, potentially overcoming drug resistance and significantly improving the outcomes for patients with GBM.
Jack and Fay Netchin Medical Student Summer Fellowship
A Medical Student Summer Fellowship is a three month, mentor-guided summer research experience, intended to motivate talented medical students to pursue a career in neuro-oncology research.
2025
Lucien Rubinstein Award Recipient
Darwin Kwok, PhD
Institution: University of California, San Francisco
Mentor: Hideho Okada, MD, PhD
Tribute: In Memory of Jameson Taylor, GBM warrior and medical student
Glioblastoma and other brain tumors are very difficult to treat because they almost always come back after standard therapies like radiation and chemotherapy. A major challenge is that these treatments change the tumor in ways that make it harder for the immune system to recognize and attack. Our project set out to understand these changes and to explore how they could be turned into new opportunities for treatment. We discovered that after therapy, brain tumors produce a new landscape of abnormal protein fragments derived from newly formed RNA junctions, which are strands of proteins precursors that connect and change shape. These newly formed RNA junctions are not normally found in healthy cells. These abnormal junctions can create unique protein fragments, or neoantigens, that the immune system could potentially recognize as foreign. By analyzing patient tumors and cell models, we built the first large atlas of these therapy-induced changes. We then used advanced computer tools to predict which of these abnormal fragments could be seen by the immune system and confirmed that many are specific to cancer cells. Even more importantly, we identified a handful of high-priority candidates that appear across multiple patients and treatments, making them especially promising for the development of new immunotherapies such as vaccines or engineered T cells. These findings open up a new way to think about treating brain tumors. By turning the changes caused by therapy into targets for the immune system, we may be able to develop longer-lasting and more effective treatments for patients.
Matthew Abikenari, MSc
Glioblastoma (GBM) is the most aggressive primary tumor of the central nervous system and remains among the deadliest cancers, with a median survival of approximately 15 months despite standard therapy. Although advances in surgery, chemotherapy, and immunotherapy have improved disease management, GBM remains incurable due to profound therapeutic resistance and its ability to suppress antitumor immunity. While tumor-associated macrophages have been extensively studied, the role of tumor-associated neutrophils (TANs) in GBM remains poorly understood. Neutrophils, best known for fighting infections, may play different roles in cancer and could either support or limit tumor growth.
The aim of this study is to determine whether TANs can help fight glioblastoma. Using mouse models, we will examine how neutrophils interact with tumor cells and immune cells, and assess whether the presence of neutrophils is associated with slower tumor growth and disease progression. Understanding whether neutrophils can restrain GBM may reveal new ways to harness the immune system for treatment and improve outcomes for patients with this disease. If successful, this work could change how we think about the innate immune system’s role in brain cancer and open entirely new paths toward therapies for a disease that currently has very few effective options.
Markus Anzaldua-Campos, BA
Institution: Washington University School of Medicine in St. Louis
Mentor: Bhuvic Patel, MD
Tribute: Fully Funded by the Gladiator Project
Glioblastoma (GBM) is one of the most aggressive brain tumors in adults. Even with standard treatment, surgery followed by chemotherapy and radiation, most patients survive less than two years.
GBM is difficult to cure in part because a single tumor contains many different kinds of cancer cells called tumor heterogeneity. Some are more aggressive than others, and when treatment is given, the tumor can shift toward cell types that are better at surviving and resisting therapy. A major challenge in developing new treatments is that many laboratory models used to select drugs for clinical trials have never been exposed to standard chemoradiation, even though most patients receive chemoradiation before entering trials. This mismatch may cause therapies to look promising in the lab but perform poorly in patients.
In this project, we will grow patient-derived glioblastoma organoids, three-dimensional smaller tumors made from a patient’s own tumor tissue and treat them with chemotherapy plus radiation to recreate the post-treatment setting. We will measure how chemoradiation changes the tumor’s cell states and then test whether these changes make the tumor more resistant or sensitive to a panel of drugs. This work will create a more realistic platform for testing therapies after standard treatment, improving how drugs are prioritized for clinical trials and helping guide better strategies for treating glioblastoma.
Noah Drewes, BS
Glioblastoma (GBM) is a deadly brain cancer, and even if patients receive surgery, radiation, and chemotherapy, the tumor comes back in almost all cases. One of the reasons GBM is so hard to treat is because cancer cells learn how to survive even after treatment and can adapt to chemotherapy. If we understand how this process works, we could develop new treatments and help patients with GBM live longer and healthier lives.
One of the most important proteins that leads to cancer survival is HIF-1a, which helps tumor cells grow new blood vessels, invade their surroundings, and behave like stem cells, which in return causes resistance to treatment. In general, HIF-1a is activated by low levels of oxygen, but in our lab, we also found that chemotherapy can cause activation of HIF-1a, even when oxygen levels are normal.
So far, we have found that chemotherapy causes increased HIF-1a in glioblastoma cells. We also found that a protein called CAMK2G can interact with HIF-1a after giving chemotherapy. Ultimately, CAMK2G could help glioblastoma cells survive chemotherapy through activation of HIF-1a.
For this project, we plan to find out if blocking CAMK2G prevents HIF-1a activation, reduces the creation resistant tumor cells, and overall makes glioblastoma less likely to recur after giving chemotherapy. This project could lead to new treatments that make current therapies work better and help prevent glioblastoma from coming back.
Min Jae Kim, BS
Institution: University of Pennsylvania
Mentor: Christina Jackson, MD
Tribute: In Memory of Joe Smeeding
Meningiomas are common brain tumors that often cause symptoms such as weakness, numbness, trouble walking, or confusion. Many meningiomas do not invade the brain, but they can press on and distort the brain’s “wiring” (white matter pathways) that carry signals needed for movement, sensation, balance, and thinking. Today, surgeons mainly estimate a patient’s risks and chances of recovery using tumor size and location on standard scans, along with clinical experience. There is no reliable, patient specific way to determine which pathways are responsible for a person’s symptoms or which pathways must be relieved during surgery to maximize recovery.
This project will use MRI and diffusion MRI, an advanced MRI technique that shows water movement in the brain, to map the white matter pathways that pass through each patient’s tumor and identify symptom specific pathway patterns linked to motor, sensory, gait, and cognitive problems. I will then test whether patients improve when surgery successfully relieves pressure on the pathways most relevant to their symptoms, by comparing pathway patterns related to the surgical cavity and to any remaining tumor after surgery. The expected outcome is a practical imaging based approach that helps predict symptom risk and likelihood of recovery, enabling more personalized counseling and supporting surgical planning that targets the circuits driving symptoms while protecting healthy brain tissue.
Cathy Li, BA
Institution: Cleveland Clinic
Mentor: Justin Lathia, PhD
Tribute: In Honor of Bobby Marshburn
Glioblastoma (GBM) is the most common and aggressive type of brain cancer in adults. Even with surgery, radiation, and chemotherapy, GBM often returns, and survival remains poor. Notably, men are more likely to develop GBM and tend to have worse outcomes than women, but the biological reasons for these differences are not fully understood. One factor that may contribute to these differences is the immune system. A type of immune cell called a regulatory T-cell, or Treg for short, normally helps prevent harmful overactivity of the immune system. However, in GBM, Tregs can protect the tumor by suppressing the immune response that would otherwise help fight cancer. Our early studies show that removing Tregs improves survival to a greater degree in male compared to female mice with GBM, suggesting that Tregs may play a stronger role in suppressing anti-tumor immunity in males. This project will examine why Tregs behave differently in males and females with GBM. First, we will study whether genetic differences between males and females, specifically differences in sex chromosomes, affect Treg levels in brain tumor and peripheral setting. Second, we will test how sex hormones such as estrogen and testosterone influence Treg function and tumor growth. By understanding how genetic and hormonal factors shape immune responses in GBM, this research may help guide the development of more effective, personalized treatments for both male and female patients.
Braxton Morrison, ScM
Institution: University of California San Francisco School of Medicine
Mentor: Jacob Young, MD
Tribute: In Memory of Hong Sun (1958-2025)
Glioblastoma is the most common and most aggressive primary brain cancer in adults. Even with the best available care—surgery, radiation, and chemotherapy—patients often face a poor outlook. Because few new treatments have been approved in the past 20 years, clinical trials are critical for giving patients access to promising therapies and for improving future care. Yet only 8–11% of newly diagnosed glioblastoma patients enroll, in part because identifying appropriate trials is slow and difficult; eligibility rules are lengthy, and the needed details are spread across many pages of medical records.
This project will evaluate whether a “smart assistant” based on large language models (AI tools that can read and organize text) can streamline trial recruitment at UCSF, a tertiary cancer center. We will build an end-to-end system that extracts key clinical details from notes and matches them to trial requirements to generate a personalized list of eligible trials for each patient (Aim 1). We will also create a carefully curated, gold-standard dataset of patients with recurrent glioblastoma to support rigorous validation of future models (Aim 2).
Impact: By reducing missed trial opportunities and staff burden, this work could increase and broaden trial enrollment, improve equity of access to experimental treatments, and accelerate testing of new therapies for glioblastoma.
Saahith Potluri, BS
Institution: Johns Hopkins University School of Medicine
Mentor: Henry Brem, MD
Tribute: Fully Funded by Southeastern Brain Tumor Foundation
Glioblastoma is a devastating brain cancer that is notoriously difficult to treat. One significant obstacle is the “blood-brain barrier,” a protective sheath around the central nervous system that, while vital for health, inadvertently blocks most anticancer medicines from reaching the tumor. This research utilizes a promising genetic therapy using a naturally occurring protein called Growth Arrest-Specific 1 (Gas1). Gas1 acts as a molecular “stop” signal, leading cancer cells to cease dividing and triggering their natural self-destruction. While Gas1 has been shown to significantly shrink glioblastoma tumors, delivering it safely into the brain has remained a major hurdle. Our study proposes a cutting-edge, two-part delivery system: packaging the Gas1 gene into microscopic nanoparticles and using focused ultrasound to gently and temporarily open the brain’s protective barrier at the exact site of the tumor. Focused ultrasound, which is already approved for human use, allows the therapy to be delivered with pinpoint accuracy without the need for invasive surgery. Successful results from this study could potentially provide a roadmap for delivering powerful, tumor-fighting genes directly to the brain. By demonstrating that focused ultrasound can successfully drive Gas1 therapy to diminish GBM in mice, we aim to accelerate its clinical translation. Our goal is to redefine the standard of care and offer new hope to those facing this cancer.
Roland Scott, BA
Institution: Columbia University
Mentor: Brian Gill, MD
Tribute: In Memory of Jameson Taylor, GBM Warrior and Medical Student
Gliomas are aggressive brain tumors that have complex relationships with the surrounding brain tissue. As they grow, they can alter the behavior of nearby brain cells which can lead to seizures. Seizures are common in patients with brain tumors and are often a major source of cognitive and functional impairment at all stages of the disease. Unfortunately, there are no anti-seizure drugs designed specifically for brain tumor patients, and existing drugs work inconsistently. A new drug, AUT00201, holds particular promise as it normalizes the behavior of a select group of neurons which we have previously shown are altered by the presence of tumors. In this study we will test if this drug decreases seizures in a clinically relevant mouse model of glioma. If successful, this could pave the way for future studies in patients with brain tumors who continue to suffer from seizures despite using the current standard of care medications.
Grants Awarded in Collaboration with Other Organizations
Metastatic Brain Tumor Collaborative CNS Metastasis Research Grants
CNS Metastasis Research Grants provide $50,000 over one-year to support researchers to conduct metastatic CNS tumors or leptomeningeal disease-focused projects that are applicable to at least two different primary cancers
Brain Tumor Funders Collaborative
In 2025 the Brain Tumor funders Collaborative (BTFC) awarded two $500,000 grants to support projects focused on Liquid Biopsy for Primary Brain Tumors