The Children’s Tumor Foundation (CTF) is the drug discovery engine for NF. Everything we do is to bring treatments to patients as we work toward a cure. By connecting patients, doctors, scientists, and pharma, we drive treatments, advance care, and deliver results for millions affected by neurofibromatosis or schwannomatosis. Our patient-first collaborative approach accelerates drug development and brings life-changing therapies to patients faster – driven by our mission to end NF.
About NF
NF refers to a group of genetic conditions that cause tumors to grow on nerves. These include neurofibromatosis type 1 (NF1) and all types of schwannomatosis (SWN), including NF2-related schwannomatosis (NF2-SWN), formerly called NF2. NF occurs in 1 of every 2,000 births, affecting more than 4 million people worldwide. Anyone can be born with NF, and it affects everyone differently. NF can lead to blindness, deafness, bone abnormalities, disfigurement, learning challenges, disabling pain, or cancer.
Throughout this report, each section includes a Key Takeaway and Key Definitions to support understanding of the progress shared.
On the use of italics:
Human genes use italics: NF1, LZTR1
Proteins and diagnoses do not: NF1, merlin
Reflections from the 2025 NF Summit and NF Conference
Dear Friends,
The 2025 NF Conference and NF Summit in Washington, D.C., brought together a truly global community—the combined events drew more than 1,000 researchers, clinicians, industry leaders, regulators, patients, and families—united in our mission to end NF.
Held in the heart of the U.S. capital, the June conference was a powerful example of unity, dignity, and humanity. It was a global collaboration driving and celebrating scientific momentum. I’m especially grateful to our planning committee—Drs. Dusica Babovic-Vuksanovic, Elisabeth Castellanos Perez, and Rebecca Dodd—for curating a dynamic, cross-disciplinary agenda.
We opened the meeting with a tribute to two incredible pioneers and friends we lost this year—Dr. Vincent Riccardi and Dr. Verena Staedtke. Their contributions will continue to enlighten and guide us on our path to end NF.
Highlights included a high-level global panel on the regulatory landscape in rare diseases. Our moderator, Julie Tibbets, (Goodwin Procter LLP), led a critical conversation with Amy Comstock Rick, JD (Director of Strategic Coalitions, Rare Disease Innovation Hub, FDA), and Steffen Thirstrup, MD, PhD (Chief Medical Officer, EMA), about how to accelerate access to treatments in rare disease. Their discussion on the future of rare disease regulation offered exclusive insight into how global agencies are invested and collaborating in driving innovation—and why that matters for NF.
This year’s NF Conference marks another milestone towards ending NF. We are learning more than ever about how the different cells inside tumors talk to each other—and how that might open doors to new treatments beyond MEK for all forms of NF. From exciting trial updates to the growing use of AI, the future of NF care is becoming more connected, more hopeful, and more within reach.
The NF Summit (for patients and families) and NF Conference were fully integrated, with shared programming that brought scientists and families together in new ways— from poster tours to a joint session on pain management, moderated by Dr. Mark Hutchinson, Adelaide, Australia. I was particularly excited by the groundbreaking work on tumor microenvironments, especially Dr. Nancy Ratner’s keynote on plexiform neurofibroma formation.
To everyone who joined us in Washington: thank you. Your commitment is accelerating progress, deepening partnerships, and bringing us closer to a world without NF.
With gratitude,
Annette Bakker, PhD, CEO, Children’s Tumor Foundation
PS. Please mark your calendars for next year’s NF Summit, July 9 –11, and NF Conference, July 26 –30, 2026, both in Denver, Colorado.
Near-Term Wins in NF Research
A unifying theme emerged at the 2025 NF Conference: the gap between discovery and care is narrowing. The studies featured in this section— spanning drug trials, next-generation testing, and gene therapy—are among those best positioned for near-term impact for patients.
Emerging Clinical Trial Results: Promising New Treatments in the Pipeline
Dr. Jaishri Blakeley (Johns Hopkins University) shared interim results from the CTF-funded INTUITTNF2 platform trial, showing that brigatinib has continued benefit in patients who were tracked for an extended period after starting the trial. Compared to extended use of bevacizumab (Avastin), brigatinib may offer superior outcomes for meningioma, although more work is required to confirm this. In a second treatment group, neratinib, a targeted therapy with the potential to block tumor-driving signals in the body, showed moderate promise in treating progressive non-vestibular schwannomas and meningiomas in NF2-SWN, with an acceptable safety profile. Further enrollment is planned.
Dr. Blakeley also presented early results from a study evaluating the safety of immunotherapy (combining two agents: nivolumab and ipilimumab) in patients with newly diagnosed malignant peripheral nerve sheath tumors
Dr. Jaishri Blakeley shared interim results from the CTF-funded INTUITT-NF2 platform trial.
(MPNSTs). Most participants tolerated the treatment without major adverse effects, indicating that pre-treatment immunotherapy may be a viable strategy.
Dr. Angela Hirbe (Washington University) presented long-term data from the CTF-supported ReNeu trial of
Near-Term Wins in NF Research
mirdametinib for NF1-associated plexiform neurofibromas (PNs). The rate of major tumor shrinkage increased over time with no new safety concerns, although the on–off dosing schedule raised questions about symptom flare-ups during the off weeks.
Dr. Natalie Stec (Massachusetts General Hospital) shared results on long-term use of bevacizumab (Avastin) for NF2SWN. Many patients maintained stable hearing and tumors that didn’t grow on MRI, even with frequent pauses or discontinuation due to side effects.
Dr. Beom Hee Lee (Asan Medical Center, Seoul) shared mid-trial findings from a CTF-co-funded Phase 1/2 study of PRG-N-01 (trineumin) currently being run in Korea for NF2-SWN. Early data showed tumor volume reductions with a favorable safety profile—an encouraging sign that, if confirmed in larger studies, this could soon offer a new treatment option for people with NF2-SWN.
Key Takeaway
Multiple new and ongoing drug trials are showing promise for patients living with NF. From targeted therapies that block tumordriving signals to immunotherapies that enlist the body’s own immune system, researchers are finding safer and more effective ways to slow tumor growth, preserve hearing, and improve quality of life.
Key Definitions
Platform Trial: A type of clinical trial that tests multiple treatments in one ongoing study, allowing faster evaluation of promising therapies.
Targeted Therapy: A treatment that uses drugs or other substances to target cancer cells and spare normal cells.
Immunotherapy: A treatment that helps your own immune system fight cancer or other diseases.
Non-vestibular Schwannoma: A schwannoma tumor that grows on nerves other than the vestibular (hearing/balance) nerve.
Meningioma: A tumor that originates from the meninges, the protective membranes surrounding the brain and spinal cord.
Plexiform Neurofibroma (PN): A type of tumor that grows along nerves and can cause pain, disfigurement, or other complications.
Dr. Taylor Sundby presented work on cancer prevention in NF1 using noninvasive biomarkers.
Predictive Testing and Biomarkers
Earlier Detection, Better Outcomes
Dr. Taylor Sundby (National Cancer Institute), a CTF Clinical Research Award recipient, presented work on cancer prevention in NF1 using noninvasive biomarkers. With additional support of more than $1.5 million from CTF toward a large collaborative consortium including Drs. Angela Hirbe and John Shern, this study explored the use of liquid biopsies, including cell-free DNA and protein markers in the blood, to distinguish benign, premalignant, and malignant tumors—enabling earlier and more accurate detection of MPNSTs.
Dr. Shivani Ahlawat (Johns Hopkins University) demonstrated how MRI and core needle biopsy can differentiate benign PN from early MPNST with 92.8% diagnostic accuracy in this study.
Key Takeaway
New blood tests are making it easier to spot dangerous tumor changes earlier, without invasive procedures. By identifying molecular “red flags” in blood, researchers can better predict when tumors are turning cancerous— allowing earlier intervention.
Key Definitions
Biomarker: A biological molecule found in blood or other parts of the body that is a sign of a normal or abnormal process, or of a condition or disease.
Liquid Biopsy: A simple blood test that looks for pieces of tumor DNA or other markers in the blood.
Needle Biopsy: A thin needle takes a small tissue sample for testing.
MPNST: Malignant Peripheral Nerve
Sheath Tumor, an aggressive form of cancer that can develop in patients with NF.
Near-Term Wins in NF Research
Gene Therapy From Challenge to Possibility
Gene therapy has proven difficult for NF due to a variety of reasons, including gene size and delivery localization. However, many researchers at this year’s conference shared promising data on how to overcome these issues.
Dr. Jean-Philippe Brosseau (Université de Sherbrooke) demonstrated proof-of-principle for NF1 gene therapy in mouse models of plexiform neurofibroma. By toggling NF1 gene expression on and off, his team showed that restoring NF1 halted or even reversed tumor growth, which supports the continued development of NF1-targeted gene
Dr. Lars Riecken is exploring lipid nanoparticles (LNPs).
Dr. Lars Riecken (Fritz Lipmann Institute, Leibniz Institute on Aging), whose work in this area has received CTF funding, is exploring lipid nanoparticles (LNPs) as a novel delivery system for gene therapy in NF2-SWN. His team successfully used LNPs to deliver mRNA to Schwann cells in both cell culture and animal models. This approach could offer an alternative to viral-based delivery systems, which have limits on how much genetic material they can carry.
Dr. Jean-Philippe Brosseau demonstrated proof-of-principle for NF1 gene therapy in mouse models of plexiform neurofibroma.
Dr. Jeremie Vitte (University of California, Los Angeles) described gene replacement therapy in NF2-SWN, using viral-delivered NF2 to restore the expression of merlin (the protein product of the NF2 gene) in preclinical models. Restoring merlin suppressed the growth of schwannoma tumors, highlighting gene therapy as a promising treatment approach for NF2-SWN.
Key Takeaway
Researchers are finding ways to deliver, restore, or repair gene function in NF. By restoring missing proteins, repairing faulty ones, or using innovative delivery methods, scientists are opening the door to treatments that could slow, stop, or even reverse tumor growth.
Key Definitions
Gene Therapy: A treatment that works by replacing, repairing, or modifying faulty genes to correct the underlying cause of disease.
Lipid Nanoparticles (LNPs): Tiny fatbased particles that can safely carry genetic material (like mRNA) into cells.
mRNA (messenger RNA) acts as a messenger carrying the gene’s instructions to make a protein.
Merlin: The protein made by the NF2 gene that helps control cell growth; loss of merlin leads to tumor development.
Schwannoma: A usually benign tumor of the nerve’s insulating cells (Schwann cells). It can grow on any peripheral, cranial, or spinal nerve.
Antisense Therapy: A method that blocks the translation of faulty parts of a gene, resulting in a functional or partially functional protein.
Induced Pluripotent Stem Cells (iPSCs): Lab-made cells that can become almost any cell type, used for research and testing.
Collective Global Impact
77 Countries Represented across conference history
6 Continents Represented
NF Conference Attendees, expanded from just 20 at the first NF Conference in 1987
NF Conference
The 2025 NF Conference officially opened on Saturday, June 21, with welcome remarks from Children’s Tumor Foundation CEO Dr. Annette Bakker, a tribute to Drs. Vincent Riccardi and Verena Staedtke by Dr. Miriam Bornhorst, and introductory comments from this year’s Conference Co-Chairs: Dr. Dusica Babovic-Vuksanovic (Mayo Clinic), Dr. Elisabeth Castellanos Perez (Germans Trias & Pujol Hospital), and Dr. Rebecca Dodd (University of Iowa). The cochairs highlighted the growth in the NF Conference from 1987 to 2025, expanding from 20 U.S. participants to over 850 attendees from 77 countries represented across 6 continents.
Keynote Addresses
The NF Conference brought together leading experts from both within and beyond the NF field, fostering indepth discussions of the latest discoveries to accelerate drug development and bring new treatments to patients.
Amy Comstock Rick, JD (Director of Strategic Coalitions, FDA Rare Disease Innovation Hub, CBER/CDER), Steffen Thirstrup, MD, PhD (Chief Medical Officer, European Medicines Agency) and Julie Tibbets (Chair, Life Sciences Regulatory & Compliance, Goodwin Procter LLP) came together as leadership from the U.S. Food and Drug Administration (FDA) and European Medicines Agency (EMA) to share how regulators are working more closely than ever to speed safe and effective treatments for rare diseases, including NF.
Highlights:
Global alignment: FDA and EMA are harmonizing standards and streamlining cross-border trials.
Access & innovation: Agencies are supporting novel trial designs, data sharing, and early engagement with patient groups.
Patient tools: New trial maps, workshops, and resources aim to make the clinical trial process more transparent and accessible.
Beyond approval: The panel acknowledged real-world barriers to access, like reimbursement delays, and committed to ongoing collaboration to address them.
New resources: The FDA introduced its Rare Disease Innovation Hub, designed to centralize support for trial developers and communities.
Key Takeaway
Global regulatory leaders, top researchers, and innovators shared concrete ways to speed development of safe, effective NF treatments. From harmonizing trial standards to exploring cutting-edge targets, these talks underscored that collaboration, innovation, and patient involvement are critical to success.
Dr. Nancy Ratner (Cincinnati Children’s Hospital), whose groundbreaking research has shaped our understanding of plexiform neurofibromas (PN) and who was instrumental in the development of the MEK inhibitor mirdametinib (Gomekli) as part of the CTF-funded and driven NF Preclinical Consortium, delivered the opening keynote on her research into how the immune system can drive PN formation. Her team is now looking at other potential inhibitors for the treatment of these tumors with promising initial data in mice. Dr. Ratner is also investigating how the immune system contributes to neurofibroma growth—and whether immunotherapy might offer a new avenue for treatment.
Dr. David Gewirtz (Virginia Commonwealth University) addressed the phenomenon of therapy-induced senescence. While chemotherapy and radiation are meant to kill tumor cells, they sometimes cause the cells to stop growing without actually dying—a state called senescence. Dr. Gewirtz presented evidence that these senescent cells can “awaken” and re-enter the cell cycle, potentially driving relapse. This suggests that senolytic drugs—medications that specifically clear out these “stalled” tumor cells—might help prevent recurrence. Though not yet explored in NF1, this strategy offers a promising new direction.
Dr. William Gahl (NIH, National Human Genome Research Institute) shared the mission and impact of the NIH Undiagnosed Diseases Program, which has evaluated nearly 1,700 patients out of 6,500 applicants, and provides week-long inpatient diagnostic workups without insurance barriers. Through deep phenotyping
(connecting genetic changes to symptoms), functional assays, and global data sharing, the program has identified new disease-causing mutations and informed treatment strategies. Dr. Gahl emphasized the importance of proper diagnosis—not just for care planning, but for community-building and clarity in patient journeys. The program is open to referrals worldwide, at no cost to families, and includes training for young physicians in rare disease management.
Dr. Pelin Candarlioglu Deacon (3D and 3Rs) delivered a keynote address on microphysiological systems (MPS), in vitro preclinical models (cells or tissues studied in a dish) that better mimic human complexity, which have the potential to transform early-stage drug development. Dr. Candarlioglu emphasized that many current preclinical models fail to translate into clinical success, and MPS platforms—such as Emulate’s Liver Chip, now recognized by the FDA—offer a promising alternative. She discussed the relevance of MPS systems for NF drug development, including modeling blood-brain barrier penetration, tumor–immune interactions, and combination therapy assessments.
Key Definitions
Trial Design: The plan for how a clinical trial is conducted, including who participates and how data is collected.
Senescence: A state where cells permanently stop dividing but do not die, which can sometimes contribute to disease.
Senolytic Drugs: Medications that selectively destroy senescent cells to improve health outcomes.
In vitro preclinical models: lab-grown cells or tissues studied in a dish (not in animals or people) to test whether a drug looks promising and safe before human trials.
Immunotherapy and the Microenvironment
It has become increasingly apparent that the biology surrounding the manifestation of symptoms of all types of NF relies heavily on the environment surrounding the cell (the microenvironment) and the interactions of the immune system with affected cells. Therefore, immunotherapies offer a promising target for drug discovery.
Dr. Thomas DeRaedt (Children’s Hospital of Philadelphia), a former CTF Young Investigator Award recipient, focused on identifying targets for CAR T-cell therapy (an approach that modifies a patient’s own T-cells (white blood cells that find and help destroy problem cells) to better attack and destroy cancer cells in NF1-associated malignancies. His team has cataloged a number of peptide markers that are present across multiple NF1 tumor types and is now testing their potential for therapeutic development.
Dr. Rosie Kaplan (NCI Pediatric Oncology Branch) presented a cell therapy approach targeting immune suppression in the tumor microenvironment (an approach designed to take the brakes off the immune system around tumors). Her team reprogrammed a type of immune cell to deliver interleukin-12 (IL-12), a natural
Key Definitions
CAR T-cell Therapy: A treatment where a patient’s own immune cells are modified in the lab to better attack cancer cells.
T-cells: White blood cells, which are part of the immune system, that find and help destroy problem cells.
Peptide markers: short pieces of proteins that act like ID tags on tumor cells.
“go” signal, which revved up T-cells, shrunk tumors, and helped mice live longer. A Phase 1 study is now testing this approach in people with advanced solid tumors.
Dr. Michel Kalamarides (Sorbonne University, Paris) showed that aggressive NF2-related meningiomas aren’t static—the mix of cell types inside a single tumor shifts over time, and those shifts appear to be steered by the immune microenvironment around the tumor. His group is mapping the signals between tumor and immune cells to learn when and how these changes happen. If we can pinpoint these dynamics, we may be able to reprogram the microenvironment or combine immunotherapies to slow growth and reduce relapse.
Key Takeaway
Immunotherapy, which trains the body’s own immune system to fight disease, is gaining momentum for NF-associated tumors. By identifying specific targets on tumor cells and boosting immune activity, researchers are developing new treatments that could improve survival and reduce tumor burden.
Interleukin-12 (IL-12): A protein that boosts the immune system’s ability to fight disease.
Tumor Microenvironment: The surrounding cells, molecules, and blood vessels that help a tumor grow and survive.
Emerging Drug Combinations and Targets
Tumors often have heterogeneity, meaning that a single tumor can contain pockets of cells that look and act differently, which can complicate how these tumors are treated. Tumor heterogeneity may mean that combination treatments will be more effective than single agents.
Dr. Andrea McClatchey (Massachusetts General Hospital), a former Young Investigator Award (YIA) recipient and current co-chair of the YIA committee, presented her lab’s findings on the microscopic
Key Definitions
Tumor Heterogeneity: When a single tumor contains different types of cells, which can respond differently to treatment.
SHP2 Inhibitor: A drug that blocks the SHP2 protein, which is involved in cell growth signals.
TEAD Inhibitor: A drug that blocks a protein that helps regulate gene activity linked to tumor growth.
Preclinical Models: Laboratory experiments, often in cells or animals, used to test a treatment before human trials.
complexity of schwannoma tumors. Her work shows that NF2-deficiency contributes to tumor heterogeneity and that different drugs may have variable effects depending on the composition of these tumors. Understanding this built-in variety points to more tailored care, and combination or stepwise therapies (given in stages) that cover more of the tumor, so it’s less likely to resist treatment or grow back.
Dr. Jiawan Wang (Johns Hopkins University) shared findings that combining drugs that are SHP2 inhibitors with TEAD inhibitors more effectively suppresses tumor growth in preclinical models
Dr. Janet Oblinger (Nationwide Children’s Hospital) and Dr. Lindy Zhang (Johns Hopkins University), a current Drug Discovery Initiative awardee, in separate presentations shared findings on combination treatments for MPNSTs by blocking either the SHP2 and CDK4/6 proteins or eIF4A (a translation initiation factor) and XPO1 (a nuclear export protein). Each showed promising and synergistic results from these combined treatments.
Dr. Dawn Quelle (University of Iowa) found that using two existing cancer treatments together (which are already used in breast cancer) may help boost the body’s immune attack on MPNSTs by increasing signals that fight the tumor. Additionally, Dr. Dana Mitchell (Indiana University) showed that while blocking FAK—a protein that helps tumor cells stick, move, and survive—had limited impact on its own in NF2-SWN, pairing it with the MEK inhibitor selumetinib led to markedly better results in preclinical models.
Key Takeaway
Combining treatments may be more effective than single drugs for NF tumors, which often contain cells with different characteristics. Researchers are testing powerful drug pairings that block multiple tumor-growth signals at once, showing encouraging results in preclinical studies.
New Treatment Approaches
Growing the basic understanding of the biochemical pathways involved in tumor development continues to identify potential new drug targets.
Alexa Sheehan (University of Iowa), a CTF Young Investigator Awardee, discovered that when PRC2—a protein complex that normally keeps certain genes switched off—is lost in MPNST, tumors become more aggressive. This happens because the loss of PRC2 activates specific enzymes that remodel the environment around the tumor. Her findings indicate that blocking these enzymes may help slow down the spread of tumors.
Key Takeaway
By uncovering new ways tumors grow and survive, scientists are identifying fresh drug targets for NF. These discoveries offer new hope for treatments that can slow or stop NFrelated tumors.
Dr. Liang Hu (Cincinnati Children’s Hospital Medical Center) demonstrated that NF1-deficient tumor cells depend on a protein called KRAS to thrive. His research showed that in animal models, a drug that activates PKC (a cell-signaling protein) turned down the effect of KRAS, which in turn triggered tumor cell death and reduced tumor burden in animal models. This points to potential new targets for NF1.
Dr. Sylwia Ammoun (University of Plymouth) tested two MERTK inhibitors in mouse models of schwannoma and meningioma. Both agents reduced tumor cell proliferation, and one of them slowed meningioma growth, supporting further therapeutic development.
Dr. Frank Huang (Mayo Clinic) presented MCO-3, a new drug candidate that hits two targets at once, discovered by high-throughput screening, which demonstrated potent and selective activity against MPNST cell lines, resulting in prolonged survival in mouse models, with no observed toxicity.
CTF Young Investigator Awardee Alexa Sheehan is uncovering how changes in tumor biology may lead to new treatment strategies for MPNST.
Key Definitions
KRAS: A protein involved in cell growth; changes in the KRAS gene can lock the protein “on,” which may drive tumor growth.
PKC Agonist: A drug that activates protein kinase C, which can influence cell survival and death.
MERTK Inhibitor: A drug that blocks MERTK, a protein linked to tumor growth and survival.
High-Throughput Screening: A method to quickly test thousands of potential drugs in the lab.
AI-Driven Discovery
The advances of artificial intelligence (AI) in the medical space continue to show clear promise to accelerate the NF field.
Dr. Shannon McWeeney (Oregon Health and Science University) shared a multi-modal AI “triangulation network” that synthesizes biological and clinical data to uncover actionable insights. Her framework has already been used to virtually screen safe anti-cancer drug combinations, predict responses to therapy, and identify new small molecule candidates.
Dr. Ali Bashashati explored the use of AI to redefine cancer pathology and risk categorization.
Key Takeaway
Artificial intelligence is transforming NF research by finding patterns humans might miss. From predicting which drug combinations will work best to analyzing tumor scans more accurately, AI tools are helping speed the search for effective treatments.
Dr. Ali Bashashati (University of British Columbia) explored the use of AI to redefine cancer pathology and risk categorization. His platform integrates genetic data with images of tumor tissue under a microscope and has identified a novel subset of endometrial tumors with worse outcomes. This finding underscores the power of AI-assisted diagnostics for guiding physicians in identifying the right therapy for the right patient.
Abhijeet Parida, MSc (Children’s National Hospital), introduced CAVS-NF1, an AI-powered, web-based tool for rapid and consistent MRI volumetric analysis of optic pathway gliomas (OPGs). The tool is free and HIPAAcompliant: nf1.hope4kids.io
Dr. Sasha Scott (Sage Bionetworks), a past CTFfunded trainee, compared painful versus non-painful schwannomas from non-NF2 schwannomatosis patients and identified differentially expressed genes that may drive pain signaling. She also applied machine learning–based drug prediction to nominate candidate therapeutics for future testing in preclinical models.
Key Definitions
Multi-Modal AI: AI that combines different types of data, like genetic information and medical images, for deeper insights.
Pathology: The study of diseases by examining tissues, cells, and organs.
MRI Volumetric Analysis: Using imaging software to measure tumor size and changes over time.
Innovative Tumor Modeling
Translational research (the ability to move potential treatments to clinical trials from the basic lab) requires reliable and specific models to accurately predict which treatments are likely to be most effective. Preclinical models are most useful when they recreate multiple aspects of the environment in patients.
Modeling for MPNST transition continues to be a focus for NF researchers. Dr. Alice Soragni (University of California, Los Angeles) introduced a platform for drug screening using mini-ring 3D patient-derived organoids (patient-grown 3D tumor clusters shaped like rings), which can be used for high-speed, highvolume drug testing. These models mimic real-life tumor characteristics more closely than others, enabling a more efficient translation of the findings into the clinic.
Dr. Sara Gosline (Pacific Northwest National Laboratory), in collaboration with teams from the University of Minnesota, Johns Hopkins University, and Washington University, presented a patientderived xenograft microtissue (PDX-MT) platform for NF1 MPNSTs. Coupled with advanced analysis and imaging, these strategies show strong potential for personalized therapeutic development.
Dr. Kiymet Bozaoglu (Murdoch Children’s Research Institute) presented a stem cell–based platform for studying neurodevelopment in NF1. By turning stem cells from people with NF1 into nerve tissue in the lab, her team enables direct investigation of how NF1 alters early brain development and provides a test bed for candidate therapeutic interventions before clinical translation.
Dr. Stephanie Brosius developed an immune-competent mouse model for NF1-associated glioblastoma.
Dr. Stephanie Brosius (Children’s Hospital of Philadelphia) presented an immune-competent mouse model for NF1-associated glioblastoma. These models are important to more accurately capture the complex nature of human biology. Her team demonstrated that glioma stem cells from the mouse model produce tumors that mirror the primary disease, offering a robust tool for preclinical testing.
Dr. Sarah Gosline developed a PDX-MT platform to advance NF1 MPNST
Dr. Lars Riecken (Fritz Lipmann Institute, Leibniz Institute on Aging) shared his lab’s development of a new mouse model using patient-derived tumor tissue to study NF2-related meningiomas. His research suggests that NF-related tumors behave more like evolving ecosystems rather than static growths, which could lead to more targeted and effective therapies.
Georgia Daraki (Fritz Lipmann Institute, Leibniz Institute on Aging), a 2024 CTF Young Investigator Awardee, presented a mouse model of LZTR1-related schwannomatosis, paralleling human disease. The team plans to test drugs that block a major growth pathway (ERK) and clear out macrophages, immune cells that can help tumors grow.
Garrett Draper (University of Minnesota) built preclinical models of atypical neurofibromatous neoplasms of uncertain biologic potential (ANNUBP) by using CRISPR to tweak Schwann cells (the cells that insulate nerves) so they behave like these borderline tumors—more worrisome than a typical neurofibroma but not full cancer. These models will allow researchers to better understand the tumor’s biology and test treatments that could keep ANNUBP from turning into malignant tumors.
Key Definitions
Preclinical Model: A laboratory system, such as cells or animals, used to test treatments before they are tried in humans.
Mini-ring 3D patient-derived organoids: Tiny donut-shaped 3D clusters grown from a patient’s tumor, that can be used in a high-throughput manner.
Organoids: Miniature, simplified versions of organs grown in the lab from patient cells.
CRISPR: A powerful tool for making precise changes to DNA.
Patient-Derived Xenograft (PDX): A model where human tumor tissue is implanted into mice to study disease and test treatments.
CTF Young Investigator
Awardee Georgia Daraki developed a mouse model of LZTR1-related schwannomatosis.
ANNUBP: a nerve-sheath tumor (seen in NF1) that looks more worrisome than a typical neurofibroma but isn’t full cancer (MPNST)
Key Takeaway
Better lab models mean better chances of finding effective treatments. Researchers are creating models that closely mimic human NF tumors, allowing them to test drugs more accurately and move the most promising candidates into clinical trials faster.
Genetic and Metabolic Discoveries
Understanding what genetic changes occur in affected individuals and how tumor cells “feed” (their cellular metabolism) has been a hallmark of identifying potential treatments.
Dr. Luis Parada (Memorial Sloan Kettering Cancer Center), noting the overlap in genetic drivers between NF1-associated MPNSTs and glioblastoma, screened over 200,000 compounds and identified two metabolism-targeting candidates that show activity in both disease models. This suggests that targeting cellular metabolism could help slow or block malignant transformation.
Dr. Semira Ortiz (Pennington Biomedical Research Center) investigated the effect of aerobic exercise on an NF1-driven rat model of breast cancer. Exercise significantly delayed tumor onset and improved survival, indicating a potential role for physical activity in managing NF1-associated breast cancer risk.
Dr. Seth Tomchik (University of Iowa) investigated behavioral and metabolic pathways downstream of Ras using fruit fly models of NF1. His group showed that NF1-related phenotypes map to distinct signaling
Key Takeaway
New genetic and metabolic insights are revealing how and why NF tumors form, and how to stop them. From identifying cancer-driving mutations to finding energy weaknesses in tumor cells, these discoveries are opening new opportunities for prevention and treatment.
cascades, suggesting that targeting pathway-specific nodes may allow symptom-focused therapies rather than one-size-fits-all molecular interventions.
Dr. Semira Ortiz (Pennington Biomedical Research Center) identified mitochondrial complex I dysfunction as a consistent marker across mouse models carrying NF1 mutations. This energy deficit may contribute to malignant transformation, suggesting both a biomarker and a mechanistic entry point for further research.
It has been known that patients with NF1 have a single variation in one of their two NF1 genes, and many symptoms of NF1 are associated with a new mutation in the other copy of the gene. Dr. Thomas Oliver (Wellcome Sanger Institute) revealed that many normal tissues from NF1 patients harbor somatic mutations of the second NF1 gene. This widespread mutation burden could help explain cancer risk and progression even in seemingly unaffected tissues.
Key Definitions
Cellular Metabolism: The chemical processes that occur within living cells to maintain life.
Mitochondrial Complex I
Dysfunction: An impaired first step of the cell’s energy-making chain.
Somatic Mutation: A genetic change acquired during a person’s lifetime, not inherited from parents.
Mosaicism: When different cells in the same person have different genetic makeups.
Overlapping NF1 and Schwannomatosis Phenotypes
Drs. Katharina Wimmer, Alessandro De Luca, Eric Legius, Radhika Dhamija, Michael Ronellenfitsch, Pia Vaassen, and Kimia Hashemi, MSc, discussed various conditions that mimic the presentation of NF1, NF2-SWN, and SWN, complicating treatment decisionmaking. These include: Constitutional Mismatch Repair Deficiency (CMMRD), LZTR1 and ERBB2 variants, intestinal and spinal neurofibromatosis, RASopathies, and KRAS-driven localized hypertrophic neuropathy. Experts emphasized the need for broader genetic panels, attention to pain etiology, and awareness of the variety of conditions that may result in similar presentations, or phenotypes. These results also stressed the need for genetic testing in multiple tumors (and locations within one tumor) due to mosaicism.
Key Takeaway
Some conditions can look like NF but are actually caused by different genetic changes. Identifying these look-alike conditions through genetic testing ensures patients get the right diagnosis and treatment — and helps avoid unnecessary worry about cancer risks when they do not apply.
Dr. Alessandro De Luca presented research on LZTR1 variants and café-aulait macules.
Dr. Eric Legius presented an update on intestinal neurofibromatosis.
Key Definitions
Phenotype: The observable traits or symptoms caused by a person’s genes and their interaction with the environment.
Genetic Panel: A test that looks for changes in multiple genes at once.
RASopathies: Genetic conditions (including NF) linked to the RAS/ MAPK pathway, which is a chain of signals inside cells that carries “grow/ divide” messages.
CMMRD: Constitutional Mismatch Repair Deficiency, a rare inherited condition that increases cancer risk.
Dr. Yemima Berman advances NF1 care through clinical trials aimed at improving muscle function.
Musculoskeletal Manifestations
of NF1
Bone and muscle problems can be a difficult aspect of NF1, affecting strength, posture, and mobility. Here, we spotlight solutions moving toward improved care for these difficult manifestations.
Dr. Yemima Berman (University of Sydney) shared results from a CTF-funded study on L-carnitine for muscle weakness in NF1. A small pilot in children showed tolerability and full compliance, and a larger placebo-controlled trial using small wearable motion sensors is underway.
Dr. Noelle Larson (Mayo Clinic) discussed NF1-associated scoliosis, which affects up to 30% of patients. Early surgical intervention is key, and new techniques like intraoperative CT (a CT scan done during surgery) and magnetic growing rods may improve outcomes, although MRI compatibility remains a concern.
Key Takeaway
Bone and muscle problems are common in NF1, but research is leading to new ways to address them. From surgical innovations for scoliosis to potential drug treatments for muscle weakness and bone repair, these advances aim to preserve mobility and quality of life.
Drs. Jonathan Rios (UT Southwestern) and Florent Elefteriou (Baylor College of Medicine), in separate talks, discussed the importance of the BMP pathway in bone formation and healing. The data from both teams suggest that MEK inhibitors with and without BMP2 (a bone-healing protein) may be useful for restoring normal bone formation.
Key Definitions
Scoliosis: A sideways curvature of the spine.
BMP Pathway: (Bone Morphogenetic Protein pathway): a group of proteins that tells cells when to become bone or cartilage, important for bone formation and healing.
MEK Inhibitor: A drug that blocks a protein in a key growth pathway, potentially aiding bone repair; selumetinib (Koselugo) and mirdametinib (Gomekli), FDA-approved treatments for NF, are both MEK inhibitors.
Cognition, Pain, and Quality of Life
Researchers continue to explore the complex nature of the impacts of NF on patients’ quality of life, including cognition, pain, and emotional-social development.
Dr. Yang Hou (Florida State University) presented the largest dataset to date on attention-deficit/hyperactivity disorder (ADHD) in NF1, showing peak symptoms around age 10 and greater severity in girls and children of parents with lower education levels.
Dr. Steven Angus (Indiana University School of Medicine) focused on challenges with attention, learning, and social/behavior deficits in NF1. His lab explored ways to stabilize neurofibromin levels by blocking its normal breakdown through F-box protein inhibition (blocking proteins that tag other proteins for the cell’s garbage-disposal system). Their findings suggest a promising new approach to treating NF1-related symptoms like ADHD and autism spectrum disorder.
Mandi Johnson, MBA (Johns Hopkins University), shared updates from the Neurofibromatosis Therapeutic Acceleration
Key Takeaway
NF affects more than just tumors — it can impact learning, attention, sleep, and emotional well-being. Researchers are uncovering the biological reasons behind these challenges and developing tools to better measure and improve the quality of life for patients with NF.
Program (NTAP) cutaneous neurofibroma natural history study, which used the CTF NF Registry to help recruit patients. This study is tracking tumor growth in nearly 500 individuals using 3D imaging as well as collecting data on hormonal effects and patient-reported outcomes. Findings will help improve the monitoring and understanding of these tumors, which are often painful and affect appearance.
Sophia Carias, BA (Massachusetts General Hospital) presented QUEST, a new CTF-funded patient-reported outcome measure for NF2-SWN trials. This tool better captures physical, emotional, and social impacts from the patient perspective.
Dr. Jodi Lukkes (Indiana University School of Medicine) explored ADHD-like behaviors in NF1 through mouse studies, which revealed “noisy” signaling in certain areas of the brain during reward-based learning. The results show how brain changes could lead to attention and impulse-control problems seen in patients.
Dr. Yang Hou presented the largest dataset to date on ADHD in NF1, highlighting key risk factors in children.
Young Investigator Day Training Tomorrow’s NF Leaders
Young Investigator Day, a satellite session that preceded the NF Conference, was designed to foster community, collaboration, and career development for early-career scientists working in neurofibromatosis research. From postbaccalaureate trainees to clinical fellows, 64 participants attended this year’s program, representing a wide range of academic and clinical training backgrounds.
Interest in the event was strong, with 76 applications received. Although the original budget planned for 50 attendees, all 69 eligible applicants were accepted in order to maintain momentum and engagement in this growing initiative. Due to visa and travel complications, 64 ultimately participated.
The program featured a full day of scientific exchange and mentorship. Trainees shared their work through platform presentations and a concluding poster session, while also benefiting from direct interaction with a distinguished group of NF experts. Mentors included long-standing leaders in the field—some newly retired, like Drs. Eric Legius and Gareth Evans—as well as
Key Takeaway
Dr. Francis Collins, former Director of the NIH and leader of the Human Genome Project.
active senior investigators such as Drs. Nancy Ratner, Marco Giovannini, Eduard Serra, and Andrea McClatchey They were joined by newer NF faculty, including Drs. Vanessa Merker and Daochun Sun, who offered a valuable peer-to-peer perspective.
In addition to scientific discussions, attendees explored professional development topics, including fellowship applications and fundraising strategies, with opportunities for small-group dialogue over lunch with mentors.
Investing in the next generation of NF researchers is critical for long-term progress. Young Investigator Day brought together early-career scientists from around the world to share discoveries, learn from leaders in the field, and build collaborations that will fuel NF breakthroughs for decades to come.
A highlight of the day was a keynote address by guest of honor Dr. Francis Collins. Best known as the former Director of the NIH and leader of the Human Genome Project, Dr. Collins also discovered the NF1 gene, a foundational milestone in NF research. His remarks focused on the evolving landscape of science, the realities of research funding, and the vital role of early-career investigators in advancing the field.
2025 Poster Competition Winners
Jadwiga Bilchak
Basic Science
1ST PLACE
Jadwiga Bilchak, PhD (CTF Young Investigator Awardee)
Connecting Sleep and Sensory Deficits in a Drosophila Model of NF1
Alexis Stillwell
Anna Nagel
In a fruit-fly NF1 model, vibrations that normally lull flies to sleep didn’t work in NF1-mutant flies—suggesting a link between altered sensory processing and sleep difficulties reported in NF1 patients. This work was also recognized as the People’s Choice winner of Young Investigator Day.
2ND PLACE
Alexis Stillwell (CTF Young Investigator Awardee)
Developmental Analyses of Skeletal Manifestations in NF1 (p.M992del “Mild” Variant)
Developed a mouse model to study a specific NF1 variant linked to skeletal development, providing a new platform for understanding bone-related complications in NF1.
3RD PLACE
Anna Nagel (CTF Young Investigator Awardee)
HDAC2 Activity in Schwannoma Cells and Consequences of Its Inhibition
Explored the role of the HDAC2 protein in schwannoma cells, investigating how its inhibition could impact tumor biology and uncovering possible therapeutic pathways.
Clinical Science
1ST PLACE
Matthew Jamnik (CTF-Funded)
Cognitive Function in Middle-Aged and Older Adults with NF1: Psychosocial Predictors
This research has found that cognitive decline in older adults with NF1 is associated with aging and psychosocial factors like social support and sense of purpose—highlighting possible targets for intervention. Participants were recruited via the CTF NF Registry.
2ND PLACE
David Bonilla
Outcomes of NF1 Patients Diagnosed with Gastrointestinal Stromal Tumors (GIST)
Reported that GISTs occur at a far higher rate in NF1 (about 7 in 100) than in the general population (about 1 in 100,000), with different presentation patterns. Introduced the RECKGIST score, based on mitotic index, to identify high-risk individuals for follow-up and intervention.
3RD PLACE
Wangcun Jia, PhD
Emergence and Development of Nascent Cutaneous Neurofibromas in Pediatric NF1 Patients
Used noninvasive imaging (spatial frequency domain and high-frequency ultrasound) to detect earlystage cutaneous neurofibromas before they surface. Preliminary findings show rapid tumor volume change, potentially accelerated during puberty.
David Bonilla
Matthew Jamnik
Wangcun Jia
Clinical Care Program
The Clinical Care Program spanned two days of the NF Conference, with sessions designed to highlight emerging best practices and challenges in the management of NF patients. Led by Drs. Laura Klesse (Chair of the CTF Clinical Care Advisory Board), Tena Rosser, and Nicole Ullrich, the program focused on clinically relevant topics with direct and immediate implications for patient care, providing participants with in-depth updates on patient management across the spectrum of NF manifestations.
As CTF continues to support research and education for all types of schwannomatosis, Dr. Brian Na (University of California, San Francisco) reviewed case studies to illustrate alternative treatment options for meningiomas, noting that clinical trials for NF2-SWN meningiomas are expanding, with nine ongoing studies, including immunotherapy.
Key Definitions
Variant of Uncertain Significance (VUS): A genetic change whose impact on disease risk is not yet known.
mTOR Inhibitor: A drug that blocks mTOR, a protein that helps control cell growth and survival.
Auditory Brainstem Implant: A device that helps restore some hearing for people who cannot use cochlear implants.
Dr. Gareth Evans showed that while loss-offunction (LoF) variants in LZTR1 are associated with schwannomatosis, they also appear frequently in individuals without symptoms, suggesting that the risk of developing schwannomas from these variants may be lower than previously understood.
Alicia Gomes, MS, CGC, presented on the classification of genetic variants in NF, with a focus on variants of uncertain significance (VUS). She described the work of the Variant Curation Expert Panel (VCEP), which is developing gene-specific classification criteria for NF1, and eventually for NF2, SPRED1, SMARCB1, and LZTR1
Two case panel discussions gave attendees a practical look at how NF is diagnosed and managed in real life, with case studies covering NF2-SWN, LZTR1-SWN, and NF1. The panels highlighted the complexity of patient care and the promise of emerging treatments like MEK and mTOR inhibitors
Dr. Laura Klesse, Chair of the CTF Clinical Care Advisory Board, co-led the Clinical Care Program.
Dr. Frank Buono addressed the growing role of AI in improving clinical evaluation.
Quality of life issues continue to be an important and complex component of clinical care. Dr. D. Bradley Welling (Harvard University) discussed hearing preservation strategies in NF2-SWN and emphasized the role of intraoperative hearing monitoring during surgical interventions. Although approximately 75% of NF2-SWN patients are not candidates for hearing preservation, new assistive technologies such as cochlear and auditory brainstem implants, captioning apps, and smart glasses are helping to improve communication and quality of life.
Dr. Isabelle Chase (Harvard School of Dental Medicine) presented clinical cases illustrating the importance of routine dental care for patients with NF1. Facial asymmetry, jaw abnormalities, and missing or malformed teeth are common and patients will benefit from multidisciplinary management.
Key Takeaway
Doctors and scientists are improving the day-to-day care of people with NF. From new genetic insights to better hearing preservation strategies, assistive technologies, and AI tools for tumor tracking, these advances are making NF care more precise, personalized, and effective.
A trio of talks by Drs. Sanjay Aneja, Frank Buono, and Kavita Sarin addressed the growing role of AI in improving clinical evaluation, including chart reviews, tumor volume analysis, and cutaneous neurofibroma tracking.
Alicia Gomes, MS, CGC, presented on variant classification in NF, including the work of the Variant Curation Expert Panel (VCEP).
Special Panels and Workshops
Dr. Michael Fisher shared updates on NF clinical trials, including new studies for NF1, NF2-SWN, and rare NF1 manifestations.
The NF Data Portal: Analyzing Data & Accelerating Research
Presented by Sage Bionetworks, Pluto Bio, and the Children’s Tumor Foundation, this hands-on workshop equipped researchers to harness the full potential of the NF Data Portal. In live demonstrations, experts showed how to access, visualize, and analyze datasets of interest for the NF field. For the first time, the workshop included “lightning talks” where researchers showcased how they successfully reused shared data to generate new insights and accelerate discovery. The session highlighted the growing culture of open science and data reuse in NF research.
Consortia and Collaboration Updates
VCEP: Variant Curation Expert Panel
Presented by Yunjia Chen, PhD (University of Alabama at Birmingham), this CTF-funded initiative (which was also presented in the Clinical Care Program) is revising outdated criteria for determining whether a gene variant is pathogenic (disease-causing). The panel is focused on five genes, four of which are NF-related (NF1, NF2, SMARCB1, and LZTR1). A new three-step reclassification process has been established, with the first two steps completed for NF1 and a manuscript in preparation. Work on the schwannomatosis genes is ongoing.
Dr. Yunjia Chen leads a CTFfunded effort to update criteria for classifying NF gene variants.
Dr. Robert Allway helped lead a hands-on workshop on the NF Data Portal.
NFCTC: NF Clinical Trials Consortium
Michael Fisher, MD (Children’s Hospital of Philadelphia), presented an overview of six active NF1 clinical trials, with a strong focus on MPNST and a new trial enrolling patients with atypical neurofibromas. Nine additional trials are in development, including two for NF2-SWN and three for under-studied NF1 manifestations: bone abnormalities, ADHD, and high-grade gliomas.
The
Nexus of
Now: Where AI, Medicine, and Advocacy Converge on Pain
Drs. Mark Hutchinson (University of Adelaide) and Kim Sullivan (Boston University) discussed how AI and immunology are reshaping the science and treatment of chronic pain — including in complex, multisystem diseases like NF. Multi-specialty collaboration, including outside of healthcare and medical research, is necessary to effectively address the various causes and manifestations of pain. Presenters highlighted a light-based skin sensor currently in trials to offer a way to quantify pain and identify potential biomarkers.
Key Takeaway
Interactive panels and workshops brought NF experts together to share data, set standards, and explore new ways to accelerate research. By fostering collaboration, these sessions ensure that discoveries move faster from the lab to patients.
Key Definitions
NF Data Portal: An online platform for sharing and analyzing NF research data.
Variant Curation: The process of evaluating genetic changes to determine their impact on disease.
NF Clinical Trials Consortium: A network of hospitals and researchers running NF clinical trials in the US.
Volumetrics: Measuring the size and changes of tumors using imaging.
Plexiform Volumetrics Workshop
As more clinical trials investigate potential therapies that reduce tumor burden, there is an increased need for standardization of measurement approaches across trial designs. Drs. Eva Dombi, Brigitte Widemann, and Andrea Gross (NIH) hosted an interactive panel to gain buy-in and establish next steps to develop a gold standard protocol for PN volumetrics, allowing researchers and physicians to compare the outcomes of various clinical studies in an “apples-to-apples” manner. This reduces the need to run new trials that directly compare one drug to another.
Dr. Brigitte Widemann coled a workshop to advance standardized methods for measuring plexiform neurofibromas in clinical trials.
Advocacy in Action: Securing the Future of Research Funding
Simon Vukelj, CTF’s Chief Marketing Officer, and Angela Lamari, VP at Capstone, explored the outlook for U.S. government research funding. Simon shared a key win—the $25 million secured for the CDMRP NF research program in the FY26 House bill—and highlighted new CTF tools to help researchers find both CTF and non-CTF funding. He framed the conversation as a practical, nonpartisan look at the policies shaping biomedical research. Angela outlined how NIH appropriations work, why funding’s economic impact in many states helps protect it, and why proposed caps on institutional indirect cost rates face major hurdles.
Their discussion also addressed the recent pause in some grants and rare disease concerns, such as “brain drain,” with this guidance: know the process, be patient, and keep your voice in front of policymakers. The session closed with Jackson Howard, Regional Coordinator for EURAXESS North America, on EU research funding opportunities through Horizon Europe.
Key Definitions
NIH (National Institutes of Health): The primary U.S. government agency for biomedical and public health research.
CDMRP (Congressionally Directed Medical Research Programs): U.S. Department of Defense funding mechanism that supports targeted biomedical research, including the NF Research Program.
Appropriations: The process by which Congress allocates federal funds to government agencies and programs.
Indirect Costs: Funding provided to cover institutional expenses (e.g., facilities, administration) that support a research project.
Brain Drain: The loss of researchers to other fields or countries.
Key Takeaway
Nonpartisan advocacy is essential to sustaining and expanding NF research funding. Focusing on the facts—not the headlines—while understanding how government funding decisions are made and engaging directly with policymakers helps protect critical research dollars.
CTF Chief Marketing Officer Simon Vukelj and Angela Lamari, VP at Capstone, explored the outlook for U.S. government research funding.
Friedrich von Recklinghausen Award Tradition and Progress in NF
The Children’s Tumor Foundation’s Friedrich von Recklinghausen Award honors members of the professional NF community who have made significant contributions to research or clinical care in neurofibromatosis or schwannomatosis. It is named for Friedrich Daniel von Recklinghausen (1833–1910), the German physician who first described what we now know as neurofibromatosis type 1.
The Children’s Tumor Foundation presented the 2025 Friedrich von Recklinghausen Award to Pierre Wolkenstein, MD, PhD (Henri-Mondor Hospital, Paris-Est University/ Université Paris-Est Créteil) at the NF Conference.
A Career of Impact
A dermatologist by training and a visionary leader, Professor Wolkenstein has devoted nearly four decades to advancing NF, particularly NF1. Since 2004 he has led the French National Referral Center for Neurofibromatoses, building it into a world-class program serving more than 3,000 patients. As Chair of Dermatology at Henri-Mondor Hospital and Dean of the Faculty of Medicine at Université Paris-Est Créteil, he has united clinical excellence, academic rigor, and policy advocacy.
His groundbreaking work on cutaneous neurofibromas and quality of life in NF1—reflected in 400+ publications— has helped define standards of care. As a mentor, he has cultivated a thriving community of trainees, including the next generation of leaders at the Paris NF Center.
Leadership at Home and Abroad
A natural convener and collaborator, Professor Wolkenstein has served as President of the European Neurofibromatoses Group and co-chaired the first joint CTF–European NF Group global meeting in Paris (2018). He has also advised France’s Ministry of Health. With the forthcoming publication of the KOMET study in The Lancet (senior author), 2025 is a fitting moment to recognize his enduring contributions to NF science, care, and community.
Congratulations
CTF, together with his colleagues and peers worldwide, is proud to honor Professor Wolkenstein with the 2025 Friedrich von Recklinghausen Award for outstanding achievement over 38 years and unwavering commitment to the NF community.
