The Children's Tumor Foundation
11/12/2025 | Press release | Distributed by Public on 11/12/2025 10:01
New CTF-Funded Research Reveals a Promising Strategy to Overcome Drug Resistance in NF2-Related Schwannomatosis
New CTF-Funded Research Reveals a Promising Strategy to Overcome Drug Resistance in NF2-Related Schwannomatosis
November 12, 2025Awards & Grants, Featured, Featured EU, NF2-SWN, Science & Research
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The Children's Tumor Foundation is proud to celebrate a major scientific milestone from one of our Young Investigator Award (YIA) recipients. A newA woman wearing a white lab coat stands in a laboratory, smiling at the camera. Shelves with lab supplies are visible in the background. study by Haley Hardin, a postdoctoral student in the lab of Dr. Cristina Fernández-Valle, has just been published in Oncogene, a leading journal from Nature Publishing Group. Haley was a 2022-2024 CTF Young Investigator Awardee, and this publication reflects exactly why early-career funding matters: it opens the door to discoveries that can change how NF is understood and treated.
You can read more about the study here.
What the Research Found
NF2-related schwannomatosis (NF2-SWN) causes people to develop multiple tumors called schwannomas, often leading to hearing loss, balance problems, chronic pain, and other serious neurological challenges. Today, there are no approved drug treatments for these tumors, which makes research like this essential.
In this study, researchers dug into an important question: Why do schwannoma cells survive even when a drug slows their growth?
Earlier work showed that the MEK inhibitor trametinib can slow tumor growth in mice, but the tumor cells quickly adapted and stayed alive. Haley Hardin and colleagues used new human schwannoma cell models to uncover how the cells pull off this escape act.
Here's what they found, in plain language:
When treated with trametinib, schwannoma cells avoid dying by switching on survival programs.
They grow larger, reinforce their internal "skeleton," and turn on genes that help them stick together more tightly.
A key group of proteins, called BET proteins, helps drive this survival response.
When researchers block BET proteins in combination with trametinib, the tumor cells can't adapt, and they die.
Importantly, cell death is only observed when BET blockers are paired with trametinib. Combining BET blockers with another drug, brigatinib, did not have the same effect.
In short:
Targeting BET proteins in combination with MEK inhibition may be a promising way to overcome drug resistance in NF2-SWN and help tumor-killing treatments work the way they're meant to.
Why This Matters
For families affected by NF2-SWN, this kind of research is a beacon of possibility. Understanding how tumors resist treatment is a crucial step toward developing therapies that truly stop tumor growth or shrink tumors altogether.
This study highlights:
The importance of carefully pairing drugs to develop combination therapies to block tumor escape routes
The value of new human schwannoma models
The power of early-career research funding to accelerate scientific breakthroughs
CTF's Young Investigator Awards are designed to launch the careers of researchers like Haley, giving them the support and freedom to pursue bold ideas that can open new therapeutic doors. This publication is a direct reflection of the impact donors make when they invest in the next generation of scientists.
Congratulations to Haley Hardin and the Fernández-Valle Lab
CTF celebrates this achievement and the promise it brings for the NF community. Please join us in congratulating Haley and her team on this important contribution to the future of NF2-SWN research.
More updates to come as this work progresses - and as always, thank you to our donors and community for fueling discoveries that move us closer to treatments and, one day, cures.
The Children's Tumor Foundation published this content on November 12, 2025, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on November 12, 2025 at 16:01 UTC. If you believe the information included in the content is inaccurate or outdated and requires editing or removal, please contact us at [email protected]