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KAIST-Yonsei Team Identifies Origin Cells for Malignant Brain Tumor Common in Young Adults
<Dr. Jung Won Park, (Upper Right) Professor Jeong Ho Lee, Professor Seok-Gu Kang>
IDH-mutant glioma, caused by abnormalities in a specific gene (IDH), is the most common malignant brain tumor among young adults under the age of 50. It is a refractory brain cancer that is difficult to treat due to its high recurrence rate. Until now, treatment has focused primarily on removing the visible tumor mass. However, a Korean research team has discovered for the first time that normal brain cells acquire the initial IDH mutation and spread out through the cortex long before a visible tumor mass harboring additional cancer mutations forms, opening a new path for early diagnosis and treatment to suppress recurrence.
KAIST announced on January 9th that a joint research team led by Professor Jeong Ho Lee from the Graduate School of Medical Science and Engineering and Professor Seok-Gu Kang from the Department of Neurosurgery at Yonsei University Severance Hospital has identified that IDH-mutant gliomas originate from Glial Progenitor Cells (GPCs) present in normal brain tissue.
Glial Progenitor Cells (GPC): Cells that exist in the normal brain and can become the starting point for malignant brain tumors if genetic mutations occur.
Through precise analysis of tumor tissue obtained via extensive resection surgery and the surrounding normal cerebral cortex, the research team discovered that "cells of origin" harboring the IDH mutation already existed within brain tissue that appeared normal to the naked eye.
< Brain-Derived Refractory Brain Tumor Origin Cells (AI-Generated Image) >
This result proves for the first time that malignant brain tumors do not emerge suddenly at a specific point in time, but rather begin within a normal brain and progress slowly over a long period.
The research team then used "spatial transcriptomics"—a cutting-edge analysis technology that shows "which genes are operating where" simultaneously—to confirm that these origin cells with mutations were indeed Glial Progenitor Cells (GPCs) located in the cerebral cortex.
Furthermore, they successfully reproduced the process of brain tumor development in an animal model by introducing the same genetic "driver mutation" found in patients into the GPCs of mice.
This study is a significant expansion of previous research identifying the "origin" of IDH wildtype malignant brain tumors. In 2018, the joint research team led a paradigm shift in brain tumor research by revealing that IDH wildtype glioblastoma, a representative malignant brain tumor, originates not from the tumor body itself, but from neural stem cells in the subventricular zone—the source of new brain cells in the adult brain (Lee et al., Nature, 2018).
The current study clarifies that even though "IDH wildtype glioblastoma" and "IDH-mutant glioma" are both types of brain cancer, their starting cells and points of origin are entirely different, proving that different types of brain tumors have fundamentally different developmental processes.
< Mechanistic Elucidation of Malignant Brain Tumor Development Induced by IDH Mutations and Subsequent Genetic Alterations in Normal Cortical Glial Progenitor Cells >
Professor Seok-Gu Kang (Co-Corresponding Author) stated, "Brain tumors may not start exactly where the tumor mass is visible. A target approach focused on the origin cells and the site of origin according to the brain tumor subtype will serve as a crucial clue to changing the paradigm of early diagnosis and recurrence suppression treatment."
Based on these research results, Sovagen Co., Ltd, a faculty startup from KAIST, is developing an innovative RNA-based drug to suppress the evolution and recurrence of IDH-mutant malignant brain tumors. Additionally, Severance Hospital is pursuing the development of technologies to detect and control early mutant cells in refractory brain tumors through the Korea-US Innovative Result Creation R&D project.
Dr. Jung Won Park (Postdoctoral Researcher at KAIST Graduate School of Medical Science and Engineering), a neurosurgeon and the sole first author of the study, said, "This achievement was made possible by combining KAIST’s world-class basic science research capabilities with the clinical expertise of Yonsei Severance Hospital. The question I kept asking while treating patients—'Where does this tumor originate?'—was the starting point of this research."
The findings were published on January 8th in the world-renowned academic journal Science.
Paper Title: IDH-mutant gliomas arise from glial progenitor cells harboring the initial driver mutation
DOI: 10.1126/science.adt0559
Authors: Jung Won Park (KAIST, First Author), Seok-Gu Kang (Yonsei Severance Hospital, Corresponding Author), Jeong Ho Lee (KAIST, Sovagen, Corresponding Author)
This research was conducted with support from the Suh Kyung-bae Science Foundation, the National Research Foundation of Korea, the Ministry of Science and ICT, the Ministry of Health and Welfare, and the Korea Health Industry Development Institute (Physician-Scientist Training Program).
2026.01.09 View 352 -
KAIST Awakens dormant immune cells inside tumors to attack cancer
<(From Left) Professor Ji-Ho Park, Dr. Jun-Hee Han from the Department of Bio and Brain Engineering>
Within tumors in the human body, there are immune cells (macrophages) capable of fighting cancer, but they have been unable to perform their roles properly due to suppression by the tumor. KAIST researchers have overcome this limitation by developing a new therapeutic approach that directly converts immune cells inside tumors into anticancer cell therapies.
KAIST (President Kwang Hyung Lee) announced on the 30th that a research team led by Professor Ji-Ho Park of the Department of Bio and Brain Engineering has developed a therapy in which, when a drug is injected directly into a tumor, macrophages already present in the body absorb it, produce CAR (a cancer-recognizing device) proteins on their own, and are converted into anticancer immune cells known as “CAR-macrophages.”
Solid tumors—such as gastric, lung, and liver cancers—grow as dense masses, making it difficult for immune cells to infiltrate tumors or maintain their function. As a result, the effectiveness of existing immune cell therapies has been limited.
CAR-macrophages, which have recently attracted attention as a next-generation immunotherapy, have the advantage of directly engulfing cancer cells while simultaneously activating surrounding immune cells to amplify anticancer responses.
However, conventional CAR-macrophage therapies require immune cells to be extracted from a patient’s blood, followed by cell culture and genetic modification. This process is time-consuming, costly, and has limited feasibility for real-world patient applications.
To address this challenge, the research team focused on “tumor-associated macrophages” that are already accumulated around tumors.
They developed a strategy to directly reprogram immune cells in the body by loading lipid nanoparticles—designed to be readily absorbed by macrophages—with both mRNA encoding cancer-recognition information and an immunostimulant that activates immune responses.
In other words, in this study, CAR-macrophages were created by “directly converting the body’s own macrophages into anticancer cell therapies inside the body.”
<Figure . Schematic illustration of the strategy for in vivo CAR-macrophage generation and cancer cell eradication via co-delivery of CAR mRNA and immunostimulants using lipid nanoparticles (LNPs)>
When this therapeutic agent was injected into tumors, macrophages rapidly absorbed it and began producing proteins that recognize cancer cells, while immune signaling was simultaneously activated. As a result, the generated “enhanced CAR-macrophages” showed markedly improved cancer cell–killing ability and activated surrounding immune cells, producing a powerful anticancer effect.
In animal models of melanoma (the most dangerous form of skin cancer), tumor growth was significantly suppressed, and the therapeutic effect was shown to have the potential to extend beyond the local tumor site to induce systemic immune responses.
Professor Ji-Ho Park stated, “This study presents a new concept of immune cell therapy that generates anticancer immune cells directly inside the patient’s body,” adding that “it is particularly meaningful in that it simultaneously overcomes the key limitations of existing CAR-macrophage therapies—delivery efficiency and the immunosuppressive tumor environment.”
This research was led by Jun-Hee Han, Ph.D., of the Department of Bio and Brain Engineering at KAIST as the first author, and the results were published on November 18 in ACS Nano, an international journal in the field of nanotechnology.
※ Paper title: “In Situ Chimeric Antigen Receptor Macrophage Therapy via Co-Delivery of mRNA and Immunostimulant,” Authors: Jun-Hee Han (first author), Erinn Fagan, Kyunghwan Yeom, Ji-Ho Park (corresponding author), DOI: 10.1021/acsnano.5c09138
This research was supported by the Mid-Career Researcher Program of the National Research Foundation of Korea.
2025.12.31 View 949 -
Mathematicians Solve Cellular Noise, a Long-standing Challenge in Biology
< (From left) Researcher Dongju Lim, Researcher Seokhwan Moon, Professor Jae Kyoung Kim (KAIST), Professor Jinsu Kim (POSTECH), Professor Byung-Kwan Cho (KAIST) >
Why does cancer sometimes recur even after successful treatment, or why do some bacteria survive despite the use of powerful antibiotics? One of the key culprits identified is "Biological Noise"—random fluctuations occurring inside cells. Even when cells share the same genes, the amount of protein varies in each, creating "outliers" that evade drug treatments and survive. Until now, scientists could only control the average values of cell populations; controlling the irregular variability of individual cells remained a long-standing challenge.
A joint research team—led by Professor Jae Kyoung Kim (Department of Mathematical Sciences, KAIST), Professor Jinsu Kim (Department of Mathematics, POSTECH), and Professor Byung-Kwan Cho (Graduate School of Engineering Biology, KAIST)—has theoretically established a "Noise Control Principle." Through mathematical modeling, they have found a way to eliminate biological noise and precisely govern cellular destiny. This achievement in securing precision control technology at the single-cell level is expected to be a new milestone in solving challenges in cancer treatment and synthetic biology.
While cells in our bodies strive to maintain homeostasis for survival, their internal environments are constantly changing. Existing genetic circuit technologies could regulate the average protein levels of a cell population but often ended up amplifying the "noise"—the variance between individual cells. The research team compared this to a "shower that fluctuates between boiling and freezing." Even if the average water temperature is set to 40°C, a normal shower is impossible if the water alternates between scalding and icy. Similarly, a small number of cells that escape control due to this "trap of the average" become the primary cause of cancer recurrence or antibiotic resistance. To solve this, the team devised a new mathematical model called the "Noise Controller (NC)."
The researchers first investigated whether they could control the variance of outputs—which differs from cell to cell—using a "dimerization reaction," where the final products of a system bind together to form pairs. In the process, they confirmed that the dimerization reaction could act as a sensor to detect fluctuations (noise) in the cellular state. However, initial attempts showed that this method alone had limits in reducing differences between cells. Consequently, they determined that a device was needed to immediately reduce substances if they were overproduced. They combined this with a "degradation-based actuation" principle, which promptly breaks down proteins when they become excessive. As a result, they theoretically implemented "Noise Robust Perfect Adaptation (Noise RPA)," which maintains a constant noise level despite external environmental changes. Through this, they succeeded in suppressing cell-to-cell deviation to a Fano factor of 1—the minimum level achievable by universal biological systems.
< Figure 1. Conceptual Diagram of Noise Controller (NC) Effects: When no control technology is used (top, gray), the average value of the cell population changes due to external stimuli. With existing control technology (middle, blue), the average value is maintained, but the deviation between individual cells (noise) remains large. In contrast, using the Noise Controller (bottom, green) maintains the average while also reducing the noise level of individual cells. >
The research team proved the model's performance by virtually applying it to the DNA repair system of E. coli. In the existing system, the amount of DNA-repairing proteins varied so greatly between cells that approximately 20% of the cells failed to repair and died. However, by applying the Noise Controller (NC) to unify protein levels across all cells, the mortality rate was slashed to 7%. The team significantly boosted cell survival rates through sophisticated mathematical principles alone. This is highly significant as it moves beyond the "average control" paradigm to realize "single-cell control," dealing with each cell with precision.
< Figure 2. Structure of the Noise Controller (NC).In the conventional control scheme (left), the final output (X2) produces one of the controller proteins (Z2), and this protein is degraded together with the other controller protein (Z1) that generates the system input (X1).In contrast, the noise controller (NC) established in this study (right) has a largely similar structure, but is characterized by the production of the controller protein (Z4) through a dimerization reaction of the final output. This protein directly degrades the system input (X1).Through this mechanism, mathematical expressions for the mean of the final output (lower left equation) and its noise (lower right equation) can be derived >
Professor Jae Kyoung Kim, who led the research, stated, "The significance lies in bringing cellular noise—which was previously dismissed as luck or coincidence in biological phenomena—into the realm of controllable factors through mathematical design." He added, "It will play a vital role in fields requiring precise cellular control, such as overcoming cancer treatment resistance and developing high-efficiency smart microorganisms." Co-corresponding author Professor Jinsu Kim of POSTECH emphasized, "This research demonstrates the power of mathematical modeling, starting from theoretical formulas of intracellular noise using reaction network theory and leading to the design of actual biological mechanisms."
< Figure 3. Actual Biological Circuit Structure of the Noise Controller (NC): A representation of the mathematical model established by the research team implemented as a genetic circuit, which is an actual biological system. The existing control technology (left) consists of a reaction where the final product produces an anti-sigma factor (RsiW), which then binds with the sigma factor (SigW) that generates the system’s input value. The Noise Controller (NC) (right) similarly utilizes the binding reaction between an anti-sigma factor (RseA) and a sigma factor (ECF); however, the primary differences are that the anti-sigma factor (RseA) is produced through the dimerization reaction of the final product , and that the anti-sigma factor (RseA) directly degrades the system’s input value >
The results of this study were published on December 24 in the international academic journal Nature Communications (IF=15.7).
2025.12.29 View 556 -
Breakthrough in Intractable Intestinal Disease Treatment Using Xenogeneic-Free Intestinal Stem Cells
< (From left) Professor Sung Gap Im (KAIST), Dr. Seonghyeon Park (KAIST), M.S candidate Sang Yu Sun (KAIST), Dr. Mi-Young Son (KRIBB), (Top right) Dr. Tae Geol Lee (KRISS), Dr. Jin Gyeong Son (KRISS) >
Intestinal Stem Cells (ISCs) derived from a patient's own cells have garnered significant attention as a new alternative for treating intractable intestinal diseases due to their low risk of rejection. However, clinical application has been limited by safety and regulatory issues arising from conventional culture methods that rely on animal-derived components (xenogeneic components). A KAIST research team has developed an advanced culture technology that stably grows ISCs without animal components while simultaneously enhancing their migration to damaged tissues and regenerative capabilities.
KAIST announced on December 23rd that a joint research team—led by Professor Sung Gap Im from the Department of Chemical and Biomolecular Engineering, Dr. Tae Geol Lee from the Nano-Bio Measurement Group at the Korea Research Institute of Standards and Science and Dr. Mi-Young Son from the Stem Cell Convergence Research Center at the Korea Research Institute of Bioscience and Biotechnology has developed a polymer-based culture platform that dramatically improves the migration and regeneration of ISCs in a xenogeneic-free environment.
To overcome obstacles in the clinical application of stem cell therapies—such as the risk of virus transmission to patients when using substances derived from mouse fibroblasts or Matrigel—the joint research team developed "PLUS" (Polymer-coated Ultra-stable Surface). This polymer-based culture surface technology functions effectively without any animal-derived materials.
< Figure 1. Precise control of polymer coating and surface modification via initiated Chemical Vapor Deposition (iCVD) process >
PLUS is a synthetic polymer surface coated via a vapor deposition method. By precisely controlling surface energy and chemical composition, it significantly enhances the adhesion and mass-culture efficiency of ISCs. Notably, it maintains identical culture performance even after being stored at room temperature for three years, securing industrial scalability and storage convenience for stem cell therapeutics.
Through proteomics analysis*, the research team identified that the expression of proteins related to cytoskeletal reorganization significantly increased in ISCs cultured on the PLUS environment.
Proteomics Analysis: A method used to simultaneously analyze the types and quantitative changes of all proteins present within a cell or tissue.
Specifically, the team confirmed that increased expression of cytoskeleton-binding and actin-binding proteins leads to a stable restructuring of the internal cellular architecture. This provides the power source for stem cells to move faster and more actively across the substrate.
< Figure 2. Elucidation of the mechanism for enhanced ISC migration through precision proteomics analysis >
Real-time observations using holotomography microscopy revealed that ISCs cultured on PLUS exhibited a migration speed approximately twice as fast as those on conventional surfaces. Furthermore, in a damaged tissue model, the cells demonstrated outstanding regenerative performance, repairing more than half of the damage within a single week. This proves that PLUS activates the cytoskeletal activity of stem cells, thereby boosting their practical tissue regeneration capabilities.
The newly developed PLUS culture platform is evaluated as a technology that will significantly enhance the safety, mass production, and clinical feasibility of ISCs derived from human pluripotent stem cells (hPSCs). By elucidating the mechanism that simultaneously strengthens the survival, migration, and regeneration of stem cells in a xenogeneic-free environment, the team has established a foundation to fundamentally resolve safety, regulatory, and productivity issues in stem cell therapy.
Professor Sung Gap Im of KAIST stated, "This research provides a synthetic culture platform that eliminates the dependence on xenogeneic components—which has hindered the clinical application of stem cell therapies—while maximizing the migration and regenerative capacity of stem cells. It will serve as a catalyst for a paradigm shift in the field of regenerative medicine."
Dr. Seonghyeon Park (KAIST), Sang Yu Sun (KAIST), and Dr. Jin Gyeong Son (KRISS) participated as first authors. The research findings were published online on November 26th in Advanced Materials, the leading academic journal in materials science.
Paper Title: Tailored Xenogeneic-Free Polymer Surface Promotes Dynamic Migration of Intestinal Stem Cells
DOI: 10.1002/adma.202513371
This research was conducted with support from the Ministry of Science and ICT, the Ministry of SMEs and Startups, the National Research Foundation of Korea, the National Council of Science and Technology Research, KRISS, KRIBB, and the National NanoFab Center.
2025.12.23 View 517 -
KAIST, Production Temperature ↓ by 500°C, Power Output ↑ 2x… Next-Generation Ceramic Electrochemical Cell Reborn
<(Top row, from left) Professor Kang Taek Lee, Ph.D candidate Yejin Kang, Dr. Dongyeon Kim, (Bottom row, from left) M.S candidate Mincheol Lee, Ph.D candidate Seeun Oh, Ph.D candidate Seungsoo Jang, Ph.D candidate Hyeonggeun Kim>
As power demand surges in the AI era, the “protonic ceramic electrochemical cell (PCEC),” which can simultaneously produce electricity and hydrogen, is gaining attention as a next-generation energy technology. However, this cell has faced the technical limitation of requiring an ultra-high production temperature of 1,500°C. A KAIST research team has succeeded in establishing a new manufacturing process that lowers this limit by more than 500°C for the first time in the world.
KAIST (President Kwang Hyung Lee) announced on the 4th of December that Professor Kang Taek Lee’s research team in the Department of Mechanical Engineering developed a new process that enables the fabrication of high-performance protonic ceramic electrochemical cells at temperatures more than 500°C lower than before, using “microwave + vapor control technology” that leverages microwave heating principles and the diffusion environment of chemical vapor generated from specific chemical components.
The electrolyte—the key material of protonic ceramic electrochemical cells—contains barium (Ba), and barium easily evaporates at temperatures above 1,500°C, which has been the main cause of performance degradation. Therefore, the ability to harden the ceramic electrolyte at a lower temperature has been the core issue that determines cell performance.
As power demand surges in the AI era, the “protonic ceramic electrochemical cell (PCEC),” which can simultaneously produce electricity and hydrogen, is gaining attention as a next-generation energy technology. However, this cell has faced the technical limitation of requiring an ultra-high production temperature of 1,500°C. A KAIST research team has succeeded in establishing a new manufacturing process that lowers this limit by more than 500°C for the first time in the world.
KAIST (President Kwang Hyung Lee) announced on the 4th of December that Professor Kang Taek Lee’s research team in the Department of Mechanical Engineering developed a new process that enables the fabrication of high-performance protonic ceramic electrochemical cells at temperatures more than 500°C lower than before, using “microwave + vapor control technology” that leverages microwave heating principles and the diffusion environment of chemical vapor generated from specific chemical components.
The electrolyte—the key material of protonic ceramic electrochemical cells—contains barium (Ba), and barium easily evaporates at temperatures above 1,500°C, which has been the main cause of performance degradation. Therefore, the ability to harden the ceramic electrolyte at a lower temperature has been the core issue that determines cell performance.
To solve this, the research team devised a new heat-treatment method called “vapor-phase diffusion.” This technique places a special auxiliary material (a vapor source) next to the cell and irradiates it with microwaves to quickly diffuse vapor. When the temperature reaches approximately 800°C, the vapor released from the auxiliary material moves toward the electrolyte and tightly bonds the ceramic particles. Thanks to this technology, a process that previously required 1,500°C can now be completed at just 980°C. In other words, a world-first ceramic electrochemical cell fabrication technology has been created that produces high-performance electricity at a “low temperature” without damaging the electrolyte.
A cell fabricated with this process produced 2 W of power stably from a 1 cm² cell (roughly the size of a fingernail) at 600°C and generated 205 mL of hydrogen per hour at 600°C (about the volume of a small paper cup, among the highest in the industry). It also maintained stability without performance degradation during 500 hours of continuous operation.
In other words, this technology reduces the production temperature (−500°C), lowers the operating temperature (600°C), doubles performance (2 W/cm²), and extends the lifespan (500-hour stability), achieving world-class performance in ceramic cell technology.
The research team also enhanced the reliability of the technology by using digital twins (virtual simulations) to analyze gas-transport phenomena occurring in the microscopic internal structure of the cell − phenomena that are difficult to observe in actual experiments.
<Figure 1. (a) Schematic of the vapor-diffusion-based process; (b) Surface microstructure of the electrolyte; (c) Internal barium composition ratio of the electrolyte according to processing conditions; (d) Comparison of power-generation performance with previous studies>
< Figure 2. (a) Three-dimensional reconstructed image of the protonic ceramic electrochemical cell fuel electrode according to processing conditions (b) Pore structure (c) Gas-transport simulation results >
Professor Kang Taek Lee emphasized, “This study is the world’s first case of using vapor to lower the heat-treatment temperature by more than 500°C while still producing a high-performance, high-stability cell.” He added, “It is expected to become a key manufacturing technology that addresses the power challenges of the AI era and accelerates the hydrogen society.”
Dongyeon Kim (KAIST PhD) and Yejin Kang (KAIST PhD candidate) participated as co–first authors. The research results were published in Advanced Materials (IF: 26.8), one of the world’s leading journals in energy and materials science, and were selected as the Inside Front Cover article on October 29.
(Paper title: “Sub-1000°C Sintering of Protonic Ceramic Electrochemical Cells via Microwave-Driven Vapor Phase Diffusion,” DOI: https://doi.org/10.1002/adma.202506905)
This research was supported by the MSIT’s Mid-career Researcher Program and the H2 Next Round Program.
2025.12.05 View 1095 -
A KAIST team develops the world's first modular co-culture platform for the one-pot production of rainbow-colored bacterial cellulose.
<(From Left) Distinguished Professor Sang Yup Lee, Ph.D candidate Pingxin Lin, Ph.D candiate Zhou Hengrui>
The integration of systems metabolic engineering with co-culture strategies that couples bacterial cellulose production with natural colorant biosynthesis enabled the one-pot generation of rainbow-colored bacterial cellulose, establishing a sustainable biomanufacturing platform that can replace petroleum-based textiles and eliminate chemical dyeing processes.
A research group at KAIST has successfully developed a modular co-culture platform for the one-pot production of rainbow-colored bacterial cellulose. The team, led by Distinguished Professor Sang Yup Lee from the Department of Chemical and Biomolecular Engineering, engineered Komagataeibacter xylinus for bacterial cellulose synthesis and Escherichia coli for natural colorants overproduction. A co-culture of these engineered strains enabled the in situ coloration of bacterial cellulose. This research offers a versatile platform for producing living materials in multiple colors, and provides new opportunities for sustainable textiles, wearable biomaterials, and functional living materials that combine optical and structural properties beyond the reach of conventional textile technologies.
Bacterial cellulose is an attractive and biodegradable alternative to petroleum-derived fabrics due to its high purity, mechanical strength, and water-retention properties. However, the limited color range of bacterial cellulose, which is typically white, has limited its broader application in the textile industry, where more vibrant colored fabrics are increasingly desired. Conventional dyeing methods rely on petroleum-based colorants and toxic reagents, creating environmental and processing challenges. These challenges have driven the demand for alternative production methods.
To address these issues, KAIST researchers, including Ph.D. Candidate Hengrui Zhou, Ph.D. Candidate Pingxin Lin, Professor Ki Jun Jeong, and Distinguished Professor Sang Yup Lee, combined systems metabolic engineering with co-culture strategies to develop a bio-based route that integrates bacterial cellulose formation with natural pigment synthesis, enabling the production of colored living materials in a single step without additional chemical processing.
The team’s work, entitled “One-pot production of colored bacterial cellulose,” was published in Trends in Biotechnology on November 12,2025.
This research details the one-pot production of multicolored bacterial cellulose using a modular co-culture platform that integrates a bacterial cellulose-overproducing K. xylinus strain with natural colorant-producing E. coli strains. The team focused on addressing the limitations in bacterial cellulose coloration caused by environmental challenges and complex processing requirements. By employing vesicle engineering and optimizing co-culture parameters, the researchers achieved one-pot production of red, orange, yellow, green, blue, navy, and purple bacterial cellulose, eliminating the need for external dyes and toxic chemical treatments.
To enhance dyeing efficiency, E. coli strains were engineered for the overproduction and secretion of natural colorants. It was determined that the intracellular accumulation of these pigments disrupts cellular metabolism and physiology, thereby inhibiting their production. To overcome this limitation, vesicle engineering has emerged as a key strategy to mitigate these cytotoxic effects, including the induction of inner- and outer-membrane vesicles and the modulation of cell morphology, enabling the more efficient secretion of colorants and increased overall production. The engineered E. coli strains were optimized in fed-batch fermentation, achieving record-breaking production of 16.92 ± 0.10 g/L of deoxyviolacein, 8.09 ± 0.17 g/L of violacein, 1.82 ± 0.07 g/L of proviolacein, and 936.25 ± 9.70 mg/L of prodeoxyviolacein, the highest reported titers to date for all four violacein derivatives.
< Figure 1. Rainbow-colored bacterial cellulose (microbial fiber) with applied color >
A co-culture platform combining the K. xylinus with E. coli strains was further developed and optimized, enabling the in situ one-pot coloration of bacterial cellulose in vibrant green, blue, navy, and purple. Fed-batch fermentation further improved the performance of the platform, achieving the world-first one-pot production of multicolored bacterial cellulose on a larger scale. To expand the bacterial cellulose color palette, engineered carotenoid-producing E. coli strains were incorporated, enabling the successful synthesis of red, orange, and yellow bacterial cellulose. This milestone demonstrates the potential of microbial fermentation as a sustainable alternative to petroleum-based textile processes.
“We can anticipate that this microbial cell factory-based one-pot production of rainbow-colored bacterial cellulose has the potential to replace current petroleum-based textile processes,” said Ph.D. Candidate Hengrui Zhou. “The systems metabolic engineering strategies developed in this study could be broadly applied for the production of diverse sustainable textiles, wearable biomaterials, and functional living materials that combine optical and structural properties beyond the capabilities of conventional textile technologies.” He added, “This platform reduces the environmental impact while greatly expanding design possibilities. Beyond serving as a proof-of-concept, this technology offers a promising route toward scalable, eco-friendly fabrics with in situ coloration. Its modular design allows the incorporation of diverse natural colorant pathways, enabling the creation of living materials in multiple colors.”
< Figure 2. Schematic of a microbe-based platform for one-step production of rainbow-colored bacterial cellulose >
“As demand for sustainable textiles and living materials continues to grow, we expect that the integrated biomanufacturing platform developed here will play a pivotal role in producing diverse functional biomaterials with additional design possibilities in a single step, without additional chemical processing,” explained Distinguished Professor Sang Yup Lee.
This work was supported by the Development of Next-generation Biorefinery Platform Technologies for Leading Bio-based Chemicals Industry project (2022M3J5A1056072) and the Development of Platform Technologies of Microbial Cell Factories for the Next-generation Biorefineries project (2022M3J5A1056117) from the National Research Foundation supported by the Korean Ministry of Science and ICT.
Source:
Hengrui Zhou (1st), Pingxin Lin (2nd), Ki Jun Jeong (3rd), and Sang Yup Lee (Corresponding). “One-pot production of colored bacterial cellulose”. Trends in Biotechnology (Published) doi: 10.1016/j.tibtech.2025.09.019
2025.11.19 View 1432 -
Unraveling the Secret of Cell Movement
<(From left) Professor Won Do Heo (KAIST), Postdoctoral Researcher Heeyoung Lee (KAIST, First Author), Professor Kwang-Hyun Cho (KAIST), Professor Kapsang Lee (Johns Hopkins University, USA), Dr. Sangkyu Lee (IBS), Dr. Dongsan Kim (LIBD), Dr. Yeaji Seo (Hulux) (Co-First Authors)>
Cell movement is an essential biological process, whether it's cancer cells metastasizing to other parts of the body or immune cells migrating to heal a wound. However, the principle by which cells autonomously determine their direction of movement without external stimuli has remained unknown until now.
Through this research, KAIST and an international joint research team have elucidated the principle by which cells decide their direction and move on their own, offering a crucial clue for identifying the causes of cancer metastasis and immune diseases and establishing new treatment strategies.
KAIST announced on the 10th of November that the research team led by Endowed Chair Professor Won Do Heo of the Department of Biological Sciences, in collaboration with the research team of Endowed Chair Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering, and Professor Kapsang Lee's research team at Johns Hopkins University in the US, has for the first time in the world identified the 'autonomous driving mechanism' by which cells determine their direction of movement without external signals.
The research team developed a new imaging technique called 'INSPECT (INtracellular Separation of Protein Engineered Condensation Technique)' that allows direct visualization of how proteins interact within living cells. Using this technology, they revealed the principle of the cell's internal program for autonomously deciding its direction of movement.
The team newly analyzed the operation of the key proteins that regulate cell movement, the Rho family proteins (Rac1, Cdc42, RhoA). The results showed that these proteins do not merely divide the front and back of the cell, as previously theorized, but that the cell's decision to move straight or change direction depends on which protein it binds with.
The INSPECT technology artificially implements the phenomenon of 'phase separation,' where proteins, upon binding, naturally form segregated regions that do not mix well. This technique allows for the direct visualization of how proteins actually bind within the cell using a fluorescent signal.
<Figure 1. INSPECT: A technique for visualizing Intracellular Protein-Protein Interactions">
The research team used the proteins ferritin and the fluorescent protein DsRed to make the clusters, or 'condensates,' visible to the eye when proteins bind together like small droplets.
Using this technology, the team analyzed a total of 285 pairs of interactions by combining 15 types of Rho proteins with 19 types of binding proteins, confirming actual binding in 139 pairs. Specifically, they identified that the Cdc42–FMNL protein combination is the core circuit responsible for the cell's 'straight movement,' while the Rac1–ROCK protein combination is responsible for the cell's 'change of direction.'
The research team slightly modified a part of the Rac1 protein (the 37th amino acid), which is crucial for cell direction control, to prevent it from binding well with the 'steering wheel' protein, ROCK. As a result, the cells could not change direction and continued to move in a straight line.
In contrast, in normal cells, Rac1 and ROCK bind well, forming a structure called 'arc stress fiber' at the front of the cell. This fiber enables the cell to make near-perpendicular turns when changing direction.
Furthermore, in an experiment where the environment the cells were attached to was changed, normal cells adjusted their moving speed according to the surrounding environment, but the Rac1F37W cells (cells with a broken 'steering wheel') maintained the same speed regardless of environmental changes. This demonstrates that the Rac–ROCK protein axis subtly controls the cell's ability to recognize and adapt to its surrounding environment.
<Figure 2. Analysis of the Signaling Network through Screening of Protein Interactions that Bind to a Cell Migration-Controlling Protein>
Professor Won Do Heo stated, "This research reveals that cell movement is not a random motion but is precisely controlled by an intrinsic program created by the ensemble of Rho signaling proteins and cell migration-related proteins." He added, "The newly developed INSPECT technology is a powerful tool for visualizing intracellular protein interactions and will be broadly utilized to uncover the molecular mechanisms of various life phenomena and diseases, such as cancer metastasis and neuronal cell migration."
This research, in which Dr. Heeyoung Lee of KAIST, Dr. Sangkyu Lee (currently at IBS), Dr. Yeji Seo (currently at Hulux Co., Ltd.), and Dr. Dongsan Kim (currently at LIBD) participated as co-first authors, was published in Nature Communications on October 31st.
Journal Name: A Rho GTPase-effector ensemble governs cell migration behavior
DOI: https://doi.org/10.1038/s41467-025-64635-0
The research was supported by the Samsung Future Technology Foundation and the National Research Foundation of Korea.
2025.11.10 View 896 -
KAIST Uncovers the Mechanism Behind Overactive Immune Cells
<(From Right) Professor Eui-Cheol Shin, Ph.D candidate So-Young Kim, Professor Su-Hyung Park, Professor Hyuk Soo Eun, Dr. Hoyoung Lee>
“Why do immune cells that are supposed to eliminate viruses suddenly turn against our own body?”
There are instances where killer T cells—which are meant to precisely remove virus-infected cells—malfunction like overheated engines, attacking even healthy cells and damaging tissues. A KAIST research team has now identified the key mechanism that regulates this excessive activation of killer T cells, offering new insights into controlling immune overreactions and developing therapies for immune-related diseases.
KAIST (President Kwang Hyung Lee) announced on November 5 that a research team led by Professors Eui-Cheol Shin and Su-Hyung Park from the Graduate School of Medical Science and Engineering, in collaboration with Professor Hyuk Soo Eun from Chungnam National University College of Medicine, has uncovered the molecular basis of nonspecific activation in killer T cells and proposed a new therapeutic strategy to control it.
Killer T cells (CD8⁺ T cells) selectively eliminate infected cells to prevent viral spread. However, when excessively activated, they can attack uninfected cells, causing inflammation and tissue damage. Such overactive immune responses can lead to severe viral infections and autoimmune diseases.
In 2018, Professor Shin’s team was the first in the world to discover that killer T cells can be nonspecifically activated by cytokines and randomly attack host cells—a phenomenon they termed “bystander activation of T cells”. The current study builds on that discovery by revealing the molecular mechanism driving this abnormal process.
The team focused on a cytokine called interleukin-15 (IL-15). Experiments showed that IL-15 can abnormally excite killer T cells by a bystander activation mechanism, causing them to attack uninfected host cells. However, when there is a concurrent antigen-specific stimulation, IL-15-induced bystander activation is suppressed.
The researchers further identified that this suppression occurs through an intracellular signaling process. When the concentration of calcium ions (Ca²⁺) changes, a protein called calcineurin activates, which in turn triggers a regulatory protein known as NFAT, suppressing IL-15-induced bystander activation of killer T cells. In other words, the calcineurin–NFAT pathway activated by antigen stimulation acts as a brake on overactivation by a bystander mechanism.
The team also discovered that some immunosuppressants, which are known to block the calcineurin pathway, may not always suppress immune responses—in certain contexts, they can instead promote IL-15-induced bystander activation of killer T cells. This finding underscores that not all immunosuppressants work the same way and that treatments must be carefully tailored to each patient’s immune response.
Through gene expression analysis, the researchers identified a gene set that increase only in abnormally activated killer T cells induced by IL-15 as markers. They further confirmed that these same markers were elevated in bystander killer T cells from patients with acute hepatitis A, suggesting that the markers could be used for disease diagnosis.
<In a normal immune response, killer T cells are activated by antigen stimulation and selectively eliminate only virus-infected cells, thereby controlling viral replication and promoting the patient’s rapid recovery. However, when killer T cells are nonspecifically overactivated by interleukin-15, they may randomly attack normal cells as well, causing excessive tissue damage and leading to severe disease. Future research may identify diseases in which such nonspecific hyperimmune responses occur, making it possible to develop new drugs to control them>
This study provides crucial clues for understanding the pathogenesis of various immune-related diseases, including severe viral infections, chronic inflammatory disorders, autoimmune diseases, and organ transplant rejection. It also paves the way for developing novel immunoregulatory therapies targeting IL-15 signaling.
Professor Eui-Cheol Shin explained that, “this study shows that killer T cells are not merely defenders—they can transform into ‘nonspecific attackers’ depending on the inflammatory environment. By precisely regulating this abnormal activation, we may be able to develop new treatments for intractable immune diseases.”
This research was published in the journal Immunity on October 31, with Dr. Hoyoung Lee and Ph.D. candidate So-Young Kim as co–first authors.
Title: “TCR signaling via NFATc1 constrains IL-15-induced bystander activation of human memory CD8⁺ T cells”, DOI: doi.org/10.1016/j.immuni.2025.10.002
The study was supported by the National Research Foundation of Korea (NRF), the Korea Health Industry Development Institute (KHIDI), and the Institute for Basic Science (IBS).
2025.11.06 View 1537 -
KAIST Fabricates Green Hydrogen Cells in Just 10 Minutes Like Using a Microwave
<(From Left) Ph.D candidate Hyeongmin Yu, Ph.D candidate Seungsoo Jang, Ph.D candidate Donghun Lee, Ph.D candidate Gayoung Yoon, Professor Kang Taek Lee>
Solid oxide electrolysis cells (SOECs), a key technology for producing green hydrogen without carbon emissions, require a high-temperature “sintering” process to harden ceramic powders. Researchers at KAIST have successfully shortened this process from six hours to just ten minutes, while also reducing the required temperature from 1,400°C to 1,200°C. This innovation dramatically cuts both energy consumption and production time, marking a major step forward for the green hydrogen era.
KAIST (President Kwang Hyung Lee) announced on the 25th of October that a research team led by Professor Kang Taek Lee from the Department of Mechanical Engineering has developed an ultra-fast manufacturing method capable of producing high-performance green hydrogen electrolysis cells in only ten minutes.
The core of this technology lies in sintering—a process in which ceramic powders are baked at high temperatures to form a dense, tightly bonded structure. Proper sintering is critical: it ensures that gases do not leak (as hydrogen and oxygen mixing could cause explosions), oxygen ions move efficiently, and the electrodes adhere firmly to the electrolyte to allow smooth current flow. In short, the precision of the sintering process directly determines the cell’s performance and lifetime.
To address these challenges, the KAIST team applied a “volumetric heating” technique that uses microwaves to heat the material uniformly from the inside out. This approach shortened the sintering process by more than thirtyfold compared to conventional methods. Whereas traditional sintering requires prolonged heating above 1,400°C, the new process uses microwaves to heat the material internally and evenly, achieving stable electrolyte formation at just 1,200°C within 10 minutes.
In conventional fabrication, the essential materials—ceria (CeO₂) and zirconia (ZrO₂)—tend to intermix at excessively high temperatures, degrading material quality. KAIST’s new method allows these two materials to bond firmly at the right temperature without mixing, producing a dense, defect-free bilayer electrolyte.
The total “processing time” includes heating, holding, and cooling. The conventional sintering process required about 36.5 hours, whereas KAIST’s microwave-based technique completes the entire cycle in only 70 minutes—over 30 times faster.
<Figure 1. (a) Schematic illustration of the microwave-based ultrafast sintering process and the conventional sintering process (b) Cross-sectional SEM images of the bilayer ceramic electrolyte according to the sintering process>
The resulting electrochemical cells demonstrated remarkable performance: they produced 23.7 mL of hydrogen per minute at 750°C, maintained stable operation for over 250 hours, and exhibited excellent durability. Using 3D digital twin simulations, the team further revealed that ultra-fast microwave heating improves electrolyte density and suppresses abnormal grain growth of nickel oxide (NiO) particles within the fuel electrode, thereby enhancing hydrogen production efficiency.
<Figure 2. 3D reconstruction, contact area, and electrochemically active site images of the solid oxide electrochemical cell according to the sintering process>
Professor Kang Taek Lee stated, “This research introduces a new manufacturing paradigm that enables the rapid and efficient production of high-performance solid oxide electrolysis cells.” He added, “Compared to conventional processes, our approach drastically reduces both energy consumption and production time, offering strong potential for commercialization.”
This study was co-first-authored by Hyeongmin Yu and Seungsoo Jang, both Ph.D. candidates in Mechanical Engineering at KAIST, with Donghun Lee and Gayoung Youn as collaborators. The research was published online on October 2 in Advanced Materials (Impact Factor: 26.8) and was selected as the Inside Front Cover feature paper for its scientific significance.
※ Paper title: “Ultra-Fast Microwave-Assisted Volumetric Heating Engineered Defect-Free Ceria/Zirconia Bilayer Electrolytes for Solid Oxide Electrochemical Cells”, DOI: 10.1002/adma.202500183)
This work was supported by the Ministry of Science and ICT through the H2 Next Round Program, the Mid-Career Researcher Program, and the Global Research Laboratory (GRL) Program.
2025.10.29 View 1342 -
KAIST Develops AI Technology That Predicts and Assembles Cell Drug Responses Like Lego Blocks
<(From left) Dr. Younghyun Han, (top center) Dr. Chun-Kyung Lee, (bottom center) Prof. Kwang-Hyun Cho,Ph.D. candidate Hyunjin Kim>
Controlling the state of a cell in a desired direction is one of the central challenges in life sciences, including drug development, cancer treatment, and regenerative medicine. However, identifying the right drug or genetic target for that purpose is extremely difficult. To address this, researchers at KAIST have mathematically modeled the interaction between cells and drugs in a modular “Lego block” manner—breaking them down and recombining them—to develop a new AI technology that can predict not only new cell–drug reactions never before tested but also the effects of arbitrary genetic perturbations.
KAIST (President Kwang Hyung Lee) announced on the 16th of October that a research team led by Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering has developed a generative AI-based technology capable of identifying drugs and genetic targets that can guide cells toward a desired state.
“Latent space” is an invisible mathematical map used by image-generating AI to organize the essential features of objects or cells. The research team succeeded in separating the representations of cell states and drug effects within this space and then recombining them to predict the reactions of previously untested cell–drug combinations. They further extended this principle to show that the model can also predict how a cell’s state would change when a specific gene is regulated.
The team validated this approach using real experimental data. As a result, the AI identified molecular targets capable of reverting colorectal cancer cells toward a normal-like state, which the team later confirmed through cell experiments.
This finding demonstrates that the method is not limited to cancer treatment—it serves as a general platform capable of predicting various untrained cell-state transitions and drug responses. In other words, the technology not only determines whether or not a drug works but also reveals how it functions inside the cell, making the achievement particularly meaningful.
<Latent Space Direction Vector–Based Cell Transition Modeling>
The research provides a powerful tool for designing methods to induce desired cell-state changes. It is expected to have broad applications in drug discovery, cancer therapy, and regenerative medicine, such as restoring damaged cells to a healthy state.
Professor Kwang-Hyun Cho stated, “Inspired by image-generation AI, we applied the concept of a ‘direction vector,’ an idea that allows us to transform cells in a desired direction.” He added, “This technology enables quantitative analysis of how specific drugs or genes affect cells and even predicts previously unknown reactions, making it a highly generalizable AI framework.”
The study was conducted with Dr. Younghyun Han, Ph.D. candidate Hyunjin Kim, and Dr. Chun-Kyung Lee of KAIST. The research findings were published online in Cell Systems, a journal by Cell Press, on October 15.
※ Paper title: “Identifying an Optimal Perturbation to Induce a Desired Cell State by Generative Deep Learning” (DOI: 10.1016/j.cels.2025.101405)
The study was supported by the National Research Foundation of Korea (NRF) through the Ministry of Science and ICT’s Mid-Career Researcher Program and the Basic Research Laboratory (BRL) Program.
2025.10.16 View 1663 -
KAIST Discovers Role of Huntingtin Protein in Building the Cell Skeleton
<(From Left) Professor Ji-Joon Song, Ph.D candidate Jaesung Kim, Dr. Hyeongju Kim of KAIST’s Department of Biological Sciences>
Huntington’s disease is a rare genetic disorder and a representative neurodegenerative disease, characterized by loss of motor control, cognitive decline, and psychiatric problems. An international research team has discovered that the “huntingtin protein,” the causal protein of Huntington’s disease (whose mutations are the direct cause of the disease), also performs a new function: directly organizing the cytoskeleton, the fine structural framework inside cells. This discovery is expected to contribute not only to understanding the pathogenic mechanism of Huntington’s disease, but also to research on neurodevelopmental disorders such as Alzheimer’s disease and Parkinson’s disease, as well as muscle- or mobility-related diseases such as muscular dystrophy.
KAIST (President Kwang Hyung Lee) announced on September 30 that a research team led by Professor Ji-Joon Song of the Department of Biological Sciences, in collaboration with the Institute of Science and Technology Austria (ISTA), Sorbonne University/Paris Brain Institute, and the Swiss Federal Institute of Technology Lausanne (EPFL), has uncovered—through cryo-electron microscopy (cryo-EM) and cell biology methods—the structural principle by which the huntingtin protein arranges cytoskeletal microfilaments (F-actin) into bundles.
Until now, the huntingtin protein was known only to “use” the cytoskeleton, being involved in vesicle transport or microtubule-based transport. The team, however, demonstrated that huntingtin physically organizes the cytoskeleton itself. This study is considered the first in the world to prove this new role of the huntingtin protein at the molecular level.
The researchers confirmed that huntingtin binds directly to cytoskeletal microfilaments (F-actin), and that pairs of huntingtin proteins bundle the cytoskeleton into arrays at intervals of about 20 nanometers.
Such cytoskeletal bundles play a crucial role in the development of neural connectivity. Indeed, structural development of neurons was found to be impaired in nerve cells deficient in the huntingtin protein.
<Elucidation of the Mechanism of Cytoskeletal Microfilament Bundle Formation by Huntingtin Protein and Its Impact on Neuronal Development>
First author Jaesung Kim, a PhD candidate at KAIST, stated, “This study provides a new perspective for understanding the molecular mechanism of the huntingtin protein, the cause of an incurable disease that has long remained a mystery.”
Professor Ji-Joon Song of KAIST’s Department of Biological Sciences explained, “This achievement not only provides an important clue to understanding the pathogenic mechanism of Huntington’s disease, but is also expected to have a far-reaching impact on research into cytoskeleton-related diseases,” and added that “it opens new avenues for exploring the role of the huntingtin protein in diverse biological phenomena such as cell division, migration, and mechanical signal transduction.”
This research was conducted with Jaesung Kim (PhD candidate, KAIST), Hyeongju Kim (now at Harvard University), Rémi Carpentier (Paris Brain Institute), Mariacristina Capizzi (Paris Brain Institute), and others as co-first authors, and was published on September 19 in Science Advances, a sister journal of Science.
※ Paper title: “Structure of the Huntingtin F-actin complex reveals its role in cytoskeleton organization,” DOI: https://doi.org/10.1126/sciadv.adw4124※ Co-corresponding authors: Ji-Joon Song (KAIST), Florian Schur (ISTA), and Sandrine Humbert (Sorbonne University/Paris Brain Institute).
This research was supported by the Ministry of Health and Welfare’s Global Research Collaboration Program (Korea–Switzerland Biohealth International Joint Research) and the Korea–Austria Cooperation Program.
2025.09.30 View 1565 -
KAIST, Cancer Cell Nuclear Hypertrophy May Suppress Spread
<(From Left) Ph.D candidate Saemyeong Hong, Dr. Changgon Kim, Professor Joon Kim, Professor Ji Hun Kim>
In tissue biopsies, cancer cells are frequently observed to have nuclei (the cell's genetic information storage) larger than normal. Until now, this was considered a sign that the cancer was worsening, but the exact cause and effect had not been elucidated. In this study, the KAIST research team found that cancer cell nuclear hypertrophy is not a cause of malignancy but a temporary response to replication stress, and that it can, in fact, suppress metastasis. This discovery is expected to lead to the development of new diagnostic and therapeutic strategies for cancer and metastasis inhibition.
KAIST (President Kwang Hyung Lee) announced on the September 26th that a research team led by Professor Joon Kim of the Graduate School of Medical Science and Engineering, in collaboration with the research teams of Professor Ji Hun Kim and Professor You-Me Kim, discovered the molecular reason why the nucleus enlarges in cancer cells. This achievement provides an important clue for understanding nuclear hypertrophy, a phenomenon frequently observed in pathological examinations but whose direct cause and relationship with cancer development were unclear.
The research team confirmed that DNA replication stress (the burden and error signal that occurs when a cell copies its DNA), which is common in cancer cells, causes the 'actin' protein inside the nucleus to aggregate (polymerize), which is the direct cause of the nuclear enlargement.
<Mechanisms Inducing Nuclear Enlargement in Cancer Cells and Its Impact on Cellular Physiology>
This result suggests that the change in cancer cell nuclear size may not simply be a "trait evolved by the cancer cell for its benefit." Rather, it suggests that it is a temporary, makeshift response to stress, and that it may impose constraints on the cancer cell's potential for metastasis.
Therefore, future research needs to explore whether changes in nuclear size can become a target for cancer treatment or a clue related to the suppression of metastasis. That is, nuclear hypertrophy may be a temporary response to replication stress and should not necessarily be seen as indicating the malignancy of the cancer.
This conclusion was substantiated through: (1) Gene Function Screening (inhibiting thousands of genes sequentially to find the key genes involved in nuclear size regulation); (2) Transcriptome Analysis (confirming which gene programs are activated when the nucleus enlarges); (3) 3D Genome Structure Analysis (Hi-C), which revealed that nuclear hypertrophy is not just a size change but is connected to changes in DNA folding and gene arrangement; and (4) Mouse Xenograft Models (confirming that cancer cells with enlarged nuclei actually have reduced motility and metastatic ability).
Professor Joon Kim of the Graduate School of Medical Science and Engineering said, "We confirmed that DNA replication stress disrupts the nuclear size balance, explaining the underlying mechanism of long-standing pathological observations," adding, "The possibility of utilizing nuclear structural changes as a new indicator for cancer diagnosis and metastasis prediction has now opened up."
Dr. Changgon Kim (currently a Hematology and Oncology specialist at Korea University Anam Hospital) and Saemyeong Hong, a PhD candidate from the KAIST Graduate School of Medical Science and Engineering, participated as co-first authors in this study. The results were published online in the international journal PNAS (Proceedings of the National Academy of Sciences of the United States of America) on September 9th.
※ Paper Title: Replication stress-induced nuclear hypertrophy alters chromatin topology and impacts cancer cell fitness ※ DOI: https://doi.org/10.1073/pnas.2424709122
Meanwhile, this research was supported by the Mid-career Researcher Program and the Engineering Research Center (ERC) program of the National Research Foundation of Korea.
2025.09.29 View 1509