Background: Prostate cancer progression exhibits significant variability influenced by biological and racial factors. DNA methylation profiling has shown potential in early cancer detection, but its integration with machine learning across racially diverse populations remains limited. Objective: This study aimed to develop a prostate cancer stage classifier for the majority White cohort using DNA methylation data and a multilayer perceptron (MLP) model in order to classify prostate cancer stages into early (stages I-II) and late (stages III-IV) stages and assess its performance when applied to other racial groups to highlight the need for race-specific models. Methods: Methylation and phenotype data from the TCGA-PRAD (The Cancer Genome Atlas Prostate Adenocarcinoma) dataset were processed using differentially methylated position (DMP) analysis to identify CpG sites correlated with cancer stages. These features were further refined through recursive feature elimination (RFE) and used to train MLP models. Shapley Additive Explanations (SHAP) and Local Interpretable Model-Agnostic Explanations (LIME) were used to interpret the model and identify key DNA methylation features contributing to model predictions. Results: The best-performing model achieved 95% accuracy and up to 99% area under the curve on the majority race (White) training data using 90 selected features. However, performance declined sharply in racial minority groups, revealing the effects of sample imbalance and race-specific methylation patterns. Feature importance examination indicated strong patterns within certain CpG sites driving model predictions. Conclusions: We propose a race-aware MLP model for prostate cancer stage classification using DNA methylation data, which has been optimized through DMP and RFE-based feature selection. SHAP and LIME confirmed the predictive relevance of selected CpG sites, supporting model transparency. The results highlight high performance within the White cohort but reveal poor generalization to racial minority groups, emphasizing the importance of race-specific modeling strategies.
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ThermoCas9: Gene Editor Targets Cells with Disease-Related Hypomethylation
Research led by Wageningen University in the Netherlands and the Van Andel Institute (VAI) in Michigan has shown that ThermoCas9, a variant of CRISPR, can distinguish tumor DNA from healthy DNA and selectively cut only the former, marking a potential step toward a highly precise cancer therapy.
The method relies on DNA methylation, a process in which methyl groups are added to DNA to regulate whether genes are on or off. In cancer cells, DNA methylation is altered and can therefore act as a molecular “fingerprint” that differentiates tumor cells from healthy ones.
“ThermoCas9 is the first CRISPR-associated enzyme to respond to differences in the most abundant type of DNA methylation in human and other eukaryotic cells,” explained co-senior author John van der Oost, PhD, from Wageningen University. “This means we now have a system that we can target specifically toward tumor cells.”
The study, published in Nature, represents the first time a CRISPR-based method has relied on methylation to target human cancer cells.
“ThermoCas9 uses methylation like an address to precisely target cancer cells while leaving healthy cells untouched,” added co-senior author Hong Li, PhD, from VAI. “The findings could be a game changer.”
After analyzing ThermoCas9’s structure and finding that it can distinguish between unmethylated and methylated genes, Li and team introduced the enzyme into different types of healthy human cells with distinct methylation landscapes and into breast and colorectal cancer cells.
They found that ThermoCas9 cut DNA in the tumor cells while leaving healthy DNA intact, suggesting that the system can detect subtle chemical differences between healthy and tumor cells and act on them.
“ThermoCas9 is a perfect example of the value of fundamental research; you have to know how these individual pieces work together,” said Li. “We used biochemistry and structural biology to discover a mechanism that we one day hope will lead to more precise, effective cancer treatment.”
Although the study highlights the potential of ThermoCas9 as a cancer treatment, it does not show that the selective DNA damage it inflicts leads to tumor cell death. The researchers next steps will focus on damaging tumor DNA sufficiently to trigger cell death.
Of note, aberrant methylation patterns also play a role in diseases other than cancer, including autoimmune disorders. It is therefore possible that ThermoCas9 or a similar CRISPR tool could evolve into a versatile molecular strategy that recognizes diseased cells by their chemical “signature” and selectively disables them.
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Epigenetic Target Could Sensitize Pancreatic Cancer to Immunotherapy
Researchers have found an epigenetic switch that pancreatic cancer cells use to protect themselves against genomic instability. In a study published in Cancer Research, the team reports that blocking the epigenetic regulator DPY30 triggered immune cell infiltration into pancreatic tumors in mice, sensitizing them to immunotherapy.
Frequently diagnosed at advanced stages, pancreatic cancer is often resistant to conventional therapies and shows limited response to immunotherapy. This leaves patients with few effective treatment options.
“As cancer biologists, we are intrigued by the remarkable ability of pancreatic cancer cells to tolerate genomic instability and sustained replication stress while continuing to proliferate and evade immune surveillance,” said Francesca Citron, PharmD, PhD, instructor of genomic medicine at The University of Texas MD Anderson Cancer Center and lead author of the study. “This paradox led us to investigate the adaptive mechanisms that enable cancer cells to buffer genomic instability, particularly by protecting replication forks and preventing catastrophic DNA damage.”
The researchers were interested in finding out whether epigenetic regulators may play a direct role in safeguarding the integrity of replication forks, where DNA is copied as cells divide. Under stress, DNA replication is typically disrupted, for instance as cancer cells continue dividing and accumulating mutations that result in genomic instability. However, Citron’s team discovered that pancreatic cancer cells rely on DPY30 to protect DNA replication forks under stress and continue multiplying in spite of genomic instability.
DPY30 belongs to a group of proteins that together form the WRAD/COMPASS complex, which is involved in epigenetics regulation. The study found that this component was able to switch the entire complex from playing a global epigenetics function to a localized role at stressed replication forks, where DPY30 stabilized.
“Historically, WRAD core components, particularly DPY30, have been primarily studied in the context of histone methylation and transcriptional regulation,” said Citron. “Our findings significantly expand this paradigm by demonstrating that these factors play a direct role in maintaining replication fork stability under conditions of stress. Importantly, we also establish a link between this mechanism and modulation of the tumor immune microenvironment, providing a conceptual bridge between replication stress and immune response.”
In a mouse model of pancreatic cancer, DPY30 inhibition destabilized replication forks, leading to increased genomic instability and activating inflammatory signaling pathways. This then triggered the recruitment of tumor-infiltrating lymphocytes and turned previously immunologically “cold” tumors into “hot” tumors that responded to immunotherapy.
“Inhibiting DPY30 leads to increased replication-associated DNA damage, which in turn robustly enhances immune signaling pathways,” said Citron. “This dual effect, on genome stability and immune activation, opens new therapeutic opportunities to impair replication fork protection while simultaneously stimulating anti-tumor immune responses.”
Furthermore, biopsies from pancreatic cancer patients showed that higher levels of DPY30 expression were associated with higher tumor grades, a poorer prognosis and lower response rates to immunotherapy. Together, these findings point at DPY30 as both a therapeutic target and a biomarker to stratify patients who are most likely to benefit from immunotherapy.
Going forward, the researchers plan to dive deeper into how HPY30 influences immune cell recruitment and activation within the tumor microenvironment. In parallel, they will be exploring pharmacological strategies to inhibit DPY30 and testing their efficacy in preclinical studies. Citron added: “Ultimately, our goal is to develop rational combination therapies that drive more effective and durable responses in patients.”
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Epigenetics at Birth Links Microbiome to Neurodevelopment, Potentially ASD and ADHD
The results of a study headed by researchers at Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, indicate that the gut microbiome and epigenetics are intertwined, and that both contribute to neurodevelopment.
The researchers showed that epigenetic changes present at birth can impact how an infant’s gut microbiome develops during their first year. They also identified specific epigenetic changes and gut microbes that were associated with signs of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) when the children were three years old.
“Certain bacteria seem to offer protection, which is exciting because it suggests there could be ways to support a child’s development through diet or probiotics in the future,” said research lead and gastroenterologist Francis Ka Leung Chan, MD. Chan is co-senior author of the team’s published paper in Cell Press Blue, titled “Epigenome-microbiome interplay in early life associates with infants’ neurodevelopmental outcomes,” in which they stated, “We showed that epigenetic alterations at birth were associated with early-life microbiome development and that they determine the risks of neurodevelopmental consequences in children.”
The first years of life are critical for brain development and immune system maturation. Though previous studies have shown that both early epigenetic changes and gut microbiome development can impact health in later life, little is known about how these two systems interact. “Recent data suggest that epigenetic programming of gene expression profiles is sensitive to the early-life environment and can impact health outcomes in children,” the authors wrote. “One environmental cue known to trigger host epigenetic modifications is the genes of bacteria, fungi, and viruses inside the human body, collectively known as the microbiome.”
Co-senior author and public health researcher Hein Min Tun, PhD, of The Chinese University of Hong Kong, commented, “We wanted to see how the epigenome and microbiome interact in early life and if their interaction could influence a child’s risk of developing neurodevelopmental conditions like ASD and ADHD.” The authors added, “New understanding of host-microbe-epigenome interactions and mechanisms of epigenetic changes in early life can be leveraged for the prevention, early detection, and novel interventions of common childhood diseases.”
For their study the researchers characterized DNA methylation patterns from the umbilical cord blood of 571 infants. They paired this information with gut microbiome data collected from 969 infants at two, six, and 12 months of age, and from their parents during the third trimester of pregnancy. When the children reached 36 months of age, the researchers used a behavioral questionnaire to assess their neurodevelopment and investigate links between the microbiome, epigenome, and early signs of ASD and ADHD.
“This, to our knowledge, represents the first longitudinal study with multiple sample types to depict the intimate interplay between perinatal exposures, epigenetic hallmarks, and gut microbiome development and neurodevelopmental outcomes within the first three years of life,” the authors stated.
They found that an infant’s epigenome at birth was associated with birth mode, length of gestation, having older siblings, and maternal allergies, but it was not affected by their parents’ gut microbiomes. Microbiome development, on the other hand, was associated with birth mode, antibiotics, having older siblings, and breastfeeding. Infants who were born by Caesarean section (CS) showed different patterns of DNA methylation for several genes involved in immune responses and brain development. “Some of the changes in methylations of immune- and nervous-system-related genes, associated with CS delivery, are linked to neurodevelopmental outcomes,” they noted.
Their reported findings, the team suggested, “… resonate with studies linking CS to increased risks of immune-mediated and neurodevelopmental disorders, providing mechanistic plausibility through epigenomic and microbial dysbiosis.” The team also showed that an infant’s epigenome at birth impacted how their microbiome developed during their first year. Specifically, infants developed less diverse gut microbiomes at 12 months of age when they showed higher rates of DNA methylation in immune genes involved in recognizing pathogens. “We found that methylation rates in the major histocompatibility complex (MHC) region of infants at birth were linked to differences in the diversity of the infant gut microbiome at 12 months,” they commented.
The behavioral survey revealed that signs of ASD and ADHD in three-year-olds were associated with specific epigenetic patterns and the presence of certain gut microbes. “Importantly, we reported that epigenetic modifications were associated with an increased susceptibility to neurodevelopmental conditions in children, and these effects were in part mediated by microbial colonization.”
However, other microbial species seemed to mitigate these effects: infants with epigenetic patterns associated with ASD or ADHD were less likely to show signs of the disorders if they acquired Lachnospira pectinoschiza and Parabacteroides distasonis, respectively, during their first year. “We discovered a kind of conversation happening: a baby’s epigenetic setting at birth can influence their risk for neurodevelopmental disorders, but the presence of certain ‘good’ bacteria in their gut can step in and modify the risk,” Tun reported. “The foundations for brain health are laid very early, even before birth. However, we don’t want people to think this means a child’s developmental path is fixed at birth. These are complex conditions with many causes, and we’ve only uncovered a small piece of a very large puzzle.”
The researchers are continuing to follow the children who participated in the study to see how these early-life factors relate to their health as they grow. They note that laboratory experiments are needed to confirm the associations between gut microbes and neurodevelopment. In their discussion, the team wrote, “In conclusion, our findings revealed dual alterations to the neonatal epigenome and gut microbiome by perinatal factors and highlight the role of the ‘holo-epigenome’—the integrated host epigenome and microbiome—as a key mediator of neuro-immune outcomes. Interventions targeting microbial restoration or epigenetic modulation during critical developmental windows may mitigate risks of neurodevelopmental disorders.”
First author and gastroenterologist Siew Chien Ng, MD, PhD, added, “The ultimate goal is to develop safe, non-intrusive early interventions such as specific probiotics or live biotherapeutics, that could help nurture a healthy gut microbiome and potentially reduce the risk of neurodevelopmental challenges.”
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Cancer Drug Shortfalls Tied to How BET Inhibitors Hit BRD2 and BRD4 Differently
For more than a decade, BET inhibitors have been touted as one of cancer therapy’s most promising drug classes. The logic was straightforward: many tumors rely on oncogenes that depend on BET (bromo- and extra-terminal domain) proteins—chromatin‑binding regulators that help switch genes on. Block the BET family, the thinking went, and cancer cells should lose their transcriptional fuel. In the lab, the strategy often worked. But in clinical trials, the results were far more uneven: modest responses, substantial side effects, and little clarity about which patients might benefit.
A new study from the Max Planck Institute of Immunobiology and Epigenetics (MPI‑IE) may finally explain why. Published in Nature Genetics, the work uncovers a previously underappreciated division of labor within the BET family—one that helps clarify why drugs that block all BET proteins at once have struggled in the clinic. The paper is titled, “Histone acetylation-dependent clustering of BRD2 instructs transcription dynamics.”
Most BET inhibitors were designed to block a shared bromodomain that all BET proteins use to bind chromatin. That approach assumed the proteins—BRD2, BRD3, BRD4, and BRDT—perform similar roles. But the new study paints a more nuanced picture. Using rapid protein degradation, chemogenomics, and super‑resolution microscopy in mouse embryonic stem cells, the team dissected the distinct contributions of BRD2 and BRD4 to transcription.
Their findings reveal that BRD4 drives the well‑known step of releasing paused RNA polymerase II into productive elongation. BRD2, however, acts earlier. It helps recruit and organize the transcription initiation machinery at promoters, particularly under conditions where pause‑release is impaired. As the authors wrote, BRD2’s role becomes “particularly critical under the conditions of impaired pause release,” a mechanistic insight that reframes how BET proteins collaborate during gene activation.
The MPI‑IE team likens BRD2 to a stage manager. “BRD2 sets up the stage: assembling the props, costumes, and actors to ensure preparations run smoothly. BRD2 then gives BRD4, the actor, the ‘start’ signal to begin with the performance,” said senior author Asifa Akhtar, PhD. Blocking both proteins simultaneously—exactly what current BET inhibitors do—disrupts two different steps of transcription at once, producing unpredictable and context‑dependent effects.
“Our data shows that the setup work happening before is just as critical for gene activation,” explained Akhtar.
A key discovery is that BRD2’s recruitment depends on histone H4 acetylation placed by the enzyme MOF. When MOF was rapidly depleted or deleted, BRD2 lost its grip on chromatin, while BRD3 and BRD4 remained largely unaffected. “The findings support a model in which acetylated chromatin creates a platform that allows regulatory proteins like BRD2 to concentrate and prepare the transcription machinery,” noted first author Umut Erdogdu, PhD.
The team also showed that BRD2 forms dynamic clusters at promoters. Removing only the BRD2 region responsible for clustering stalled transcription almost as completely as deleting the entire protein.
The study suggests a path forward: instead of blocking all BET proteins indiscriminately, future therapies may need to distinguish between BRD2‑ and BRD4‑specific functions. “Thus, these findings support a model in which histone acetylation-dependent spatiotemporal dynamics of BRD2 coordinate the transcription machinery to regulate transcription initiation,” the authors wrote.
For a field long puzzled by the uneven performance of BET inhibitors, BRD2’s newly revealed role offers a compelling piece of the puzzle—and a clearer blueprint for next‑generation cancer therapeutics.
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Life Biosciences Raises $80M to Fund First Trial of Anti-Aging Gene Therapy
Life Biosciences has announced an $80 million Series D round, which will fund the completion of a recently started Phase I clinical trial of a gene therapy designed to restore old, damaged cells to a younger, healthier state.
The Boston-based biotechnology company was co-founded in 2017 by David A. Sinclair, PhD, professor of genetics at Harvard Medical School and founding director of the Paul F. Glenn Laboratories for the Biological Mechanisms of Aging. Sinclair is known internationally as a leading researcher on human aging and longevity, especially for his work on epigenetic changes as drivers of aging and using reprogramming factors to reset the age of cells and tissues.
The oversubscribed round will support company operations into the second half of 2027, including the conclusion of a Phase I trial launched earlier this year to assess the safety and tolerability of Life Biosciences’ lead program, ER-100. The funds will also go towards exploring new candidates and advancing the company’s broader pipeline of therapeutics for age-related diseases.
Aging is the main driver and risk factor for most chronic diseases, with over 75% of people over 65 being estimated to suffer from at least one chronic condition. As the world population continues to age, Life Biosciences aims to delay aging processes by rejuvenating cells and restoring their function across many age-related diseases.
The company’s Partial Epigenetic Reprogramming (PER) platform is designed to partially reprogram the epigenome of old and injured cells through the expression of three Yamanaka factors: OCT4, SOX2, and KLF4 (together known as OSK). These transcription factors have been shown to reset organ-specific epigenetic code without creating induced-pluripotent stem cells, addressing the effects of aging without the risk of fully differentiating cells or inducing the formation of tumors.
This strategy has the potential to address a wide range of age-related diseases across multiple organs and systems within the human body. Life Biosciences’ Phase I clinical trial, which is currently actively recruiting, will assess the safety and tolerability of ER-100 in patients with open-angle glaucoma (OAG) and non-arteritic anterior ischemic optic neuropathy (NAION). The trial will also assess early efficacy endpoints, including multiple measurements of visual function.
Optic neuropathies like OAG and NAION are driven by damage to retinal ganglion cells, neurons that send sensory signals from the eye to the brain. These cells cannot naturally regenerate, meaning patients suffer permanent vision impairment. Unlike current treatments, which are unable to address the underlying mechanisms of neuronal degeneration, ER-100 aims to directly protect and promote the regeneration of RGC to preserve and restore sight in these patients.
Jerry McLaughlin, chief executive officer of Life Biosciences, stated that the financing “reflects the growing interest in our platform and the opportunity we have to reverse multiple diseases of aging.”
He added: “This support enables us to advance our lead program, ER-100, through key clinical milestones while continuing the expansion of our pipeline, positioning Life Biosciences to deliver disease-modifying solutions for patients.”
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Synaptic remodeling and the female depression exposome: a mini-review of neuroendocrine, epigenetic, and social determinants
Depression is a multifactorial, chronic disorder and represents a leading cause of disability, with women exhibiting nearly twice the lifetime prevalence compared to men. Growing evidence indicates that this disparity cannot be explained by hormonal or psychosocial factors, but rather by dynamic interactions between environmental exposures, neuroendocrine signaling, and epigenetic regulation across development. This mini-narrative review aimed to examine how sex-specific exposome components interact with epigenetic mechanisms and synaptic remodeling processes to influence vulnerability to Major Depressive Disorder in women. The reviewed evidence demonstrates that fluctuations in ovarian hormones modulate HPA axis responsivity, neuroinflammatory signaling, and glutamatergic transmission through epigenetic regulation of stress-responsive genes such as NR3C1, SLC6A4, and BDNF, consequently influencing synaptic remodeling within corticolimbic circuits. Environmental and social exposures, particularly early-life adversity and psychosocial stressors, further interact with microglial activation and chromatin remodeling to produce long-lasting alterations in hippocampal and prefrontal plasticity. Collectively, these findings support a model in which sex-dependent neuroendocrine sensitivity amplifies exposome-driven epigenetic programming across the lifespan. Future research directions emerging from this synthesis include longitudinal life-course studies integrating multi-omic biomarkers, quantitative exposome assessment, and neuroimaging approaches to identify modifiable environmental targets and advance precision, sex-informed preventive and therapeutic strategies in depression.
Vitamin A status is associated with sleep, clock genes, and symptoms in children with autism spectrum disorder
BackgroundVitamin A signals through retinoic acid receptors and may influence neurodevelopment and the expression of clock genes. However, the biological pathway linking vitamin A status to sleep disturbance in ASD remains insufficiently defined. This study aimed to examine associations between vitamin A status and sleep problems, core symptoms, and clock genes in children with ASD, and to explore the mechanistic role of RARβ in regulating core clock genes.MethodsThis observational study included 361 children with ASD. Clinical symptoms were assessed using the Children’s Sleep Habits Questionnaire (CSHQ); the Childhood Autism Rating Scale (CARS) and the Social Responsiveness Scale (SRS). Peripheral blood mononuclear cell (PBMC) mRNA levels of RARβ and clock genes (BMAL1 and CLOCK) were quantified by qPCR. RARβ expression was knocked down in mice by stereotaxic injection of adeno-associated virus.ResultsChildren with lower vitamin A levels exhibited more severe sleep problems and autistic symptoms. Vitamin A levels showed a weak positive correlation with the expression of RARβ and BMAL1. RARβ knockdown reduced the expression of RARβ and clock genes in mouse brain tissue. Chromatin immunoprecipitation quantitative PCR (ChIP-qPCR) confirmed RARβ occupancy at a predicted CLOCK regulatory region.ConclusionThis study provided evidence that vitamin A status was linked to sleep problems, symptom severity, and expression of clock genes in the morning in ASD. We also found that RARβ signaling may regulate the expression of clock genes. This finding provides new insights into the mechanisms underlying sleep disturbances in ASD, but further functional studies are needed to confirm these findings.
Methylome-Wide Association Study of Obsessive-Compulsive Disorder
Obsessive-compulsive disorder (OCD) is a debilitating psychiatric condition influenced by both genetic and environmental risk factors. Epigenetic modifications, such as DNA methylation, may offer insights into biologically meaningful differences associated with the disorder.
Epigenetic Strategy Restores Tumor Suppressor in Acute Myeloid Leukemia Models
Scientists from The Jackson Laboratory (JAX) and their collaborators elsewhere have found a potential way to treat cases of acute myeloid leukemia that involves turning a key cancer fighting gene back on. Besides potentially treating AML without harsh chemotherapy regimens, their work also highlights a promising strategy for studying gene-silencing mechanisms in other diseases. Full details of the study, which was done in mice, are available in a paper published in Science Translational Medicine titled “Epigenetic reactivation of the tumor suppressor ZBTB7A by KDM4 inhibition in human acute myeloid leukemia.”
Normally, tumor suppressor genes work to prevent cells from becoming cancerous. But in cancers like AML, some of these genes are switched off epigenetically. These changes to gene activity are difficult to track because standard DNA sequencing technologies are designed to find mutated DNA. “If we can identify which genes have been silenced and understand how to turn them back on, that could open up entirely new therapeutic possibilities,” said Eric Wang, PhD, an assistant professor JAX who led the research. “Instead of only trying to kill these cells, we may be able to restore the mechanisms that normally keep them under control.”
Though scientists have made great strides in developing therapies for AML, prognosis for the disease is still relatively poor. Part of the challenge is that AML cells remain in an immature, stem cell-like state. According to the paper, Wang and his team developed a tool that combines fluorescence in situ hybridization and flow cytometry with CRISPR gene editing technology to map gene activity in cells. They used the tool, called FISHnCRISP, to identify a tumor-suppressing gene called ZBTB7A that is silenced in AML patients. By restoring ZBTB7A expression, the scientists forced the cancer cells into a state where they grew less aggressively.
Digging into the details, AML cells produce a longer version of ZBTB7A’s regulatory tail, that contains sites that attract a protein called ZFP36L2, which reduces the gene’s activity. Additionally, a family of enzymes known as KDM4 modify how DNA is packaged inside AML cells, which effectively silences ZBTB7A expression. Data from experiments in mice with AML showed that when KDM4 enzymes were blocked, ZBTB7A regained its expression, reducing leukemia burden while leaving normal blood formation largely unaffected.
Importantly, “there are drug candidates out there to inhibit KDM4, and in our study we just repurposed one of them to treat AML cells,” Wang said. “We won’t know unless we test it in clinical trials, but this approach could be better than chemotherapy, because we showed it’s not toxic at all to normal blood cells.”
Future studies will focus on refining the approach and determining whether it might be combined with existing treatments. The team plans to test an experimental drug that targets KDM4, which is currently being tested in a clinical trial for solid tumors.
“We demonstrated that downregulating ZBTB7A causes this hyperinflammatory state that promotes cancer growth” and “now, we’re proposing this epigenetic approach to force AML cells to differentiate into white blood cells that eventually undergo cell death,” Wang said. “We could potentially translate our research into an early phase clinical trial more readily than developing a whole new compound from scratch.”
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