At the heart of the delivery problem lies a sobering reality: getting mRNA to the right immune cells in the right place is extraordinarily difficult. Synthetic lipid nanoparticles, the workhorse platform behind COVID-19 vaccines and increasingly explored for cancer, are efficient but flawed. When injected into the bloodstream, they become coated with apolipoprotein E, a blood-borne protein that effectively addresses them to the liver. The result is hepatocyte sequestration—most of the payload ends up in hepatic tissue, leaving scant therapeutic material to reach the lymph nodes where antigen-presenting cells reside. For a cancer vaccine whose entire purpose is to prime tumor-specific T cells, this diversion represents a fundamental bottleneck.

Engineered exosomes offer an elegant biological escape from this constraint. These tiny vesicles, naturally secreted by cells and featuring a native lipid bilayer rich in cholesterol and sphingomyelin, shield their mRNA cargo from ribonucleases that would otherwise degrade it within minutes in the bloodstream. More critically, exosomes display surface markers such as CD47, the well-known “don’t eat me” signal that engages SIRPα receptors on macrophages and blocks phagocytosis. By wearing this molecular disguise, engineered exosomes achieve markedly extended circulation half-lives, allowing them to navigate the body’s immune surveillance long enough to deliver their genetic instructions to lymphoid-resident antigen-presenting cells—the gatekeepers of adaptive immunity.

The review’s authors describe a carefully orchestrated immune cascade that begins at the injection site. When these mRNA-loaded exosomes are administered intramuscularly, they provoke a controlled, localized inflammatory response. This acute inflammation acts as a siren call, recruiting host immune cells to the site, where they acquire the tumor antigens encoded by the vaccine’s mRNA. The antigen-bearing cells then migrate to regional lymph nodes, where they initiate the activation and clonal expansion of tumor-specific T cell populations. What emerges from this process is a fleet of activated effector cells that traffics directly into the tumor microenvironment, dismantling the immunosuppressive stroma that has kept the tumor hidden.

The consequences of this infiltration are profound. Cytotoxic CD8+ T cells and natural killer cells, now present in force within the tumor, aggressively target malignant cells expressing the vaccine-encoded neoantigens. But the transformation runs deeper than a simple influx of killer cells. The tumor microenvironment itself undergoes remodeling—from a cold, immunologically silent niche characterized by physical extracellular matrix barriers, altered biochemical signaling, and suppressive regulatory leukocytes, into a hot, inflamed environment where immune activity is the norm. This shift has a crucial clinical implication: it sensitizes the tumor to immune checkpoint inhibitors, the blockbuster drugs that have revolutionized treatment of some cancers but fail in many patients precisely because their tumors lack pre-existing immune infiltration.

Perhaps the most striking insight of the review is that the durability of this anti-tumor immunity is not achieved by altering the genome itself. Instead, the vaccine-induced cytokine network drives what the authors call epigenetic priming—precise chromatin remodeling within both myeloid and lymphoid cell lineages. Through specific histone modifications, including enrichment of H3K27ac at promoter regions, and targeted DNA demethylation at the promoters of key immune effector genes such as IFNG and GZMB, the platform establishes a state of trained innate immunity. In parallel, it expands pools of central and tissue-resident memory T cells. These epigenetic changes ensure that peripheral immune effectors remain transcriptionally poised, their chromatin open and accessible, ready to execute rapid recall responses the moment they re-encounter tumor cells. The immune system, in effect, remembers the cancer—not through genetic change, but through a molecular bookmarking of the genes needed to fight it.

Yet this epigenetic plasticity is a double-edged sword. Keeping chromatin in a hyper-accessible state demands strict temporal control. Left unchecked, the same mechanisms that prime powerful anti-tumor responses could drive chronic low-grade inflammation or, worse, trigger autoimmune attacks against healthy tissues. The review emphasizes that controlling the duration and intensity of these epigenetic programs will be essential to translating the platform safely into clinical practice. Balancing potency with precision—maintaining the trained immune state long enough to eradicate cancer without letting it spill over into self-reactivity—remains one of the central engineering challenges ahead.

The path from laboratory to clinic also demands a manufacturing revolution. The gold standard for isolating exosomes in research settings, ultracentrifugation, simply cannot produce the consistent, pharmaceutical-grade product needed for human therapies. The authors argue that current good manufacturing practice (cGMP)-compliant methods—specifically tangential flow filtration and size-exclusion chromatography—must replace older techniques to resolve the inherent heterogeneity of vesicle populations. Without this manufacturing standardization, even the most elegant biological design will struggle to meet regulatory requirements for consistency, purity, and scalability.

Looking ahead, the researchers envision a modular system that could make truly personalized cancer vaccines scalable rather than bespoke. The concept is a pre-manufactured, standardized exosome chassis—a biological delivery vehicle produced in advance and quality-controlled—into which patient-specific multiomic neoantigen libraries can be rapidly loaded. Rather than designing each patient’s vaccine from scratch, clinicians would sequence a patient’s tumor, identify its unique mutation-derived neoantigens, and slot those antigen-encoding mRNAs into the ready-made exosome platform. This modularity, the review argues, is what would transform personalized precision oncology from an aspirational concept into a practical, widely deployable therapeutic modality.

The broader significance of this work lies in its synthesis of two rapidly maturing fields: mRNA therapeutics and extracellular vesicle biology. Antiviral mRNA vaccines have already proven the raw power of nucleic acid platforms at population scale. But aggressive solid malignancies present a fundamentally different challenge—one of local immune tolerance, physical exclusion of effector cells, and actively immunosuppressive microenvironments. By combining multivalent mRNA payloads, capable of encoding multiple tumor antigens simultaneously, with surface-functionalized exosomes engineered to evade clearance and home to immune-rich tissues, the platform described in this review offers a coherent strategy to dismantle those barriers. If the mechanistic blueprint holds up in clinical testing, it could mark a turning point in how medicine approaches tumors that have, until now, remained stubbornly invisible to the immune system—and resistant to the immunotherapies designed to unmask them.

Metastasis is responsible for much of the danger associated with cervical cancer. While early-stage disease can often be treated successfully, cancer cells that invade surrounding tissue, enter the bloodstream or lymphatic system, and establish secondary tumors are substantially more difficult to control. These changes are not driven solely by mutations in DNA sequence. Cancer cells also reprogram the way genes are switched on and off, using epigenetic mechanisms that can reshape cellular behavior without altering the underlying genetic code.

One of the most important epigenetic mechanisms is DNA methylation. In this process, chemical groups known as methyl groups are added to DNA, often at regions rich in cytosine and guanine nucleotides called CpG sites. Depending on their location, these modifications can reduce or enhance gene activity by changing how transcription factors and chromatin-regulating proteins interact with the genome. DNMT3A is an enzyme involved in establishing new DNA-methylation patterns, making it a potential controller of gene programs linked to cancer invasion and metastasis.

The study focuses on ESM1, a secreted proteoglycan associated with endothelial cells and blood-vessel biology. ESM1 has previously attracted attention because abnormal levels of the molecule have been observed in several cancers, where it may influence tumor growth, vascular remodeling, inflammation, and interactions between malignant cells and their surrounding microenvironment. The new work places ESM1 within an epigenetic regulatory pathway, connecting it to DNMT3A and, ultimately, to the activity of ID3.

ID3, or inhibitor of DNA binding 3, belongs to a family of regulatory proteins that influence cell differentiation, proliferation, and responses to signals from neighboring cells. Rather than binding directly to DNA in the same way as many conventional transcription factors, ID3 can regulate gene expression by interacting with basic helix-loop-helix transcription factors and limiting their ability to activate specific genetic programs. In cancer, the consequences of altered ID3 activity can vary depending on the tissue and molecular context. In cervical cancer, the findings reported in this study identify ID3 expression as a key component of a pathway that restrains metastatic behavior.

The proposed mechanism is that ESM1 influences DNMT3A, which then contributes to epigenetic regulation of the ID3 gene. By controlling the methylation environment surrounding ID3, this pathway can determine how much ID3 is produced by cervical cancer cells. When ID3 expression is maintained at levels that oppose invasion, tumor cells may become less capable of moving through surrounding tissues, invading blood vessels, or colonizing distant organs. Conversely, disruption of this regulatory relationship could create a cellular state more favorable to metastasis.

This type of mechanism is significant because it links an extracellular or microenvironment-associated molecule with a durable change in gene regulation inside the cancer cell. ESM1 is positioned outside or at the interface of cells, where it can participate in signaling and tissue organization, while DNMT3A operates in the nucleus, writing methylation patterns onto DNA. The connection between the two suggests that signals associated with the tumor environment may be translated into long-lasting epigenetic instructions that affect metastatic potential.

The findings also highlight why metastasis cannot be understood by examining cancer-cell mutations alone. Two tumors with similar genetic alterations may behave differently if their epigenetic landscapes differ. DNA methylation can function as a reversible regulatory layer, meaning that the activity of genes such as ID3 may potentially be modified by changes in signaling, enzyme activity, or therapeutic intervention. However, the reversibility of epigenetic marks does not automatically make them easy or safe to target. DNMT enzymes regulate many genes in normal cells, and broad interference with their activity could produce unwanted effects.

From a treatment perspective, the ESM1–DNMT3A–ID3 axis may eventually serve several purposes. Its components could help identify patients whose tumors have a higher risk of metastatic spread, provided the relationship is confirmed in larger clinical cohorts. The pathway might also guide the development of therapies designed to restore protective gene expression or interfere with signals that promote invasion. At present, the study represents a mechanistic advance rather than a clinical treatment recommendation. Further research will be needed to determine how consistently the pathway operates across cervical cancer subtypes, whether it predicts patient outcomes, and whether manipulating it can prevent metastasis in animal models or human trials.

The report adds a new layer to the rapidly expanding picture of cervical cancer biology, in which tumor cells, blood vessels, immune signals, and epigenetic enzymes communicate as part of a dynamic system. By identifying ESM1-mediated DNMT3A regulation of ID3 as a suppressive pathway, the researchers provide a potential explanation for how metastatic behavior is restrained at the molecular level. If future studies validate these findings, the pathway could become a focal point for biomarker research and precision strategies aimed not merely at shrinking cervical tumors, but at stopping them from spreading.

Subject of Research: ESM1-mediated epigenetic regulation of DNMT3A and ID3 in cervical cancer metastasis

Article Title: ESM1-mediated DNMT3A suppresses cervical cancer metastasis through epigenetic regulation of ID3 expression

Article References: Yu, CL., Lin, CL., Lee, HL. et al. ESM1-mediated DNMT3A suppresses cervical cancer metastasis through epigenetic regulation of ID3 expression. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-03239-z

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-026-03239-z

Keywords: Cervical cancer, metastasis, ESM1, DNMT3A, ID3, DNA methylation, epigenetics, cancer biology

AML’s bleak prognosis often stems from the cancer cells’ ability to adapt and evade frontline treatments, especially combinations of hypomethylating agents and venetoclax. The TP53 gene mutation, in particular, confers a formidable therapeutic resistance by disabling the cell’s natural damage control mechanisms and fostering unchecked proliferation. NTX-301, however, retains potent activity in AML models that have developed resistance to conventional therapies, effectively reducing leukemia cell survival in experimental and patient-derived xenograft models.

What sets NTX-301 apart is its selective epigenetic reprogramming, which targets the Hippo signaling pathway — a crucial regulator of cell growth and organ size that has recently been implicated in cancer progression and treatment resistance. Unlike traditional hypomethylating agents that broadly alter DNA methylation patterns, NTX-301 precisely modulates the expression of genes within the Hippo pathway. This modulation includes enhancement of tumor-suppressor components and suppression of YAP, a protein associated with cancer cell survival and stemness.

The activation of the Hippo pathway by NTX-301 not only curtails leukemia cell growth but also dismantles key resistance mechanisms, explaining its efficacy in refractory AML. Moreover, when combined with venetoclax, NTX-301 produces synergistic effects that extend beyond bulk leukemia cells to target leukemia stem and progenitor cells, which are typically responsible for relapse and disease persistence.

These insights reveal a dual therapeutic strategy: reactivating suppressed tumor-inhibiting pathways while simultaneously disabling cellular survival programs. The implications for clinical translation are significant, as this approach may offer a much-needed option for patients with relapsed AML, venetoclax-resistant disease, and those harboring TP53 mutations — cohorts historically limited in treatment choices.

Further research is warranted to validate NTX-301’s efficacy in clinical settings and to identify biomarkers predictive of response. The study’s authors highlight the potential of epigenetic therapies that specifically engage the Hippo pathway as an innovative frontier to overcome resistance, offering new hope against a lethal and stubborn disease.

This research marks a pivotal moment in leukemia therapeutics, opening avenues that blend molecular precision with overcoming adaptive resistance. As NTX-301 advances through further development, it holds the promise of transforming outcomes in AML, one of the most aggressive blood cancers currently confronting patients and clinicians alike.

Subject of Research: Acute Myeloid Leukemia, Epigenetic Therapy, Hippo Signaling Pathway
Article Title: The novel hypomethylating agent NTX-301 reprograms epigenetic and Hippo signaling pathways and exhibits pre-clinical activity in venetoclax-resistant and TP53-mutant AML
News Publication Date: July 13, 2026
Web References: https://aacrjournals.org/clincancerres/article/doi/10.1158/1078-0432.CCR-25-4843
Image Credits: The University of Texas MD Anderson Cancer Center
Keywords: Acute Myeloid Leukemia, Epigenetic Therapy, NTX-301, Treatment Resistance, TP53 Mutation, Hippo Pathway, Venetoclax Resistance, Leukemia Stem Cells

Synovial sarcoma’s hallmark is a unique chromosomal translocation that fuses two genes, SS18 and SSX, generating the SS18::SSX fusion oncoprotein. This aberrant protein acts as a molecular driver of cancer, orchestrating epigenetic and transcriptional reprogramming that sustains the malignant identity and proliferative capacity of these cells. The exact mechanisms through which the fusion oncoprotein hijacks cellular processes have remained elusive, complicating efforts to develop targeted therapies.

Recently, a multidisciplinary group of researchers from Sanford Burnham Prebys Medical Discovery Institute, alongside collaborators at UCLA, UC San Diego, and the University of Edinburgh, published groundbreaking findings that illuminate a novel vulnerability in synovial sarcoma’s molecular armor. By integrating publicly available genomic datasets with their own experimental screenings in cell-based and animal models, this team identified the SUMO2 gene as a critical dependency selectively essential for synovial sarcoma cell growth.

SUMO2 encodes a small ubiquitin-like modifier protein that participates in post-translational modifications known as SUMOylation. This cellular process modulates protein function, localization, and interactions, thereby influencing epigenetic landscapes and gene expression patterns. Their data suggest that SS18::SSX fusion oncoprotein activates SUMO2, facilitating the cancer cells’ aberrant epigenetic programs and promoting sarcomagenesis.

To explore the therapeutic potential of targeting SUMO2, the researchers employed TAK-981, a small molecule inhibitor that impedes the SUMOylation pathway by blocking SUMO2 conjugation. Treatment with TAK-981 significantly impaired synovial sarcoma cell viability in vitro, accompanied by downregulation of gene networks under the control of the SS18::SSX fusion oncoprotein. The inhibitor not only disrupted the proliferation of cancerous cells but also lowered cellular levels of the fusion oncoprotein itself, underscoring a feedback mechanism that may enhance treatment efficacy.

Complementing cellular studies, in vivo experiments in mouse models demonstrated that SUMO2 inhibition curtailed tumor growth, reinforcing the notion that targeting this pathway can effectively attenuate sarcomagenesis. These findings also imply that TAK-981 might sensitize synovial sarcoma cells to standard chemotherapeutic regimens, suggesting a combinatorial strategy could yield synergistic effects in the clinical setting.

The significance of these results lies in bridging the gap between genomic data and actionable therapeutic interventions. By leveraging public cancer dependency maps and validating hits in biologically relevant models, the investigators exemplify the power of precision medicine approaches in uncovering cancer-specific vulnerabilities. Their work exemplifies how data-driven methodologies guide innovative drug discovery, particularly for rare cancers lacking effective targeted therapies.

Despite advancements, synovial sarcoma remains a formidable disease with roughly a 50-60% five-year survival rate for patients with metastatic progression. The ability of this malignancy to metastasize predominantly to the lungs, combined with the absence of tailored treatments, underscores the urgent need for new modalities. The discovery of SUMO2’s central role offers promise not only as a monotherapy target but as a gateway to understanding cancer epigenetics in fusion-driven sarcomas.

According to Dr. Rema Iyer, lead author and recent graduate from Sanford Burnham Prebys Graduate School of Biomedical Sciences, the complexity of synovial sarcoma’s epigenetic rewiring has hindered targeted drug development. The study’s insights into SUMO2 highlight a viable node for therapeutic intervention that had previously escaped attention because of the intricate interplay of oncoproteins and cellular epigenomic states.

Senior author Dr. Ani Deshpande, professor at Sanford Burnham Prebys and leader of the Cancer Genome and Epigenetics Program, emphasizes that SUMO2 inhibitors like TAK-981 carry strong potential for clinical translation. Given prior evidence of TAK-981’s efficacy in preclinical models of acute myeloid leukemia and pancreatic cancer, these findings strengthen the rationale for advancing this inhibitor into clinical trials for synovial sarcoma patients.

The methodology underpinning this research involved rigorous comparative screening across various platforms: analyses of DepMap’s expansive genomic datasets, cell culture model systems, and live animal experiments. This multi-layered approach allowed for a robust identification of genes essential to synovial sarcoma growth, out of which SUMO2 emerged as a consistent and druggable target.

While the immediate therapeutic implications center on SUMO2 inhibition, the broader impact resides in the conceptual framework that fusion oncoproteins like SS18::SSX impose epigenetic dependencies exploitable by precision drugs. Researchers worldwide now may consider SUMOylation pathways as fertile ground in the fight against other fusion-driven sarcomas and potentially beyond.

This study marks a critical advance in synovial sarcoma research, paving the way for targeted, mechanism-based therapies. It is a testament to the synergy between cutting-edge genomic technology and translational science, promising a future where even the rarest and most aggressive cancers can be tackled with tailored, effective interventions.

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Subject of Research: Animals

Article Title: Targeting SUMO2 reverses aberrant epigenetic rewiring driven by SS18::SSX fusion oncoproteins and impairs sarcomagenesis

News Publication Date: 13-Aug-2025

Web References:

• The EMBO Journal article
• DepMap Consortium

References: DOI 10.1038/s44318-025-00526-w

Keywords: Cancer, Metastasis, Sarcoma, Oncoproteins

Epigenetics, which refers to heritable changes in gene expression that do not involve alterations in the DNA sequence itself, plays a pivotal role in cellular behavior, particularly in cancer biology and immune regulation. This study dives deep into how the epigenetic remodeling of mast cells—the body’s frontline defenders—and cancer cells collectively modulates the biochemical signaling networks that favor tumor progression. By decoding these modifications, the research offers a fresh perspective on the tumor microenvironment, an ecosystem critical to cancer development and metastasis.

Mast cells have traditionally been recognized for their role in allergic reactions and host defense; however, their involvement in tumor biology has gained significant traction in recent years. These versatile immune cells secrete a spectrum of cytokines and proteases, influencing inflammation and the immune milieu. Intriguingly, the study reveals that epigenetic changes in mast cells can drastically shift their cytokine secretion profiles, transforming them from fighters against pathogens into inadvertent accomplices in cancer growth. This duality presents a fascinating biological paradox and spotlights mast cells as potential epigenetic targets in oncology.

The crux of the investigation centers on how cancer cells manipulate their own epigenetic states alongside those of nearby mast cells to orchestrate a tumor-promoting environment. The researchers employed state-of-the-art genome-wide epigenomic profiling techniques, such as chromatin immunoprecipitation sequencing (ChIP-seq) and DNA methylation mapping, to delineate modifications in histone marks and DNA methylation patterns. These epigenetic marks collectively influence gene activation and repression, thereby modulating cytokine gene expression crucial for tumor-immune interactions.

One of the key findings of this study is the identification of a specific epigenetic signature that underpins the aberrant cytokine production in both mast and cancer cells. This signature comprises hypomethylated promoter regions in genes encoding pro-tumorigenic cytokines like interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta (TGF-β). These changes promote an inflammatory milieu conducive to tumor immune evasion, angiogenesis, and extracellular matrix remodeling—all hallmarks of cancer progression.

Importantly, the research highlights the bidirectional nature of epigenetic reprogramming in the tumor microenvironment. Not only do cancer cells induce epigenetic alterations in mast cells via paracrine signaling and extracellular vesicles, but mast cells also reciprocally influence the epigenetic landscape of cancer cells. This crosstalk leads to a feed-forward loop of cytokine production that exacerbates tumor aggressiveness and resistance to therapy.

Delving further into the mechanistic details, the team uncovered that key epigenetic regulators, including DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), are involved in setting and maintaining these pro-tumoral epigenetic states. Pharmacological inhibition of these enzymes in experimental models was sufficient to reverse the aberrant cytokine profiles, reducing tumor growth and metastatic potential. These insights offer tantalizing prospects for epigenetic therapy strategies aimed at reprogramming the tumor microenvironment.

Another layer of complexity is added by the discovery that non-coding RNAs, particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), serve as critical epigenetic modulators in this context. These molecules fine-tune gene expression post-transcriptionally, with some aberrantly expressed in mast and cancer cells, further fueling the tumor-promoting cytokine networks. The integration of non-coding RNA regulation with classical epigenetic modifications presents a holistic view of gene regulatory networks in cancer immunobiology.

The translational implications of this study are profound. By targeting the epigenetic machinery that governs mast cell and cancer cell interactions, it may be possible to dismantle the supportive tumor niche and enhance the efficacy of existing immunotherapies. Current immune checkpoint inhibitors have revolutionized cancer treatment but face limitations due to the immunosuppressive microenvironment. Modulating epigenetic programs in these influential cells could sensitize tumors to immune attack and prevent relapse.

Furthermore, this research challenges the traditional notion of mast cells solely as inflammatory effectors, positioning them squarely within the epigenetic landscape of cancer immunology. It paves the way for the development of novel biomarkers based on epigenetic and cytokine signatures that could predict tumor behavior and patient prognosis. Detecting these molecular fingerprints in patient samples might allow for personalized therapeutic approaches that consider both tumor and immune components.

The holistic understanding of tumor-promoting cytokine networks provided by this epigenetic lens also extends beyond oncology. Chronic inflammatory diseases, autoimmune disorders, and even infectious diseases could be re-examined through the paradigm of immune cell reprogramming. This study thus not only deepens our grasp of cancer pathology but also enriches the broader field of immunology with refined mechanistic insights.

Critically, the authors underscore the need for further research into the temporal dynamics of epigenetic reprogramming. Tumor progression is a multistage process where the immune microenvironment evolves constantly. Longitudinal analyses and single-cell epigenomic profiling stand out as promising approaches to unravel the stepwise changes in mast cells and cancer cells, potentially uncovering windows of opportunity for therapeutic intervention.

Moreover, the study’s comprehensive methodological approach involving in vitro cell culture systems, animal models, and patient-derived tumor samples strengthens the validity of the findings and their relevance to human disease. By bridging experimental models with clinical observations, the research provides a robust framework for translating epigenetic insights into tangible clinical benefits.

The implications of epigenetic reprogramming in tumor-promoting cytokine networks are equally significant in light of tumor heterogeneity. Different cancer types and even subpopulations within a tumor may exhibit distinct epigenetic patterns governing cytokine production. Personalized epigenetic profiling could thus become an integral part of precision oncology, tailoring interventions to the unique epigenomic landscape of each patient’s tumor.

In sum, this seminal work not only uncovers the intricate layers of epigenetic regulation that drive mast cell and cancer cell-mediated tumor promotion but also charts a promising course toward innovative therapeutic paradigms. The convergence of epigenetics, immunology, and oncology heralds a new era in cancer research with the potential to transform patient outcomes and circumvent the formidable barriers posed by tumor microenvironmental complexity.

As the scientific community continues to unravel the epigenetic choreography of cellular actors within tumors, studies like this exemplify the power of integrative research to pave the way for next-generation cancer treatments. With precision epigenetic interventions on the horizon, the prospect of shifting the balance from tumor promotion to tumor eradication becomes not just conceivable but imminent.

Subject of Research: Epigenetic reprogramming of mast cells and cancer cells and its impact on tumor-promoting cytokine networks.

Article Title: Epigenetic reprogramming of mast and cancer cells modifies tumor-promoting cytokine networks.

Article References:
Schcolnik-Cabrera, A., Ramírez-Yautentzi, M., Soria-Castro, R. et al. Epigenetic reprogramming of mast and cancer cells modifies tumor-promoting cytokine networks. Med Oncol 42, 371 (2025). https://doi.org/10.1007/s12032-025-02941-9

Image Credits: AI Generated