1,615 publications from this institution
<p>Supplementary Figures S1-S4. Common histological subtypes of NSCLC orthoallografts (S1); In vitro characterization of primary cell lines derived from NSCLC orthoallografts (S2); Lung colonization and tumor formation upon reintroduction of mKLC cell lines (S3); Inoculation of mKLC single cell clones gives rise to NSCLC heterogeneity in vivo (S4).</p>
Personalized medicine is defined by therapy decisions tailored to individual patients, aiming to improve therapeutic efficiencies and to minimize side effects. The current clinical practice includes targeted therapies for disease-related alterations and molecular biomarker-based patient stratification. However, recent advances in screening technologies have enabled more comprehensive identification strategies and suggest a plethora of additional valuable biomarkers and druggable molecules for future clinical applications. Beside genetic alterations, in particular, DNA methylation biomarkers emerge into the field by presenting stable DNA modifications with predictive potential for drug treatment efficiencies, especially in a cancer context. Although not directly affecting the genetic code, DNA methylation exhibits regulatory functions with high impact on disease onset and progression. In this article, the authors summarize the current knowledge of DNA methylation biomarkers for treatment efficiencies and evaluate their translational value into clinical use.
Effective anticancer immunotherapy treatments constitute a qualitative leap in cancer management. Nonetheless, not all patients benefit from such therapies because they fail to achieve complete responses, suffer frequent relapses, or develop potentially life-threatening toxicities. Epigenomic signatures in immune and cancer cells appear to be accurate and promising predictors of patient outcomes with immunotherapy. In addition, combined treatments with epigenetic drugs can exploit the dynamic nature of epigenetic changes to potentially modulate responses to immunotherapy. Candidate epigenetic biomarkers may provide a rationale for patient stratification and precision medicine, thus maximizing the chances of treatment success while minimizing unwanted effects. We present a comprehensive up-to-date view of potential epigenetic biomarkers in immunotherapy and discuss their advantages over other indicators.
B-cell acute lymphoblastic leukemia (B-ALL) remains a major clinical challenge in hematologic oncology, characterized by a continuous evolution of molecular drivers that shape its heterogeneity across the age spectrum. Pediatric B-ALL is generally associated with high cure rates, while adult forms of the disease are often more aggressive and less responsive to treatment. This review examines the age-specific genetic and epigenetic landscapes that contribute to this disparity, revealing how the nature and timing of molecular alterations point to fundamentally different leukemogenic processes. Favorable genetic aberrations, such as ETV6::RUNX1 and hyperdiploidy, are predominant in children, whereas adults more frequently present with high-risk features, including BCR::ABL1 fusions and IKZF1 deletions. Epigenetic distinctions are similarly age-dependent, involving divergent patterns of DNA methylation, histone modifications, and non-coding RNA expression. For example, pediatric B-ALL frequently harbors mutations in epigenetic regulators like SETD2 and CREBBP, while adult B-ALL is more commonly affected by alterations in TET2 and IDH1/2. These molecular differences are not only prognostic but also mechanistic, reflecting distinct developmental trajectories and vulnerabilities. Understanding these age-driven transitions is essential for improving risk stratification and developing precision therapies tailored to the unique biology of B-ALL across the lifespan.
