Background/Objectives: Differentiating between benign and malignant ovarian adnexal masses before surgery is a significant diagnostic challenge. This study examined a wide range of circulating plasma molecules (immune and inflammatory) to identify potential markers to classify tumors as benign or malignant. The goal was to develop a proof-of-concept tool for preoperative risk stratification. Methods: Twenty-three plasma molecules were evaluated in women with benign lesions (n = 68) and women with malignant ovarian tumors (n = 25). To evaluate the behavior of each marker in a normal population, women without adnexal pathology were also included (n = 11). The results were compared using the Kruskal–Wallis test with Dunn post hoc pairwise comparisons, the Benjamini–Hochberg correction for multiple comparisons, and ROC analysis. TGF-β isoforms and CA125 were measured in the complete cohort (n = 104), while the remaining molecules were assessed in a reduced cohort (n = 51). Two classification approaches were developed using TGF-β3 and IL-13: a sequential two-step algorithm and an ordinal logistic regression model. Apparent performance was corrected for optimism using Harrell’s bootstrap procedure. Results: Ten molecules reached statistical significance. Among the significant molecules, TGF-β3 identified ovarian lesions regardless of malignant status (AUC = 0.983), while IL-13 showed perfect malignancy-specific separation from benign cases (AUC = 1.000). Their combination in an ordinal logistic regression model produced three non-overlapping diagnostic strata across all three groups, significantly outperforming CA125, HE4, and ROMA at the malignancy-separation boundary (DeLong p < 0.05) in our exploratory cohort. Conclusions: TGF-β3 and IL-13 represent a biologically complementary marker pair whose combined ordinal regression model shows promising performance and warrants prospective validation in larger, multicenter independent cohorts as a preoperative risk-stratification tool for ovarian adnexal masses.

Advances in genomics and immunology have redefined the understanding of immune regulation, disease susceptibility and therapeutic response. This review synthesizes evidence across multiple biological scales—including germline variation, somatic mutations, epigenomic architecture and single-cell immune heterogeneity—to elucidate how genomic mechanisms shape immune function in health and disease. Emphasis is placed on the translational relevance of these mechanisms, particularly in the context of cancer immunotherapy, autoimmune risk stratification and emerging engineered-immunity platforms such as CRISPR-based editing and CAR T-cell therapies. The analysis also highlights the persistent underrepresentation of populations from Mexico, Colombia and Ecuador in genomic datasets, underscoring the need for inclusive precision-medicine strategies. By integrating mechanistic, technological and clinical dimensions, this review outlines the conceptual foundations of immunogenomics and identifies the opportunities and challenges that will shape its evolution as a global, population-relevant discipline.

Pharmacogenomics has emerged as an essential component of personalized therapy in internal medicine, offering a framework to understand how genetic variability influences drug response, safety, and treatment effectiveness. This review synthesizes international evidence to identify clinically relevant gene–drug interactions, evaluate global implementation strategies, and examine their applicability to healthcare systems in Mexico, Colombia, and Ecuador. The analysis demonstrates that cytochrome P450 enzymes—particularly CYP2C19, CYP2D6, and CYP3A4—continue to play a dominant role in predicting therapeutic outcomes, with strong evidence supporting interactions such as CYP2C19–clopidogrel, CYP2D6–codeine, and SLCO1B1–simvastatin. These associations consistently appear in international guidelines and represent high-impact opportunities for improving cardiovascular, psychiatric, and oncologic care. Global implementation models from North America, Europe, and Asia highlight the importance of structured policies, laboratory capacity, and electronic health record integration, while emerging experiences from Africa and Southeast Asia emphasize scalable, resource-adapted strategies. In Latin America, Mexico demonstrates the highest readiness for pharmacogenomic adoption, followed by Colombia with promising institutional initiatives, and Ecuador with early-stage development requiring capacity-building. The review also discusses the expansion of pharmacogenomics into multi-omic approaches, including epigenetics and nutrigenomics, which are expected to refine predictive accuracy but require advanced informatic infrastructure and clinician training. Overall, pharmacogenomics provides a powerful opportunity to enhance therapeutic precision, reduce adverse drug reactions, and promote equitable and efficient healthcare delivery. Its successful implementation in Latin America will depend on coordinated policy development, investment in infrastructure, and the integration of genomic education into clinical training programs.

Metabolic diseases constitute a growing global health burden and increasingly demand integrative biological frameworks that transcend organ-specific perspectives. This review synthesizes evidence demonstrating that metabolic deterioration arises from the interaction of three interconnected mechanisms: NLRP3 inflammasome activation, gut microbiota dysbiosis, and cellular aging/senescence. Using a structured scientific methodology, we examined mechanistic, translational, and clinical research across immunology, microbiology, and geroscience. The results highlight that inflammasome activity exerts systemic metabolic effects, influencing insulin resistance, liver injury, vascular remodeling, and renal dysfunction. In parallel, microbiota alterations follow a graded pattern that mirrors disease severity, aging trajectories, and immune dysregulation. Cellular senescence emerges as both a consequence and amplifier of metabolic stress, contributing to chronic inflammation and multi-organ vulnerability through SASP-mediated signaling. When integrated, these mechanisms form a self-reinforcing pathogenic triad that offers a more accurate explanation for the multisystemic nature and progression of metabolic disease. The model presented underscores the need for multidimensional therapeutic strategies that target inflammation, microbial ecology, and aging biology simultaneously. This triad-based framework is particularly relevant for regions undergoing rapid epidemiologic transitions, including Mexico, Colombia, and Ecuador, where metabolic disorders continue to rise.

Aging is associated with a progressive increase in chronic low-grade inflammation, known as inflammaging, which has been identified as a key mechanism underlying the development of multimorbidity. This review aims to analyze the role of inflammaging in aging and its impact across internal medicine, immunology, and gynecology. A structured narrative review was conducted using high-impact scientific literature, focusing on biological mechanisms, clinical implications, and interdisciplinary perspectives. The findings indicate that inflammaging is driven by interconnected processes such as immune dysregulation, cellular senescence, mitochondrial dysfunction, metabolic imbalance, and hormonal changes. These mechanisms contribute to the development of chronic diseases including cardiovascular disorders, type 2 diabetes, frailty, neurodegeneration, and postmenopausal alterations. Additionally, inflammatory biomarkers such as IL-6, TNF-α, and CRP were consistently associated with disease progression. The results also highlight the importance of lifestyle interventions, metabolic control, and emerging geroscience-based therapies in modulating chronic inflammation. Overall, inflammaging represents a central biological axis that links aging with multimorbidity, supporting the need for integrated and preventive approaches in clinical practice.