Background: Microsatellite instability (MSI) is a hallmark of DNA mismatch repair (MMR) deficiency that leads to genomic instability and increased cancer risk. The tumor microenvironment (TME) significantly influences MSI‐driven tumorigenesis, and emerging evidence points to a critical role of the microbiome in shaping this complex interplay.Methods: This review comprehensively examines the existing literature on the intricate relationship between MSI, microbiome, and cancer development, with a particular focus on the impact of microbial dysbiosis on the TME.Results: MSI‐high tumors exhibited increased immune cell infiltration owing to the generation of neoantigens. However, immune evasion mechanisms such as PD‐1/CTLA‐4 upregulation limit the efficacy of immune checkpoint inhibitors (ICIs) in a subset of patients. Pathobionts, such as Fusobacterium nucleatum and Bacteroides fragilis, contribute to MSI through the production of genotoxins, further promoting inflammation and oxidative stress within the TME.Conclusions: The microbiome profoundly affects MSI‐driven tumorigenesis. Modulation of the gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and dietary changes holds promise for improving ICI response rates. Further research into cancer pharmacomicrobiomics, investigating the interplay between microbial metabolites and anticancer therapies, is crucial for developing personalized treatment strategies.

Preeclampsia (PE) is a multifactorial and multisystemic syndrome specific to human pregnancy, traditionally characterized by hypertension and proteinuria. Affecting 2%−10% of pregnancies, PE remains a leading cause of maternal and perinatal morbidity and mortality, particularly in low- and middle-income countries. This review traces the historical evolution of PE diagnosis, from early clinical observations to the incorporation of modern omics biomarkers. Early diagnostic criteria were based on observable clinical symptoms, but advancements in biomedical science have highlighted the significance of angiogenic and anti-angiogenic factors, such as sFlt-1 and PlGF, which are used as “Established Angiogenic Biomarkers.” Despite these advancements, clinical consensus on the use of these biomarkers remains elusive due to their variable sensitivity. Recent integrative approaches using omics technologies have provided deeper insights into the complex pathophysiology of PE, uncovering new pathways and “Potential Molecular Biomarkers” for early diagnosis and prediction. However, challenges remain in translating these findings into clinical practice, particularly due to the need for robust validation studies and the consideration of inter-individual and population variability. This review emphasizes the importance of continued research and validation of these biomarkers in diverse cohorts to develop effective predictive tools and improve maternal and fetal outcomes. By exploring the historical and modern perspectives on PE diagnosis, this review aims to provide a comprehensive understanding of the disease and highlight future directions in PE research.

Pathogenic germline mutations in the BRCA1 and BRCA2 (BRCA1/2) genes contribute to hereditary breast/ovarian cancer (OC) in White/mestizo Colombian women. As there is virtually no genetic data on breast cancer (BC) in Colombians of African descent, we conducted a comprehensive BRCA1/2 mutational analysis of 60 Afro-Colombian families affected by breast/OC. Mutation screening of the complete BRCA1/2 genes for small-scale mutations and large genomic alterations was performed in these families using next-generation sequencing and multiplex ligation-dependent probe amplification analysis. Four pathogenic germline mutations, including one novel mutation, were identified, comprising 3 in BRCA1 and one in BRCA2. The prevalence of BRCA1/2 mutations, including one BRCA1 founder mutation (c.5123C>A) previously identified in this sample set, was 3.9% (2/51) in female BC-affected families and 33.3% (3/9) in those affected by both breast and OC. Haplotype analysis of 2 BRCA2_c.2701delC carriers (one Afro-Colombian and one previously identified White/mestizo Colombian patient with BC) suggested that the mutation arose in a common ancestor. Our data showed that 2/5 (40%) mutations (including the one previously identified in this sample set) are shared by White/mestizo Colombian and Afro-Colombian populations. This suggests that these 2 populations are closely related. Nevertheless, variations in the BRCA1/2 mutational spectrum among Afro-Colombian subgroups from different regions of the country were observed, suggesting that specific genetic risk assessment strategies need to be developed.

El cáncer de próstata (CP) es el segundo cáncer más común en hombres y la quinta causa de mortalidad por cáncer a nivel mundial. El CP se origina en un entorno tumoral que favorece la supresión del sistema inmunológico, donde las interacciones entre las células tumorales y los tejidos cercanos influyen en el avance de la enfermedad. El microambiente peritumoral (tejido adyacente al tumor) juega un papel esencial en la progresión del CP, al proporcionar señales que regulan la respuesta inmunitaria. Debido al papel fundamental del tejido peritumoral en la patogénesis del CP, este artículo tiene como objetivo identificar los mecanismos de interacción entre el tejido peritumoral y las células tumorales, los cuales podrían facilitar la identificación de biomarcadores para el diagnóstico temprano y el desarrollo de nuevas estrategias terapéuticas.

Field cancerization describes molecular alterations occurring in histologically normal tissues surrounding tumors that may contribute to cancer initiation and progression. In prostate cancer (PCa), the molecular characteristics of peritumoral tissue (PTT) remain incompletely understood. Because microRNAs (miRNAs) play key roles in gene regulation, tumor progression, and microenvironmental remodeling, we investigated miRNA expression patterns and regulatory networks across benign tissue (BT), PTT, and tumor tissue (TT). Small RNA sequencing was performed on matched formalin-fixed paraffin-embedded samples from 40 patients with PCa. Differential expression analysis was conducted using DESeq2, adjusting for age and Gleason grade, while functional enrichment analysis and weighted gene co-expression network analysis (WGCNA) were used to identify dysregulated pathways and conserved miRNA modules. PTT exhibited a molecular profile intermediate between BT and TT, consistent with a field cancerization effect. Compared with BT, 102 miRNAs were differentially expressed in TT and 57 in PTT, with 39 miRNAs (68% of the PTT-associated miRNAs) overlapping the tumor signature. Shared dysregulated pathways included PI3K–Akt, p53, and HIF-1 signaling; whereas, PTT showed additional enrichment in pathways related to epigenetic regulation (Polycomb Repressive Complex) and cellular stress responses (mitophagy, protein processing in ER) exclusively through up-regulated miRNAs; no pathways were uniquely enriched from down-regulated miRNAs in PTT. WGCNA identified conserved miRNA modules enriched for members of the let-7, miR-200, miR-103/107, and miR-106a~363 families, which have established roles in epithelial–mesenchymal transition, tumor progression, and microenvironmental remodeling. Collectively, these findings demonstrate that histologically benign peritumoral tissues harbor tumor-associated miRNA programs and regulatory networks that closely resemble those observed in prostate tumors, providing molecular evidence of field cancerization in PCa and identifying potential miRNA-mediated mechanisms relevant to disease progression and biomarker development.

Ovarian cancer is one of the leading causes of death from gynecologic cancer. In Colombia, as in the world, its diagnosis is made in late stages due to the absence of specific symptoms of this disease. Objective The objective of the Ovarian Cancer Registry is (i) to collect clinical and histopathological data using a standardized protocol, (ii) to characterize these patients clinically and histopathological to optimize the diagnosis and treatment, to describe these clinical aspects, which will allow us to understand the clinical particularities of this disease better. Methods The Ovarian Cancer Registry is designed as a retrospective for data collection on OVAR patients. All patients under medical care at the Hospital Universitario Mayor Méderi and who have arrived in three possible routes or scenarios: (i) outpatient care, (ii) assessment in emergency services and (iii) references to the oncology service. The OVAR will have information on patients who consulted the Major Hospital from the first of January 2021 with CIE10 C56X and C482. Ethics and dissemination The University of Rosario Ethics Committee approved registry protocol V02 (08/feb/24) No. 2541-CV1830 (Bogotá, Colombia). Registry leaders acknowledge their ongoing ethical responsibilities for all research using this data. Conclusion The data from the Ovarian Cancer Registry will be instrumental in establishing optimal management strategies for OC patients, laying the groundwork for future guideline recommendations, and shaping the direction of upcoming research on the Colombian population.