To explore the regulatory aspects of mRNAs and miRNAs in suicide, we integrated transcriptomic data from GEO datasets. The analysis of mRNA expression in the prefrontal cortex of suicide victims with major depressive disorder revealed a differential profile with 27 downregulated mRNAs, including HSPA1A, HSPA1B, DNAJB1, NR4A1, and GADD45B, which are involved in proteostasis, transcriptional regulation, and apoptosis. Functional enrichment analysis using KEGG and Gene Ontology (GO) revealed significant associations with synaptic plasticity, neuronal survival, and signaling pathways, including MAPK, TGF-β, Wnt, p53, and neurotrophins. Subsequently, using the GSE34120 GEO dataset of miRNAs from the frontal cortex of suicide victims, 105 dysregulated miRNAs were identified. The networks revealed compact regulatory modules with hsa-miR-576-3p, hsa-miR-493, and hsa-miR-550, as well as highly connected central nodes such as hsa-miR-30b, hsa-miR-16a-5p, hsa-miR-181a-5p, and hsa-miR-184. The integration of both profiles allowed the elaboration of miRNA–mRNA regulatory networks in which TP53, FOXO3, RELA, and FOS interact with multiple dysregulated miRNAs. These findings support the notion that suicide involves complex post-transcriptional dysregulation, particularly related to astrocytic function and neurotrophic signaling, with potential diagnostic and therapeutic applications.

The late-onset neonatal sepsis is a severe infection occurring after 72 hours of life and remains one of the leading causes of morbidity and mortality in neonatal intensive care units. This study aimed to identify the clinical, biochemical, and microbiological characteristics of patients diagnosed with late-onset neonatal sepsis at the Neonatal Intensive Care Unit of the Children’s Hospital between 2018 and 2022. A descriptive, observational, cross-sectional, and retrospective study was conducted including 53 newborns who met the inclusion criteria. Data were collected from medical records, covering clinical, microbiological, and antimicrobial susceptibility variables, and analyzed using descriptive statistics. The prevalence of late-onset sepsis in the study population was 9.1%, higher than the global estimate of 2%. Of the cases, 52.8% were female and 47.2% male, with a mean gestational age of 37.3 weeks and an average birth weight of 2,967 grams. Microbiological isolation in blood cultures was obtained in 26.4% of cases, with coagulase-negative staphylococci as the most frequent pathogens (64.3%), followed by Gram-negative bacteria such as Escherichia coli and Enterobacter agglomerans. Extended-spectrum beta-lactamase (ESBL)-producing bacteria were also identified. The most common empirical antibiotic regimen included cefotaxime and ampicillin, though only 40% of culture-positive cases showed concordance with empirical treatment. Biochemical and hematological values remained within normal ranges in most patients. These findings highlight the local epidemiology of late-onset neonatal sepsis, providing evidence that may contribute to improved prevention strategies, diagnostic approaches, and antimicrobial stewardship in neonatal intensive care settings.

Breast carcinoma is a major cause of cancer-related mortality among women worldwide. Identifying novel molecular targets remains essential, particularly for aggressive triple-negative breast cancer (TNBC). Leucine-rich alpha-2-glycoprotein 1 (LRG1) has been linked to tumor progression and angiogenesis, but its molecular mechanisms in breast cancer are poorly defined. We evaluated the effects of recombinant human LRG1 (rhLRG1) on cell viability and migration in MDA-MB-231 TNBC cells and performed transcriptomic profiling followed by functional enrichment analyses using GenArise, Cytoscape, and R-based tools. RhLRG1 treatment significantly increased cell viability and migration. Transcriptomic analysis revealed activation of key oncogenic cascades, including the PI3K/AKT, MAPK, and RAS signaling pathways. Hub-gene analysis identified upregulated genes involved in proliferation (NRAS, STAT5B, IGF2), angiogenesis (PGF, ANGPT2), and apoptosis (CASP8, BAD), whereas downregulated genes were associated with apoptotic resistance (BCL2, MCL1) and adhesion (LAMB1, ITGB4). Functional enrichment highlighted LRG1’s role in the bioinformatic analysis of differentially expressed genes that were obtained from microarray assays. LRG1 remodels the tumor microenvironment by promoting proliferation, angiogenesis, and apoptotic sensitivity while repressing resistance-related genes. These findings position LRG1 as a potential diagnostic biomarker and therapeutic target for advanced breast carcinoma.

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy driven by the accumulation of genetic alterations in hematopoietic progenitor cells. CEBPA variants have been linked to familial AML, although multigenerational cases have been infrequently reported. We describe the case of a 6‐year‐old boy referred for hematologic abnormalities, with a history of idiopathic thrombocytopenic purpura at age 3. His family history revealed 11 cases of AML in four maternal generations, suggesting autosomal dominant inheritance. Diagnostic evaluation revealed AML with 40% bone marrow blasts, a normal karyotype, and a negative multiplex RT‐PCR panel for 28 common chromosomal translocations. Next‐generation sequencing (NGS) identified a novel heterozygous pathogenic variant in the CEBPA gene (c.273_309delinsGGCCAGGGTCT; p.Lys92Alafs∗7), which was predicted to generate a truncated protein. Given the patient’s medical history, genetic screening was performed on the patient’s first‐degree relatives. Genetic testing subsequently identified the same variant in the patient’s mother, supporting its germline origin, while his sister showed no alterations in the CEBPA gene sequence. The presence of the variant in the patient´s mother, who is asymptomatic, is consistent with autosomal dominant transmission and age‐dependent or incomplete penetrance. In this case, the patient carried a heterozygous variant, achieved complete remission after chemotherapy, and remains under surveillance. We present a pathogenic germline deletion‐insertion variant in the CEBPA gene, not previously described in the literature, associated with hereditary predisposition to AML in a four‐generation family, highlighting the variable expressivity characteristic of this syndrome and the relevance of considering a hereditary predisposition disorder in pediatric patients with AML.