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Tertiary lymphoid structures (TLS) are organized ectopic lymphoid clusters of immune cells that develop in non-lymphoid tissue to promote antigen presentation, drive cytotoxic immune responses, and enhance humoral immunity via B cell clonal expansion. Their presence within the tumor microenvironment (TME) correlates with increased patient survival and an improved response to immune checkpoint inhibitors (ICIs), positioning TLS as potential predictive and prognostic biomarkers. Despite the widespread use of ICIs across various cancers, their effectiveness remains limited in gynecological malignancies, including ovarian cancer (OC), a notably challenging disease characterized by poor responses to both single and combination ICI therapies. Interestingly, the infiltration of T cells into the OC TME is linked to enhanced progression-free survival (PFS) and overall survival (OS), yet an immunosuppressive TME frequently impedes therapeutic efficacy, suggesting cell activity within localized immune niches can impact antitumor immunity. This review explores the roles of TLS, their maturity, functionality, identification, and related gene signatures; specific immune cells and cytokines that play a role in TLS formation and antitumor response; and other modifiable elements, including gut microbiota, that may drive improving OC survival by leveraging a TLS-driven antitumor response to bolster immunotherapy outcomes.

Ovarian immature teratoma is a germ cell tumor that comprises less than 1% of ovarian cancers and is treated with surgical debulking and chemotherapy depending on stage. Growing teratoma syndrome (GTS) is the phenomenon of the growth of mature teratoma elements with normal tumor markers during or following chemotherapy for treatment of a malignant germ cell tumor. These tumors are associated with significant morbidity and mortality due to invasive and compressive growth as well as potential for malignant transformation. Current treatment modality is surgical resection. We discuss a 12-year-old female who presented following resection of a pure ovarian immature teratoma (grade 3, FIGO stage IIIC). Following chemotherapy and resection of a pelvic/liver recurrence demonstrating mature teratoma, she underwent molecular genetics based chemotherapeutic treatment. No standardized management protocol has been established for the treatment of GTS. The effect of chemotherapeutic agents for decreasing the volume of and prevention of expansion is unknown. We review in detail the history, diagnostic algorithm, and previous reported pediatric cases as well as treatment options for pediatric patients with GTS.

Background Post-hemorrhagic hydrocephalus (PHH) is a severe complication in premature infants following intraventricular hemorrhage (IVH). It is characterized by abnormal cerebrospinal fluid (CSF) accumulation, disrupted CSF dynamics, and elevated intracranial pressure (ICP), leading to significant neurological impairments. Objective This review provides an overview of recent molecular insights into the pathophysiology of PHH and evaluates emerging therapeutic approaches aimed at addressing its underlying mechanisms. Methods Recent studies were reviewed, focusing on molecular and cellular mechanisms implicated in PHH, including neuroinflammatory pathways, immune mediators, and regulatory genes. The potential of advanced technologies such as whole genome/exome sequencing, proteomics, epigenetics, and single-cell transcriptomics to identify key molecular targets was also analyzed. Results PHH has been strongly linked to neuroinflammatory processes triggered by the degradation of blood byproducts. These processes involve cytokines, chemokines, the complement system, and other immune mediators, as well as regulatory genes and epigenetic mechanisms. Current treatments, primarily surgical CSF diversion, do not address the underlying molecular pathology. Emerging therapies, such as mesenchymal stem cell-based interventions, show promise in modulating immune responses and mitigating neurological damage. However, concerns about the safety of these novel approaches in neonatal populations and their potential effects on brain development remain unresolved. Conclusions Advanced molecular tools and emerging therapies have the potential to transform the treatment of PHH by targeting its underlying pathophysiology. Further research is needed to validate these approaches, enhance their safety profiles, and improve outcomes for infants with PHH. Impact statement This review elucidates the molecular complexities of post-hemorrhagic hydrocephalus (PHH) by examining specific immune pathways and their impact on disease pathogenesis and progression. It outlines the application of genomic, epigenomic, and proteomic technologies to identify critical molecular targets in PHH, setting the stage for innovative, targeted therapeutic approaches that could improve the outcomes of neonates affected by PHH. It discusses the potential of gene and stem cell therapies in treating PHH, offering non-surgical alternatives and focusing on the underlying neuroinflammatory mechanisms.

Since moving to the United States in 1972, she undertook routine visits to her native country, India. Relevant laboratory values included: hemoglobin 11.7 g/dL, white blood cell count 9850/mm3, platelet count 468 000 mm3, blood urea nitrogen 46 mg/dL, creatinine 2.5 mg/dL, albumin 2.4 g/dL, albumin-corrected calcium 12.18 mg/dL, aspartate aminotransferase 81 U/L, alanine aminotransferase 81 U/L, carcinoembryonic antigen 1.8 ng/mL, alpha-fetoprotein 4.4 ng/mL, CA125 245 U/mL, and cancer antigen (CA) 19–9 57.4 U/mL. Other diagnoses, such as end-organ damage from poorly controlled diabetes mellitus, thyroid dysfunction, congestive heart failure, hepatic dysfunction, kidney disease, and adverse medication effects should be ruled out with laboratory evaluation. Additional ascitic fluid results included a peritoneal fluid serum-ascites albumin gradient greater than 1.1 g/dL with a lymphocytic predominance, a white blood cell count of 7826 cells/mm3, and an absolute polymorphonuclear leucocyte count of 5488 cells/mm3 (30% of total cells).

The human pons relays sensory and motor information between the brain and the body. It is a key site for pathological processes, including diffuse midline gliomas (DMGs) and multiple sclerosis (MS) which predominantly arise in childhood and middle age, respectively. Although multiple studies address disease states, a comprehensive resource for normal pons development is lacking. Here we present PEDIA-BRAIN, an encyclopedia of gene expression and chromatin accessibility from 149,771 human pons nuclei spanning the first trimester to early adulthood to serve as a resource for the scientific community. Exploration of the encylopedia identified two trajectories to mature oligodendrocytes and developmental restriction of synaptic interactions between neurons and oligodendrocyte precursor cells. To illustrate the utility of the resource, we mapped single cell transcriptomes from DMG and MS samples and identified depletion of mature oligodendrocyte subtypes as a shared feature of both diseases. Data may be browsed and downloaded at pediabrain.nchgenomics.org.

Cardiovascular magnetic resonance (CMR) is considered the gold standard imaging modality for myocardial tissue characterization. Elevated transverse relaxation time (T2) is specific for increased myocardial water content, increased free water, and is used as an index of myocardial edema. The strengths of quantitative T2 mapping lie in the accurate characterization of myocardial edema, and the early detection of reversible myocardial disease without the use of contrast agents or ionizing radiation. Quantitative T2 mapping overcomes the limitations of T2-weighted imaging for reliable assessment of diffuse myocardial edema and can be used to diagnose, stage, and monitor myocardial injury. Strong evidence supports the clinical use of T2 mapping in acute myocardial infarction, myocarditis, heart transplant rejection, and dilated cardiomyopathy. Accumulating data support the utility of T2 mapping for the assessment of other cardiomyopathies, rheumatologic conditions with cardiac involvement, and monitoring for cancer therapy-related cardiac injury. Importantly, elevated T2 relaxation time may be the first sign of myocardial injury in many diseases and oftentimes precedes symptoms, changes in ejection fraction, and irreversible myocardial remodeling. This comprehensive review discusses the technical considerations and clinical roles of myocardial T2 mapping with an emphasis on expanding the impact of this unique, noninvasive tissue parameter.