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Liquid biopsy has emerged as a minimally invasive approach for the molecular characterization and longitudinal monitoring of primary central nervous system (CNS) tumors. Although extensively validated in systemic malignancies, its clinical application in CNS tumors is challenged by the blood–brain barrier, low analyte abundance, and heterogeneous assay performance. Recent advances have expanded the spectrum of detectable tumor-derived components, including circulating tumor DNA (ctDNA), cell-free DNA, extracellular vesicles, RNA species, nucleosomes, metabolites, and lipids, across multiple biofluids such as cerebrospinal fluid (CSF), plasma, serum, urine, saliva, and tears. The aim of this study was to review the biological foundations, analytes, biofluids, clinical applications, and technical limitations of liquid biopsy in primary CNS tumors, with emphasis on diagnostic, prognostic, and surveillance value. We synthesized current evidence on tumor-derived analytes detectable through liquid biopsy, their molecular correlates, and their performance across biofluids. CSF is consistently the most informative biofluid for CNS tumors, with higher analyte concentration and superior concordance with tumor tissue compared with plasma. CtDNA in CSF reliably identifies hallmark alterations, including IDH1/2, H3K27M, TERT, BRAF, ATRX, TP53, 1p/19q codeletion, and MYCN amplification, thereby enabling better diagnosis, molecular classification, and therapeutic stratification. Plasma-based assays are less sensitive but remain valuable for longitudinal monitoring, especially when combined with ultrasensitive sequencing or fragmentomic approaches. Emerging biomarkers, including nucleosome footprints, exosomes, proteins, microRNA (miRNA)/long noncoding RNA (lncRNA)/circular RNA (circRNA) signatures, lipidomic panels, and metabolites such as d-2-hydroxyglutarate, show potential for integration into multimodal diagnostics. Liquid biopsy provides a powerful and rapidly evolving tool for the minimally invasive molecular assessment of CNS tumors. While CSF remains the optimal matrix for diagnosis and characterization, advances in ultrasensitive detection methods increasingly support the feasibility of plasma and urine for longitudinal follow-up. Integrating liquid biopsy with advanced imaging and tissue-based data will likely transform diagnostic accuracy, therapeutic decision-making, and real-time monitoring of CNS tumors.
Critically ill patients with acute leukemia often require an intensive care unit (ICU) admission. As major therapeutic advances have been made during the last decades, the aim of this study was to assess temporal trends in ICU mortality, and identify prognostic factors to inform clinician decision-making. We conducted an individual participant data meta-analysis of studies including adults with acute leukemia admitted to the ICU. Patients with a history of allogeneic hematopoietic stem cell transplantation were excluded. Mixed-effects logistic regression models, accounting for center of ICU admission as a random variable, evaluated factors associated with ICU mortality, with particular focus on year of ICU admission, age (> 65 years) and invasive mechanical ventilation. A total of 2003 patients from 55 ICUs across 19 countries were included (median age 58 years [IQR 44–67]; 72
Currently, no consensus exists regarding the definition of oligometastatic pancreatic ductal adenocarcinoma, its necessary diagnostic measures, and potential treatment approaches. To address these knowledge gaps, the OligoPanc project brought together an interdisciplinary group of experts to establish consensus using a modified Delphi process and clinical vignettes. Participants agreed that the number of metastatic lesions and the number of affected organs are key elements in defining oligometastatic pancreatic ductal adenocarcinoma. Specifically, up to three lesions in a single organ, either the liver or the lung, define oligometastatic pancreatic ductal adenocarcinoma and could be either synchronous or metachronous. Necessary diagnostics include a triple-phase contrast-enhanced CT scan of the chest and abdomen and MRI of the liver with a hepatocyte-specific contrast agent. In unclear cases, [18F]fluorodeoxyglucose-PET CT or MRI can be considered. A multidisciplinary tumour board is essential. Patient-intrinsic factors, including age, do not define oligometastatic disease but should be considered for any treatment decision. Systemic treatment before any local consolidative treatment, including surgery, stereotactic ablative radiotherapy, or other locally ablative techniques, is mandatory. The proposed definition should be incorporated into future trials to improve comparability and enable validation.
El cáncer mamario en estadios tempranos tiene un manejo local (quirúrgico y radioterapia) y sistémico específico. Este tipo de cáncer incluye el carcinoma ductal in situ y los cánceres de mama en estadios I, IIA, IIB y IIIA. Esta undécima actualización del Consenso Mexicano de Cáncer Mamario abordó el manejo de los estadios tempranos. La difusión de este consenso contribuye a la actualización y la homogeneidad de criterios de manejo del cáncer mamario, y el objetivo de este artículo es presentar la actualización en el manejo multidisciplinario del cáncer de mama.
Tumor microbes are increasingly recognized for modulating tumor behavior and therapy responses. Intratumoral microbial burden (ITMB) analysis across cancers revealed regulation of immune pathways, and activated mast cells, mostly in colorectal (CRC) and gastric (STAD) cancers. High ITMB CRC leads to interferon regulation and is associated with improved outcomes in advanced disease. Single-cell sequencing revealed induction of interferon-related genes (IRGs) within microbes-containing human CRC. GI-luminal mismatch repair deficiency (MMRd) tumors had higher ITMB than proficient tumors (MMRp). In a rectal MMRd cohort with 100% remission after immune checkpoint blockade (ICB), tumor microbes and microbes-containing mast cells increased. In ICB-sensitive syngeneic murine MMRd tumor models, local tumor microbial depletion, impaired ICB efficacy while downregulating IFN signaling. Forced upregulation of IRGs in ADAR1-deficient cancer cells restored immunotherapy responses during microbial ablation. These data highlight dynamic interplay between ITMB, host defense, and immunogenicity which seems key to determine therapy responses.
