Myeloid cells play a key role in cancer-associated immunosuppression because their accumulation and reprogramming inhibit antitumor responses and support tumor growth. To modulate their activity, we targeted Fcγ receptors (FcγRs), which are broadly expressed in myeloid subsets. Since low-affinity Fcγ receptor IIb (FcγRIIb) mediates inhibitory signaling, we designed an immunotherapy active at a low dose to limit binding to FcγRIIb while retaining interaction with higher-affinity FcγRs. We engineered an Fc-based fusion protein, whose activity is potentiated by its ability to engage both FcγRs and a coreceptor, Heparan Sulfate Proteoglycan (HSPGs). This immunotherapy, named Fc-T54, combines an HSPG-ligand, named T54, with human IgG1-Fc. Compared with Fc, Fc-T54 displayed superior binding to Fcγ receptor IIa (FcγRIIa), Fcγ receptor IIIa (FcγRIIIa) and enhanced interactions with human leukocytes, including neutrophils, B-lymphocytes, as well as with monocytes, and dendritic cells (DCs) within peripheral blood mononuclear cells. Functionally, Fc-T54 increased monocyte/macrophage and B-cell numbers, reduced neutrophil abundance, and boosted DC activation in both the human and murine systems. Subcutaneous administration of low-dose Fc-T54 - or its murine surrogate - inhibits tumor growth in immune-deserted and immune-excluded mouse models and synergizes with anti-PD-1 therapy in an immune-inflamed model. Tumor microenvironment analysis in the bladder cancer model revealed that the immunotherapy decreased the proportion of granulocytic myeloid-derived suppressor cells while increasing CD8+ T cells and natural killer cells, promoting a microenvironment more prone to tumor control. This FcγR/HSPG-engaging immunotherapy, administered subcutaneously, offers a novel approach to modulate the myeloid compartment and improve outcomes for ICI-resistant, deserted/excluded tumors, and for inflamed tumors when used in combination regimens.

Haematologic malignancies have diverse and complex genomic abnormalities, and the correct identification is essential for making the appropriate diagnosis, providing a prognosis, and planning treatment. Improved array comparative genomic hybridisation (array CGH) can provide high-resolution, genome-wide copy number variation detection, and overcomes conventional cytogenetic limitations.

The aim of this study is to determine the role of array CGH in characterising genomic aberrations of haematologic malignancies, focusing on technical advantages, added diagnostic values, and implications for disease reclassification and precision medicine.

A comprehensive literature search of PubMed, Embase, Web of Science, and Scopus was conducted to identify studies evaluating the diagnostic performance and clinical utility of array CGH in haematologic cancers.

Array CGH detects genomic alterations at kilobase-level resolution and reveals additional abnormalities in approximately 30% of cases with normal results by conventional cytogenetics. It improves molecular subtyping, identifies novel prognostic marker and, when combined with single nucleotide polymorphism arrays, enables detection of uniparental disomy and copy-neutral loss of heterozygosity, thereby enhancing diagnostic yield.

Array CGH detects up to 90% of known genomic abnormalities in haematologic malignancies, and its integration with other genomic platforms will considerably enhance diagnostic precision and clinical care for haematopoietic neoplasms.

This review emphasises the important role of array CGH's greater sensitivity to clinically relevant copy number changes compared to routine cytogenetics. Clinical applications of array CGH support precision oncology, especially when combined with single nucleotide polymorphism array or next-generation sequencing technologies.

The diagnosis of myelodysplastic neoplasms (MDS) requires examination of the bone marrow for morphologic evidence of dysplasia. We sought to determine whether a self-supervised learning (SSL) artificial intelligence-based image analysis approach can be used to reliably distinguish MDS from its clinically relevant mimics using bone marrow biopsies (BMBx). The whole-slide images (WSIs) of hematoxylin and eosin (H&E)- and reticulin-stained BMBx sections from 243 unique patients (89 MDS, 55 non-MDS cytopenic controls [NMCCs], and 99 negative control [NC] cases) were partitioned into image tiles for analysis. These image tiles were then processed using the Barlow Twins SSL model to identify histomorphologic phenotype clusters (HPCs). Review of the HPCs revealed the clusters enriched in MDS cases captured known histopathologic features of the disease, including hypercellularity (characterized by enrichment in hypercellular image tiles), dysplastic and loosely clustered megakaryocytes, increased immature hematopoietic cells, increased vascularity, fibrosis, and cell streaming patterns. For external validation, 95 MDS BMBx WSIs from an independent institution were analyzed using the trained model. The model demonstrated consistent HPC enrichment patterns, supporting its robustness and generalizability. The trained ensemble model using H&E- and reticulin-stained slides distinguished MDS from NCs with an area under the curve (AUC) of 0.82, and from age-matched NMCCs with an AUC of 0.80. These findings demonstrate the potential of SSL approaches to capture diagnostically relevant morphologic patterns and to improve the reproducibility of MDS diagnosis.

This work aims to design and characterize a novel bifunctional small molecule that simultaneously targets PD-L1 and CD73 to enhance the therapeutic efficacy of tumor immunotherapy.

Multiple methodologies were integrated for compound screening and biological characterization, including computer-aided molecular docking, homogeneous time-resolved fluorescence (HTRF) binding assay, surface plasmon resonance (SPR), and PD-1/PD-L1 NFAT reporter cell assay.

The lead compound CP-1 exhibited potent dual-target inhibitory activities. It blocked the PD-1/PD-L1 interaction with an IC₅₀ of 10.27 nM and suppressed CD73 activity with an IC₅₀ of 300.2 nM. Molecular docking simulations revealed that CP-1 stably binds to the functional domains of PD-L1 and CD73 via specific non-covalent interactions. Cellular functional assays further demonstrated that CP-1 effectively restored T cell function in the PD-1/PD-L1 reporter system, with an EC₅₀ of 0.9 μM.

CP-1 exhibits balanced, dual-nanomolar inhibitory activity against PD-L1 and CD73 and displays potent immunomodulatory effects at the cellular level. It serves as a promising lead candidate for developing novel bifunctional agents to advance tumor immunotherapy.

Primary liver cancer is a major global cause of cancer death, and hepatocellular carcinoma (HCC) is the predominant histological subtype. This literature review synthesizes current evidence on the exposome, multi-omics landscape, and artificial intelligence (AI)-based integration strategies relevant to biomarker discovery in liver cancer, with a focus on biological rationale, emerging clinical applications, and translational limitations. Key etiologic drivers include viral hepatitis, alcohol-related liver disease, and metabolic dysfunction-associated steatotic liver disease, all of which interact with environmental exposures across the life course. Biomarker discovery increasingly relies on integrated assessment of exposure-related signals together with genomic, epigenomic, transcriptomic, proteomic, metabolomic, and spatially resolved data. Hepatocarcinogenesis involves a complex interplay of chronic liver injury, environmentally patterned molecular perturbation, and dynamic tumor-host interactions. We emphasize an exposome-informed, multimodal strategy in which interpretable AI models identify clinically relevant signatures for early detection, prognostic stratification, and treatment guidance. Critical limitations of current evidence include incomplete exposure assessment, heterogeneous data platforms, retrospective study design, limited external validation, and insufficient model transparency. Emerging approaches, including proteogenomic, lipidomic, single-cell, and digital pathology-based modeling, show promise but require further validation in etiologically diverse cohorts. The purpose of this review is to critically examine how AI can integrate exposome-related information with multi-omics data for biomarker discovery in liver cancer. Here, particular attention is given to the exposure-to-biomarker sequence, immune-metabolic remodeling, liquid-biopsy translation, and the reduction of high-dimensional signatures into clinically deployable assays.

To evaluate the efficacy and postoperative survival following laparoscopic and laparotomy hepatectomy of pediatric liver neoplasm (PLN).

A retrospective analysis was conducted on 180 patients who underwent hepatectomy of PLN in our center between January 2014 and May 2025. Demographic information, perioperative clinical data, postoperative liver function recovery, complications, and survival outcomes were collected to evaluate the efficacy, postoperative complications, and survival rates after laparoscopic and laparotomy hepatectomy of PLN.

In this study, 89 patients (49.44%) were male and 91 (50.56%) were female. The median age at surgery was 5.7 years. 66 patients (36.67%) were diagnosed with benign liver neoplasms (BLN), and 114 patients (63.33%) with malignant liver neoplasms (MLN). Laparoscopy was performed in 83 patients (46.11%), while laparotomy was performed in 97 patients (53.89%). In the BLN group, there were no significant differences between the laparoscopic and laparotomy groups in terms of postoperative liver function recovery or complication rates. The postoperative survival rate was 100% in both groups. However, the length of hospital stay was significantly shorter in the laparoscopic group (P < 0.001). In the MLN group, there were no significant differences in postoperative liver function recovery or complication rates between the two surgical approaches. However, the laparoscopic group had a significantly longer operative time (P = 0.009), more frequent Pringle maneuver (P < 0.001). The 5-year cumulative survival rate was 78.13% in the laparoscopic group and 81.23% in the laparotomy group, with no significant difference between the two approaches (P = 0.732).

Surgical treatment for PLN yields favorable outcomes. Laparoscopy is recommended for BLN or MLN with localized lesions. However, for large MLN that encase vessels or show diffuse infiltration, laparotomy is recommended.

Lipomas are common benign mesenchymal neoplasms with slow growth, consisting of mature adipocytes, while giant inguinal lipomas are rare because of anatomical limitations. This report describes a 46-year-old woman who presented with a reducible left inguinal mass and an ipsilateral painless giant subcutaneous mass. She was diagnosed with a left indirect inguinal hernia and a separate inguino-labial lipoma superficial to the external oblique aponeurosis, which was not adherent to the inguinal canal, round ligament or canal of Nuck. The coexistence of the two lesions was incidental. The patient underwent combined laparoscopic totally extraperitoneal (TEP) hernia repair and TEP-guided transfascial lipoma excision. Histopathology verified a mature lipoma without atypia or features of liposarcoma. We summarize the clinical manifestations, diagnostic points, anatomy, surgical techniques, pathological results and clinical outcomes of this rare condition, and confirm that single-stage TEP-guided transfascial lipoma excision is a safe and feasible procedure.

Ubiquitin-specific protease 28 (USP28) is a deubiquitinating enzyme initially identified as a regulator that stabilizes p53 and c-MYC in response to DNA damage stress. Beyond its role in maintaining genomic integrity and cell cycle checkpoints, USP28 is implicated in diverse pathological processes. In various solid tumors, including lung, pancreatic, ovarian, and hepatocellular carcinomas, USP28 is markedly upregulated; it promotes proliferation, metabolic reprogramming, invasion, and therapeutic resistance by stabilizing oncoproteins such as c-Myc, STAT3, and SOX9. Conversely, in specific contexts like breast cancer and certain melanomas, USP28 deficiency drives malignant progression, revealing a context-dependent functional duality. These findings underscore the complexity of USP28 signaling and highlight its potential as a therapeutic target for precision medicine. This review summarizes the molecular characteristics and physiological functions of USP28, its context-dependent roles in neoplastic diseases, and its translational implications for targeted therapy and biomarker discovery.

Immune checkpoint blockade has transformed cancer therapy, yet many tumors remain intrinsically resistant or acquire resistance after initial response. Increasing evidence indicates that this failure is not determined solely by PD-1, PD-L1, CTLA-4, or T-cell exhaustion, but also by metabolically suppressive states within the tumor microenvironment. Tumor-derived metabolites can function as metabolic immune checkpoints by limiting effector immune activity, promoting regulatory or myeloid suppressive compartments, and weakening immunotherapy efficacy. This mini review summarizes recent experimental evidence showing how lactate, adenosine, tryptophan-derived metabolites, and nucleotide-derived metabolites shape immune escape and resistance to immune checkpoint blockade. Lactate links tumor glycolysis to Treg recruitment, impaired T-cell function, and lactylation-associated therapeutic resistance. The CD73-adenosine axis suppresses CD8⁺ T cells and natural killer cells while reinforcing regulatory and myeloid immune programs. Tryptophan-derived metabolites extend beyond the classical IDO1-kynurenine-AhR pathway to involve non-classical checkpoints such as Siglec-15 and broader kynurenine/indole/serotonin networks. Emerging evidence further identifies nucleotide-derived UDP signaling as a driver of macrophage-mediated immunosuppression. Finally, we discuss how targeting metabolic checkpoints in combination with immune checkpoint blockade may improve therapeutic responses. Defining the spatial and cellular contexts of metabolite-mediated immune suppression may enable more precise strategies to overcome immunotherapy resistance.

TGFBI in tumors, providing a comprehensive theoretical foundation for developing TGFBI-based precision diagnosis and treatment. Transforming growth factor-beta-induced protein (TGFBI) is a secreted extracellular matrix protein involved in various physiological and pathological processes. Its multiple roles in tumorigenesis and the remodeling of the tumor immune microenvironment (TIME) have recently drawn increasing attention. This review systematically compares the dual pro-tumor and tumor-suppressive functions of TGFBI across multiple cancer types and provides a comprehensive analysis of its immunomodulatory roles-particularly its recently identified function as a secreted immune checkpoint bridging extracellular matrix remodeling and immune suppression. By integrating evidence from single-cell and spatial transcriptomic studies, we elucidate the cell-type-specific expression patterns of TGFBI in the tumor microenvironment and propose a tumor-type-specific therapeutic stratification framework for TGFBI-targeted interventions. This review thus fills a critical gap by providing the first systematic integration of TGFBI's context-dependent functions with its translational implications.