This systematic review was conducted to inform the development of clinical practice guidelines on the management of extravasation of antineoplastic agents in patients with cancer.

PubMed®, Embase®, CINAHL®, and Cochrane databases were searched for eligible studies from June 2014 to June 2024. Citations of guidelines and a previous systematic review were reviewed for records that met eligibility criteria. Two reviewers independently screened titles, abstracts, and full texts for inclusion.

Two independent reviewers assessed all studies that met inclusion criteria using the Risk of Bias in Nonrandomized Studies of Interventions for cohort studies and JBI critical appraisal tool for case series. The certainty of evidence was assessed using GRADE (Grading of Recommendations Assessment, Development, and Evaluation) methodology.

For patients who have an extravasation of an antineoplastic agent, although there is very low certainty in the evidence overall, interventions include administration of an antidote, compress, and surgical referral or escalation of care for extravasation of central lines.

Antidotes, application of a compress, and referral for surgical or wound care are effective strategies for managing extravasation of antineoplastic agents.

CD19-targeted chimeric antigen receptor-T cell (CART19) therapy is clinically effective in patients with relapsed or refractory B-cell lymphoma (BCL), but treatment failure and recurrence need to be overcome. Preclinical studies demonstrated that Bruton tyrosine kinase inhibitor (BTKi) improved the efficacy of CART19 therapy.

We designed this open-label, non-randomized pragmatic clinical trial. The primary end point was safety, and the secondary end point was clinical response.

Thirty-seven patients included were assigned to CART19 monotherapy (n = 24) or CART19 combined with BTKi (n = 13) group on their own accord. Grade 1-2 and grade 3 cytokine release syndrome occurred in 43.2% and 2.7% of patients, respectively. One patient experienced grade 3 neurotoxicity. The most common severe adverse events were hematological toxicities, including neutropenia (in 97.3% of patients), thrombocytopenia (in 40.5%), and anemia (in 43.2%). The adverse effects were comparable between the two groups. The best objective response rates were 84.6% vs. 66.7% (p > 0.05) in patients with and without BTKi, and the best complete response rates were 61.5% vs. 25.0% (p < 0.05). The combination of BTKi significantly prolonged the overall survival but did not affect the progression-free survival or the duration of response. T cells of patients treated with BTKi were predisposed to early differentiation and less exhaustion 3 months after CART19 infusion. Single-cell RNA sequencing analysis demonstrated that T cells were dysfunctional at relapse.

BTKi combined with CART19 induced better outcomes with good safety profiles in patients with BCL.

ClinicalTrials.gov identifier: NCT05020392.

Kaposiform haemangioendothelioma (KHE) research faces challenges due to the lack of established cell lines and suitable animal models. Our study aimed to establish KHE cell lines, spheroids and refine murine models to mimic disease characteristics, advancing our understanding of KHE pathogenesis and exploring novel therapies. Primary KHE cells were sorted using CD31 antibodies and cultured into spheroids. These cells were then injected into mice, and the resulting tumours were analysed using immunohistochemistry. Preliminary exploration of the potential mechanisms of sirolimus action on KHE was conducted through transcriptome sequencing. CD31+ KHE cells were isolated and characterised from three out of six patients. The CD31+ KHE cells demonstrated positive expression of essential markers such as CD31, Ki67 and LYVE1, consistent with the profiles observed in KHE tumours. Additionally, subcutaneous tumours displayed similar positive expression of key markers, reminiscent of KHE tumours. Transcriptome sequencing revealed downregulation of ATG9B after sirolimus treatment in CD31+ KHE cells. CD31+ KHE cells can replicate human KHE in murine models, offering a valuable tool for studying pathogenesis. Our findings also suggest a potential mechanism of sirolimus action in treating KHE, warranting further investigation into novel therapeutic strategies.

Chronic Myeloid Leukaemia is driven by the BCR::ABL1 fusion gene. Although Tyrosine Kinase Inhibitors have significantly improved patient outcomes, drug resistance and disease persistence remain challenges, highlighting the need for effective preclinical models. We observed cellular heterogeneity among CML models in response to TKIs, influencing viability, metabolism, and molecular markers. With growing interest in extracellular vesicles as mediators of leukaemia progression via oncogenic cargo like BCR::ABL1, we explored whether EVs from different CML cell lines exhibit distinct features. EVs from K562 and KCL22 cells were characterised under basal conditions using Fourier Transform Infrared spectroscopy, Atomic Force Microscopy, dot blotting, and Nanoparticle Tracking Analysis. We assessed EV release and BCR::ABL1 content before and after treatment with imatinib, nilotinib, or dasatinib, alongside Ki67 expression to gauge proliferation. Fourier Transform Infrared Spectroscopy with Principal Component Analysis revealed distinct clustering of EVs by cell line. While untreated K562 and KCL22 cells showed similar EV output and BCR::ABL1 content, post-treatment K562 cells released more EVs with elevated BCR::ABL1 transcripts. KCL22 cells showed earlier reduction in Ki67 expression. These findings highlight model-dependent EV behaviour, reflecting patient heterogeneity and reinforcing the need for careful model selection in CML research.

Targeted drug delivery systems have garnered increasing research interest in cancer threapy. Bacteria have emerged as a promising vehicle due to their innate ability to the tumour microenvironment (TME) and their intrinsic immune-stimulating properties. This review explores the application of bacteria in oncology, emphasizing the tumour-targeting behaviour of specific strains, their immunomodulatory functions, and their potential as delivery platforms for the controlled release of therapeutic agents.

This review synthesizes recent advances in bacteria-mediated cancer therapy, focusing on the mechanisms underlying bacterial targeting of hypoxic and immunosuppressive regions within the tumor microenvironment (TME). We discuss how genetic modification has been employed to design recombinant bacterial strains with enhanced tumor specificity and amplified therapeutic effects. Furthermore, the integration of bacteria with nanotechnology has facilitated the development of hybrid systems capable of targeted drug delivery and triggered-release mechanisms. The combination of bacterial therapy with other treatment modalities-such as photodynamic (PDT) and sonodynamic therapies (SDT)-is also examined, emphasizing their synergistic potential in overcoming tumor heterogeneity and enhancing anti-tumor immunity. Finally, we survey the current clinical progress of bacteria-based therapeutics and offer perspectives on the future role of artificial intelligence (AI) in improving the design and application of these living medicines.

Bacteria-based delivery systems represent a multifunctional and innovative strategy in the evolution of targeted cancer therapies. Through genetic modification and nanobiotechnology approaches, bacteria can be customized to mediate multi-effect synergistic treatments for cancer, enhancing the precision, safety, and efficacy of cancer therapies. With the ongoing integration of advanced technologies, including AI, there is great potential to overcome existing limitations and accelerate the clinical translation of bacterial anticancer therapies. This interdisciplinary effort is poised to open new avenues for next-generation cancer treatments and lay the foundation for future directions in cancer research and therapeutic practice.

Bacteria exhibit inherent tumour-targeting capabilities, particularly thriving in hypoxic tumour microenvironments (TMEs) and activating potent anti-tumour immune responses through pathogen-associated molecular patterns (PAMPs) and immunomodulation. Genetic engineering and nanobiotechnology enable advanced bacterial therapies, allowing for reduced toxicity, controlled proliferation, targeted drug delivery and the expression of therapeutic payloads (e.g., cytokines, enzymes, tumour antigens) within tumours. Bacteria serve as versatile platforms for multi-modal synergistic therapy, effectively combining with immunotherapy, photodynamic therapy (PDT), thermodynamic therapy (TDT), photothermal therapy (PTT) and sonodynamic therapy (SDT) to significantly enhance tumour eradication. Artificial intelligence (AI) is poised to revolutionise bacterial cancer therapy, offering powerful tools for optimising synthetic biology designs (e.g., promoters, gene circuits), nanocarrier engineering and predicting bacterial-host interactions for more effective and safer treatments.

Mucosal melanoma is an aggressive Malignancy arising from melanocytes in mucosal membranes. Sinonasal mucosal melanoma accounts for approximately 1% of all melanomas and 4% of all sinonasal tumors. Unlike cutaneous melanoma, its etiology remains unclear, and it is often diagnosed at an advanced stage owing to nonspecific symptoms, leading to poor prognosis.

We present the case of an 80-year-old African female with nasal obstruction and recurrent epistaxis for 6 months. Clinical examination and imaging revealed an enhancing soft tissue sinonasal lesion with osseous destruction. Functional endoscopic sinus surgery was performed for tumor debulking, and histopathological analysis confirmed mucosal melanoma with immunohistochemical positivity for HMB45. Despite surgical intervention, the patient was placed on home care owing to the aggressive nature of the disease and limited treatment options. Imaging confirmed local invasion but no distant metastases.

Sinonasal mucosal melanoma is an aggressive entity requiring early diagnosis and multimodal management. Surgical resection remains the primary treatment, but novel therapeutic strategies, including immune checkpoint inhibitors, are needed to improve patient outcomes.

Triple-negative breast cancer (TNBC), is characterized by its highly aggressive nature, with chemotherapy resistance and immune evasion contributing to poor outcomes. The role of major histocompatibility complex class I (MHCI) downregulation in TNBC progression remains incompletely understood.

The present research focused on elucidating the roles of miR-518c-5p/miR-4524a-3p in immune evasion and chemoresistance in TNBC, and evaluating their clinical significance.

Bioinformatics analysis predicted miRNAs targeting HLA-A/B/C, validated by dual-luciferase assays. Functional studies in TNBC cell lines (MDA-MB-231/468 and ADR-resistant sublines) included chromium release, proliferation, invasion, and apoptosis assays. Clinical relevance was assessed in 88 TNBC patients and 88 controls using RT-PCR and survival analysis.

MiR-518c-5p/miR-4524a-3p directly targeted HLA-A, HLA-B, and HLA-C, downregulating MHCI expression and promoting immune evasion. Overexpression of miR-518c-5p/miR-4524a-3p enhanced TNBC cell proliferation, invasion, and chemoresistance to doxorubicin, while their inhibition reversed these effects. High expression of miR-518c-5p/miR-4524a-3p correlated with adverse clinical outcomes in TNBC patients, including shorter recurrence-free survival.

MiR-518c-5p/miR-4524a-3p contribute to TNBC progression by facilitating immune evasion and chemoresistance. Targeting miR-518c-5p/miR-4524a-3p may represent a promising therapeutic approach for improving TNBC treatment outcomes.

Giant cell tumor of bone is a locally aggressive bone tumor characterized by the proliferation of round-to-oval mononuclear cells and uniformly distributed osteoclast-type giant cells. Giant cell tumor of bone typically arises in long bones, whereas craniofacial involvement is rare. Atypical histological and clinical presentations can complicate diagnosis. This study presents a challenging case of giant cell tumor of bone in the mandible.

A Japanese man in his 70s presented with a slowly expanding radiolucent lesion in the left mandible, first noted a decade ago, with no subjective symptoms. Cone-beam computed tomography revealed a 27 mm × 12 mm × 23 mm radiolucent lesion with irregular borders and discontinuity of the mandibular canal. Excisional biopsy showed the proliferation of bland spindle cells with small multinucleated cells, which indicated central giant cell granuloma. However, the spindle cells were positive for H3.3G34W, a specific marker of giant cell tumor of bone, which confirmed the diagnosis of giant cell tumor of bone. Conventional histological features of giant cell tumor of bone were absent throughout the observation period.

Morphological analysis alone is insufficient for diagnosing giant cell tumor of bone, and H3.3G34W immunostaining is valuable in distinguishing it from other giant cell lesions. The possibility of giant cell tumor of bone should not be ruled out in cases involving the jaw, although its occurrence is rare.

Gastric cancer (GC) predominantly contributes to cancer mortality, with adenocarcinomas accounting for more than 95% of incidences. Early detection improves survival, but most cases are diagnosed at advanced stages due to subtle symptoms and rapid progression. The role of TIGD6 in GC is unclear.

We analyzed TIGD6 expression using TCGA data and correlated it with clinical features and outcomes in GC patients. Bioinformatics tools, including GSEA and single-cell sequencing, were used to elucidate TIGD6's role in GC. In the GC cell lines AGS and HGC-27, TIGD6 was knocked down using RNA interference, and subsequent in vitro experiments were conducted to evaluate cell proliferation, migration, and invasion capabilities.

The expression of TIGD6 was markedly elevated in GC tissues relative to normal tissues (p < 0.001). Higher TIGD6 levels were linked to residual tumors (p = 0.027), history of reflux (p = 0.019), and antireflux treatment (p = 0.0012). Increased TIGD6 expression was associated with decreased overall survival (OS, p = 0.009) and disease-specific survival (DSS, p = 0.008), and it served as an independent predictor of worse OS (p = 0.043). Knocking down TIGD6 in GC cells suppressed proliferation, migration, and invasion, while enhancing apoptosis through modulation of the Hedgehog signaling pathway.

TIGD6 is overexpressed in GC and linked to unfavorable outcomes. It could potentially function as a biomarker and therapeutic target for this malignancy. Future studies should validate its clinical relevance and explore its detailed molecular mechanisms. Collectively, this study provides the first functional, mechanistic, and immune-phenotypic characterization of TIGD6 in GC, positioning it as a dual biomarker and therapeutic target.

Osteosarcoma (OS), the most prevalent primary malignant bone tumor in adolescents, demonstrates aggressive clinical behavior and poor prognosis. This study aimed to elucidate the functional role and molecular mechanism of miR-18b-3p in OS pathogenesis.

The miRNA microarray data from the GEO database were evaluated through GEO2R. The expression patterns of miR-18b-3p and PTEN were systematically analyzed using RT-qPCR and western blotting. A dual-luciferase reporter assay validated the direct targeting relationship between miR-18b-3p and PTEN 3'-UTR. Functional experiments included CCK-8, wound healing, and transwell invasion assays, and xenograft mouse models. Bioinformatics predictions were further supported by Gene Ontology enrichment analysis, protein-protein interaction network construction, and single-cell RNA sequencing analysis.

Integrated bioinformatics interrogation identified miR-18b-3p as a prognostically characteristic gene, with its overexpression strongly correlating with reduced overall survival in OS patients (p = 0.046). Clinical specimens and cellular models revealed marked upregulation of miR-18b-3p in OS tissues and cell lines (U2OS, MG63, HOS, SAOS2) compared to normal controls. PTEN was subsequently identified as a direct downstream target through complementary binding site verification, showing inverse correlation with miR-18b-3p expression. Functional experiments demonstrated that miR-18b-3p overexpression significantly enhanced malignant phenotypes, including cellular proliferation, migration, and invasion capacity, while PTEN restoration effectively reversed these oncogenic effects. Additionally, OS cells (HOS and SAOS2) secreted miR-18b-3p, and this paracrine mechanism potentially reprogrammed the tumor microenvironment through suppressing PTEN expressed in various immune and stromal cells.

Our findings establish miR-18b-3p as a novel oncogenic regulator in OS pathogenesis through direct PTEN targeting, highlighting its potential as a therapeutic target.