Cisplatin-based chemotherapy is limited by toxicity and resistance.High-intensity focused ultrasound (HIFU) is a noninvasive ablation technique with potential to enhance chemotherapy efficacy.

To investigate the anti-tumor effects and mechanisms of cisplatin combined with HIFU in endometrial cancer.

Safe cisplatin concentrations and HIFU parameters were screened in HEEpiC-SV40 cells. Proliferation, apoptosis, migration, and invasion of Ishikawa cells were assessed using CCK-8, EdU, colony formation, TUNEL, wound healing, and Transwell assays. Pyroptosis-related markers and PI3K/AKT pathway activity were evaluated by Western blot, qRT-PCR, and ELISA. Therapeutic efficacy was further examined in a nude mouse xenograft model.

Cisplatin (5 μg/mL) combined with HIFU (1 MHz, 160 J) was identified as the optimal treatment condition. The combination significantly inhibited Ishikawa cell proliferation, migration, and invasion while promoting pyroptosis. Mechanistically, combined treatment suppressed PI3K/AKT pathway activation and increased pyroptosis-related markers. These effects were reversed by the pyroptosis inhibitor AZL-N. Moreover, PI3K/AKT activation with 740 Y-P attenuated the anti-tumor and pyroptosis-inducing effects of the combination. In vivo, cisplatin combined with HIFU markedly restrained xenograft tumor growth and promoted tumor pyroptosis, whereas 740 Y-P pretreatment counteracted these effects.

Cisplatin combined with HIFU suppresses Type I endometrial cancer progression by inhibiting PI3K/AKT signaling and promoting pyroptosis, supporting its potential as a novel combination therapeutic strategy.

Mitochondrial apoptosis is a key regulator of tumor progression, therapeutic resistance, and immune evasion in non-small cell lung cancer (NSCLC), yet promising candidate biomarkers remain inadequately defined. Using an integrative multi-omics systems biology framework, we identified 16 mitochondrial apoptosis-associated genes and uncovered a highly interconnected apoptotic network centered on MCL1, BCL2L1, BAX, CASP8, and CASP9. Comprehensive transcriptomic, genomic, and epigenetic analyses revealed recurrent genomic alterations, subtype-specific dysregulation, copy number variation-driven transcriptional changes, differential DNA methylation, and significant survival associations, highlighting their clinical relevance. Independent validation across external transcriptomic cohorts confirmed robust differential expression of the prioritized biomarkers, while physiological transcriptomic and protein atlas analyses demonstrated conserved transcript architecture, widespread tissue expression, and mitochondrial localization of MCL1. Importantly, spatial transcriptomic profiling in a mouse NSCLC model experimentally provided complementary evidence consistent with the computational findings by demonstrating markedly increased and spatially heterogeneous expression of MCL1, BCL2L1, and CASP9 within tumor tissues and their enrichment in distinct cellular populations, supporting their role in tumor heterogeneity and mitochondrial apoptosis regulation. Integrative analysis consistently prioritized MCL1 as the dominant mitochondrial apoptosis biomarker, with BCL2L1 and CASP9 emerging as additional high-confidence candidates and CASP8 and BAX serving as complementary prognostic biomarkers. These findings establish MCL1 as a promising candidate biomarker and promising precision therapeutic target, while demonstrating that the integration of multi-omics discovery with spatial transcriptomic validation provides a comprehensive molecular framework for apoptosis-driven precision oncology in NSCLC.

Contemporary models of tumor progression highlight the key role of the tumor microenvironment (TME) and the extracellular matrix (ECM) in regulating angiogenesis, metastasis, and immune resistance. Among ECM components, oncofetal fibronectin (FN) isoforms containing the EDA and EDB domains are of particular interest because they are highly expressed in solid tumors but absent from normal adult tissues. This review article synthesizes current data on the pathophysiological functions of FN variants in oncogenesis. Particular attention was paid to their role in pathological vascular remodeling, the induction of epithelial-mesenchymal transition (EMT), the formation of pre-metastatic niches, and the generation of an immunosuppressive environment. The study also critically assesses the clinical significance of FN as a biomarker and a potential target for new therapies in breast cancer, ovarian cancer and glioblastoma. The prospects for the use of innovative stromal strategies - including antibody-drug conjugates (ADCs) and immunocytokines - to overcome resistance to standard immunotherapy are also highlighted.

Sepsis is a life-threatening complication in breast cancer patients undergoing chemotherapy, particularly when compounded by anorectal conditions. The management of eroded mixed hemorrhoids in the setting of severe chemotherapy-induced neutropenia and septicemia presents a clinical dilemma, as standard surgical interventions carry prohibitive risks. This case report details a successful conservative, multimodal approach to this rare and critical scenario.

A 51-year-old female with stage IIIA human epidermal growth factor receptor 2-positive breast cancer developed a high fever (40.1°C) 1 week after her first cycle of neoadjuvant TCHP (docetaxel, carboplatin, trastuzumab, and pertuzumab) chemotherapy. She presented with severe bone marrow suppression and constipation, which led to the manual reduction of prolapsed hemorrhoids, resulting in an eroded, inflamed perianal mass.

The patient was diagnosed with septicemia (confirmed by Escherichia coli bacteremia), chemotherapy-induced grade IV bone marrow suppression (white blood cell count 0.17 × 109/L, platelet count 6 × 109/L), and mixed hemorrhoids with erosion and secondary perianal infection.

Given the high risk of surgery due to critical thrombocytopenia and neutropenia, a conservative strategy was implemented. This included broad-spectrum systemic antibiotics (meropenem, vancomycin, amikacin, amphotericin B sequentially), aggressive hematologic support (granulocyte colony-stimulating factor, blood transfusions), and meticulous multimodal local wound care. The local regimen comprised saline cleansing, infrared therapy, recombinant human epidermal growth factor gel, zinc oxide ointment, compound borneol ester suppositories, and the topical application of a self-prepared traditional Chinese medicine, "Liuhe Dan."

After 30 days of treatment, the patient became afebrile, and her perianal swelling and inflammation completely resolved. The eroded hemorrhoid healed entirely, allowing for a successful transfer to a lower-level hospital for continued supportive care.

This case demonstrates that in severely neutropenic and thrombocytopenic patients, a conservative, integrated approach combining systemic anti-infective therapy with advanced local wound care and traditional Chinese medicine can successfully manage life-threatening sepsis originating from eroded hemorrhoids. It underscores the critical importance of perianal hygiene, prompt management of chemotherapy-induced constipation and bone marrow suppression, and the potential of nonsurgical strategies in high-risk surgical candidates.

Colonic intussusception is a rare cause of intestinal obstruction in adults, and is frequently associated with an underlying malignancy. Mucinous adenocarcinoma (MAC) is an uncommon histological subtype of colorectal cancer, characterized by abundant extracellular mucin and unfavorable biological behaviors. However, its presentation as a lead point for an intussusception is rare. Here we describe a rare case of MAC causing colonic intussusception.

We describe the case of a 75-year-old woman with multiple comorbidities who presented with hematochezia, abdominal distension, intermittent colicky pain, and progressive weight loss.

Colonoscopy revealed a large intraluminal mass in the ascending colon, while contrast-enhanced computed tomography revealed ileocecal intussusception with ischemic features.

Emergency right hemicolectomy was performed. Histopathology confirmed a moderately differentiated MAC without lymph node metastasis. Molecular analysis revealed a p.Gly13Asp KRAS (KRAS proto-oncogene, GTPase; protein change: glycine to aspartate substitution at codon 13) mutation with microsatellite stability.

The patient's prolonged immobility due to dementia and prior hip fracture surgery likely contributed to chronic bowel hypomotility, potentially exacerbating symptoms.

This case presents an unusual occurrence of MAC causing adult colonic intussusception, highlighting how tumor biology may synergize with host-related factors such as immobility to accelerate clinical deterioration. Early recognition using endoscopy and computed tomography and timely surgical resection is essential to optimize outcomes.

The dysregulation of adenosine triphosphate (ATP) hydrolysis, a crucial process in energy metabolism, has been implicated in the complex landscape of tumor development and progression. This study aims to pinpoint crucial genes that characterize the ATP hydrolysis-driven molecular signature of hepatocellular carcinoma (HCC), with a view to examining their potential therapeutic applications in enhancing patient prognosis. Utilizing transcriptomic and clinical data from The Cancer Genome Atlas and Gene Expression Omnibus databases, a systematic framework was developed and validated for model construction and assessment. Univariate Cox regression analysis (P < .05) was performed on all 416 ATP hydrolysis-related genes (ARGs) to identify prognostically relevant genes. Following least absolute shrinkage and selection operator Cox regression with 10-fold cross-validation, an 11-gene signature was established, with the median training cohort risk score used as the cutoff for stratifying patients into high- and low-risk groups. Among 416 investigated ARGs, 85 displayed differential expression in HCC, with 179 demonstrating significant prognostic relevance (univariate Cox P < .05). Two distinct molecular subtypes, characterized by marked differences in prognosis and immune infiltration, were identified through unsupervised clustering. A refined 11-gene signature was constructed via least absolute shrinkage and selection operator Cox regression with 10-fold cross-validation (training area under the curve: 0.826/0.717/0.657 for 1/3/5 year; validation area under the curve: 0.608/0.603/0.621). These risk groups exhibited significantly divergent prognostic features, gene expression patterns, immune microenvironments, and drug sensitivities, suggesting the utility of this risk signature in predicting prognosis, drug responsiveness, and immune therapeutic outcomes. Ultimately, a nomogram incorporating the risk signature was devised, demonstrating favorable predictive performance in estimating HCC patient prognosis compared to other established prognostic factors. This study establishes a classification system and risk model grounded in ARGs, offering valuable insights into the prognosis and treatment responsiveness of HCC.

Artificial intelligence (AI) applications in pancreatic cancer are expanding rapidly, but the field's global structure and emerging priorities remain incompletely characterized.

The Web of Science Core Collection was searched through July 5, 2026. English-language original articles and reviews addressing AI in pancreatic cancer were eligible. After manual screening, 583 publications from 1998 to 2026 were analyzed using Biblioshiny, VOSviewer, and CiteSpace to assess publication trends, contributors, collaboration networks, co-citation patterns, keyword evolution, thematic clusters, and citation bursts.

Publication output accelerated after 2019 and reached 164 publications in 2025; the lower total in 2026 reflected partial-year coverage. The literature involved 59 countries, 1230 institutions, and 4038 authors. China produced the largest number of publications (n = 222), whereas the United States ranked second (n = 150) and had the highest country-level centrality (0.39). Shanghai Jiao Tong University was the most productive institution (n = 20), while Harvard University had the highest institutional centrality (0.22). Frontiers in Oncology was the most productive journal (n = 32). Influential studies focused on deep learning-based computed tomography, electronic health record-based risk prediction, exosome-based machine learning, and endoscopic ultrasonography. Research themes evolved from neural-network classification and texture analysis toward radiomics, deep learning, early detection, risk prediction, liquid biopsy, tumor biology, treatment-response prediction, and precision oncology.

AI research in pancreatic cancer is growing rapidly and becoming increasingly multidisciplinary, although productivity and collaboration remain uneven. Clinical translation will require prospective multicenter validation, representative datasets, transparent reporting, calibration, fairness assessment, workflow evaluation, and evidence of improved patient outcomes.

This bibliometric study aimed to map the global research landscape of immunotherapy for biliary tract cancers (BTC) from 2014 to 2023, identifying key contributors and emerging trends.

We analyzed 481 English-language articles retrieved from the Web of Science Core Collection (2014-2023) using CiteSpace. Parameters included coauthorship, co-citation, keyword co-occurrence, and burst detection.

Annual publications surged by 80% in 2021 versus 2020. China dominated output (50% of publications), with Fudan University as the top institution. Fan Jia was the most prolific author (7 papers). High-frequency keywords included gemcitabine (first-line chemotherapy), tumor microenvironment, and T cells. Burst keywords indicated emerging foci: tumor-infiltrating lymphocytes and growth factor receptor (e.g., HER2/ERBB2). The most co-cited study (Piha-Paul et al, 2020; 106 citations) reported pembrolizumab efficacy in BTC.

Research accelerated post-2020, driven by clinical trials. China, Fudan University, and Fan Jia are central to BTC immunotherapy research. Future priorities include targeting HER2 and the tumor microenvironment.

Central nervous system (CNS) involvement following blast crisis (BC) of chronic myeloid leukemia (CML) represents a challenging complication, particularly when atypical symptoms such as progressive vision loss obscure the diagnosis and delay timely intervention.

A 65-year-old male presented with isolated CNS relapse following CML-BC, manifesting as progressive visual loss. Despite being in intramedullary complete remission and having received prophylactic intrathecal chemotherapy, the patient's atypical ocular symptom raised suspicion of CNS involvement.

Cerebrospinal fluid (CSF) analysis confirmed the presence of blast cells, establishing the diagnosis of CNS relapse.

Treatment with intrathecal chemotherapy, systemic high-dose chemotherapy combined with tyrosine kinase inhibitor therapy.

The patient demonstrated visual recovery and sustained disease remission at the 14-month follow-up.

This case underscores the importance of clinical vigilance in patients with a history of leukemia who present with blurred vision or progressive vision impairment, as such manifestations,even in the absence of overt neurological symptoms, may be indicators of CNS relapse. Additionally, further investigation through animal models is warranted to characterize the blood-brain barrier penetrance of novel tyrosine kinase inhibitors (TKIs).

Lung cancer is one of the most prevalent malignancies globally and imposes a substantial burden on mortality and healthcare costs. Emerging clinical evidence suggests that lung cancer may influence brain morphology, particularly the cerebral cortex. This study employed Mendelian Randomization (MR) to investigate the potential causal relationship between lung cancer and cortical structural alterations. Single nucleotide polymorphisms associated with small cell lung cancer (SCLC) and non-SCLC (NSCLC) were instrumental variables derived from the FinnGen consortium. Summary-level data on brain cortical structures were obtained from the Enhancing Neuroimaging Genetics through Meta-Analysis consortium. MR analyses were conducted using inverse variance weighted regression, MR-Egger regression, and weighted median methods. SCLC was associated with a reduced surface area of the rostral anterior cingulate cortex (β = -0.038, 95% confidence interval [CI]: -0.057--0.019; false discovery rate-corrected P = .007). For NSCLC, we observed nominal associations with decreased cortical thickness in the paracentral (β = -0.032, 95% CI: -0.056--0.008; P = .008) and transverse temporal regions (β = -0.032, 95% CI: -0.056--0.008; P = .009), and an increased surface area of the lingual gyrus (β = 0.028, 95% CI: 0.002-0.054; P = .034). Sensitivity analyses showed no evidence of directional pleiotropy, and leave-one-out tests indicated that results were not driven by single instruments. Mediation analyses provided no support for indirect effects via insomnia, anxiety, or depression. Our findings support a causal link between SCLC and reduced rostral anterior cingulate cortex surface area and suggest additional NSCLC-related cortical alterations in sensorimotor, auditory, and visual regions. These results highlight potential neuropsychiatric and cognitive implications in lung cancer and warrant further mechanistic investigation.