Pathological complete response (pCR) following neoadjuvant chemoradiotherapy (nCRT) in locally advanced rectal cancer (LARC) is a key prognostic marker with implications for response-adapted management. Although magnetic resonance imaging (MRI) is central to response assessment, differentiating residual tumour from treatment-related changes remains challenging. Artificial intelligence (AI) and machine learning (ML) models applied to MRI show promise in predicting pCR; however, variability in methodology and performance limits clinical translation.

A search of Embase, Medline, Cochrane and Web of Science was conducted in April 2025 in accordance with Preferred Reporting Items for Reviews and Meta-Analysis (PRISMA) guidelines. Eligible studies used MRI-only AI or ML models to predict pCR following chemoradiotherapy in adults with rectal cancer. Screening, full-text review and data extraction were performed independently by two reviewers. Risk of bias was assessed using Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2).

Twenty-two studies comprising 94 predictive models were included. Most studies were retrospective, used T2-weighted MRI and demonstrated variability in MRI protocols, modelling methods and validation strategies. Only five studies conducted external validation. Median AUC was 0.801, with performance ranging from poor to excellent (AUC 0.49-0.997).

MRI-based AI models demonstrate moderate discriminative performance for predicting pCR following neoadjuvant therapy in LARC. However, methodological heterogeneity, inconsistent reporting and limited external validation currently hinder generalisability. Greater methodological standardisation and multicentre external validation are required before clinical implementation.

Due to the unclear mechanism of uterine fibroids, more risk factors need to be clarified. This study explored associated factors of uterine fibroids and established a prediction model using clinical data from our institution.

Logistic and Least Absolute Shrinkage and Selection Operator (LASSO) analyses were used to screen the key associated factors of uterine fibroids. The receiver operating characteristic (ROC) curve and DeLong test were used to analyze the prediction performance of indicators. XGBoost classification and random forest were used to rank the feature importance. A prediction model based on the key factors was established. Decision Curve Analysis (DCA), ROC, and nomogram analysis were used to assess the performance of model for predicting uterine fibroids.

Of the 303 patients enrolled, 201 had uterine fibroids. Logistic and LASSO regression analyses identified 5 core risk indicators, including age, thyroid-stimulating hormone index (TSHI), number of deliveries, abnormal menstruation, and polycystic syndrome. Both ROC and feature importance ranking analyses consistently implied the importance of age and TSHI on uterine fibroid risk. With the increase of age and TSHI, the uterine fibroids risk was significantly increased (all P for trend<0.05). The combination of age and TSHI achieved favorable performance and clinical net benefit in fibroids risk prediction, and its favorable performance was also validated in the external National Health and Nutrition Examination Surveys database.

Age and TSHI were the key associated factors of uterine fibroids, and their combination had promising clinical value for predicting uterine fibroids risk.

Central lymph nodes metastasis (CLNM) is common in papillary thyroid. Microcarcinoma (PTMC). Whilst prophylactic central lymph node dissection (CLND) can prevent further CLNM, it remains controversial. An accurate model to predict CLNM is therefore necessary for patients with PTMC.

This study incorporated 228 patients with general clinical information, thyroid related serological examination and ultrasound of CLNM prediction, divided into training and validation sets randomly at 7:3 ratio. Least Absolute Shrinkage and Selection Operator (LASSO) regression was used for key features screening. Eight machine learning models were developed, evaluated by cross-validation and performance comparison (the area under curve, calibration curve and decision curve analysis). Shapley Additive exPlanations (SHAP) value analysis provided the interpretability of the model.

Age, gender, tumor diameter, T3, T4, TPOAb and ultrasound of CLNM prediction were identified as key features of CLNM in patients. Support Vector Machine (SVM) model with 0.783 accuracy and 0.805 specificity in validation set was considered as the most favorable performance. Age, gender and tumor diameter were the top three contributing variables in SVM model.

This study established a machine learning-based framework for predicting CLNM in PTMC, with the SVM model demonstrating superior stability and clinical utility among the evaluated algorithms. While these results are preliminary, they provide a promising tool to assist in tailoring prophylactic CLND strategies, potentially reducing unnecessary surgical intervention.

Histone lactylation, a recently identified post-translational modification, is closely linked to the pathogenesis and progression of malignant tumors, making it a promising therapeutic target for acute myeloid leukemia (AML). Increasing clinical and experimental evidence indicates that elevated serum lactate dehydrogenase (LDH) levels serve as both a diagnostic biomarker and an indicator of poor prognosis in AML, reflecting enhanced glycolytic activity and chemotherapy resistance. Patrinia scabiosaefolia Fisch (PS), a traditional medicinal herb, exhibits broad pharmacological activities, including heat-clearing, detoxifying, antibacterial, antiviral, and antitumor effects. However, the molecular mechanisms underlying its antileukemic activity, particularly in AML, remain insufficiently defined. To elucidate how DEPS exerts therapeutic effects in AML through the HIF-1α-histone lactylation axis, we systematically established the association between DEPS-mediated inhibition of histone lactylation and cellular hypoxia. Lactylation pan-antibody incubation confirmed preliminarily that DEPS significantly inhibits histone lactylation modification. Lactate restoration experiments further demonstrated that DEPS markedly suppresses lactate-induced activation of HIF-1α signaling, reducing downstream metabolic proteins and VEGFA expression. Under hypoxic conditions, AML cells displayed increased proliferation and histone lactylation, both of which were attenuated by DEPS treatment. Sodium L-lactate enhanced the expression of HIF-1α and its downstream effectors (HK2, PDK1, PKM2, GLUT1, LDHA, and VEGFA), whereas subsequent DEPS exposure significantly reversed these changes. Ultimately, DEPS inhibits H3/H4 lysine lactylation, induces G2/M cell-cycle arrest, and promotes apoptosis in THP-1 and HL-60 cells, including doxorubicin-resistant HL-60 cells. Collectively, our findings reveal previously uncharacterized antileukemic mechanisms of DEPS involving suppression of the HIF-1α signaling pathway and histone lactylation. These results highlight the importance of epigenetic regulation in AML and support the therapeutic potential of DEPS in AML treatment and reversal of chemoresistance.

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors worldwide. Both experimental and clinical studies confirm the anti-HCC effects of Yiguanjian (YGJ), though its material basis and pharmacological mechanisms remain unclear. This study integrated UHPLC-Q-TOF-MS with network pharmacology, molecular docking, and MDS to explore YGJ's potential anti-HCC mechanisms and active ingredients. In vitro analysis identified 96 chemical constituents in the YGJ extract, while network pharmacology revealed 57 potential targets and 51 bioactive compounds related to HCC treatment. The top nine key targets were AKT1, CTNNB1, EGFR, IL6, STAT3, BCL2, CASP3, MMP9, and TNF-α; the top seven active compounds included kaempferol, quercetin, luteolin, senkyunolide O, jasmolone, azaron, and dihydroartemisinin. These components may regulate HCC cell processes like gene expression, signal transduction, proliferation, apoptosis, and angiogenesis through pathways such as PI3K-Akt, TNF signaling pathway, and HIF-1 signaling pathway. Molecular docking and MDS showed that kaempferol, quercetin, luteolin, and dihydroartemisinin bind favorably to TNF-α, MMP9, BCL2, and IL6 proteins. Therefore, these proteins may serve as YGJ's therapeutic targets, while the compounds contribute to its pharmacological effects.

De Garengeot's hernia is a femoral hernia involving the appendix. An appendiceal mucinous neoplasm within this hernia is exceptionally rare. We report a case of a 68-year-old woman presenting with a right inguinal mass. Ultrasonography identified the appendix within the femoral hernia sac, appearing as a tubular hypoechoic structure with inflammatory changes and a blind end tracing to the cecum. Contrast-enhanced Computed tomography (CT) revealed a well-defined cystic mass in the right femoral hernia with enhancing walls and septa and non-enhancing internal content, findings suggestive of an appendiceal mucinous neoplasm. Intraoperatively, a femoral hernia containing the appendix (De Garengeot's hernia) was identified. Postoperative pathology confirmed a distal low-grade appendiceal mucinous neoplasm within the appendix. This case highlights the complementary value of ultrasonography and CT in preoperative diagnosis and aims to improve recognition of femoral hernias by demonstrating key diagnostic features on retrospective image analysis-including localization of the hernia sac inferior to the inguinal ligament on CT and identification of the appendiceal lumen abruptly closing at the femoral ring on ultrasound-thereby enabling informative imaging reports to guide optimal clinical management.

Hodgkin lymphoma (HL) is prevalent worldwide and typically presents symptoms like sudden pain, swelling, and weight loss. Classical HL (cHL) is largely treatable with modern risk-adapted and response-based therapy. cHL represents one of the most common malignancies occurring during the course of evolution in patients living with HIV. The present manuscript aimed to present the diagnostic work-up with an emphasis on flow cytometry in patients with HIV-associated lymphoma, of important clinical benefit both in the HIV-endemic setting as well as in state-of-the-art pathology departments. Three clinical cases of HIV patients, including HIV-associated cHL, are presented in the chapter dedicated to HIV-induced lymphomas diagnosed by FC, as Supporting Information, to support the particularities of the abundance of clonal B-cell populations among different types of HIV-related lymphomas. This adds to the proof-of-concept that the specific antibody panel design may help practitioners in discriminating among similar subtypes of HIV-associated lymphomas. Recent data emphasise the importance of FC detection of cHL rapidly and effectively, adding diagnostic value to these small biopsies. FC is an important tool for clinical decision-making in the management of HL patients, providing a noninvasive and accurate biomarker evaluation. For these considerations, we can conclude that FC is a very useful research tool, and the clinical cases presented in this paper indicate their importance in the rapid diagnosis of cHL as well.

Aripiprazole (ARI), an atypical antipsychotic, has demonstrated anticancer activity in several malignancies and may be a candidate for drug repurposing as an intravesical therapy for bladder cancer, particularly non-muscle-invasive bladder cancer (NMIBC). This study evaluated whether brief, intravesical-like ARI exposure could induce cytotoxic effects in bladder cancer cells while preserving normal bladder structure and function. RT4 and T24 bladder cancer cells, together with non-malignant UROtsa urothelial cells, were exposed to ARI (1-300 μM) for 30 min or 2 h, and viability was assessed at 24, 48 and 72 h. Reactive oxygen species (ROS) generation was measured in RT4 and T24 cells after 2 h pretreatment, while caspase-3 activity and stress-associated protein expression were examined in T24 cells. In parallel, an ex vivo porcine bladder model was used to assess the effects of luminal ARI pretreatment (300 μM, 2 h) on urothelial thickness, ATP and acetylcholine release, detrusor contractility, β-adrenergic relaxation, and nerve-evoked responses. ARI reduced viability in a concentration-dependent manner in RT4, T24 and UROtsa cells, with greater cytotoxicity after 2 h pretreatment. In bladder cancer cells, ROS increased only at higher concentrations, whereas ARI increased caspase-3 activity at lower concentrations and altered multiple stress-related proteins in T24 cells. In porcine bladder, ARI preserved urothelial structure and mediator release, maintained detrusor and neurogenic function, and enhanced the inhibitory influence attributed to urothelium-derived inhibitory factor (UDIF). Collectively, these findings identify ARI as a mechanistically active yet bladder-sparing candidate for intravesical repurposing and support its further evaluation as a potential therapy for bladder cancer.

Cervical cancer treatment is often hindered by the emergence of cisplatin (DDP) resistance. Increasing evidence has indicated that statins possess anti-tumor and chemosensitization potential beyond their lipid-lowering effects. Statin utilization is found to be significantly linked to decreased cervical cancer incidence and mortality. However, whether statins affect chemosensitivity to cisplatin in cisplatin-resistant cervical cancer remains to be clarified. In cervical cancer cisplatin-resistant cell lines (SiHa-DDP and C33a-DDP) constructed from their parental cells, the effects of seven statins (simvastatin, fluvastatin, pitavastatin, lovastatin, atorvastatin, rosuvastatin, and pravastatin) on cell viability in cisplatin-resistant cells and corresponding parental cells were assessed using the CCK-8 assay. Compared with parental counterparts, the IC₅₀ values of seven statin drugs were markedly elevated in cells exhibiting cisplatin resistance. Simvastatin significantly enhanced the efficacy of cisplatin in cisplatin-resistant cervical cancer cells, demonstrating a synergistic anti-cancer effect (CI < 1). Combined therapy using simvastatin and cisplatin inhibited cell viability and migration while promoting cell apoptosis. Mechanistically, simvastatin downregulated protein expressions of caveolin-1 (CAV1), PI3K, and p-AKT. CAV1 knockdown in SiHa-DDP and C33a-DDP cells markedly increased cisplatin sensitivity, confirming its critical role in chemoresistance. Rescue experiments showed that CAV1 overexpression partially counteracted the inhibitory effects of simvastatin. In vivo, compared with monotherapies, simvastatin combined with cisplatin treatment markedly suppressed tumor growth, reduced CAV1 protein expression, decreased the percentage of Ki67-positive cells and promoted apoptosis. In all, simvastatin enhanced cisplatin sensitivity by suppressing the CAV1-mediated PI3K/AKT pathway involvement in the development of cisplatin resistance in cervical cancer cells. These findings reveal a novel mechanism in cervical cancer cells resistant to cisplatin by which simvastatin may serve as a potential adjuvant to improve the therapeutic efficacy of cisplatin-based chemotherapy.

Gastric cancer (GC) is the fifth most diagnosed malignancy and the fifth leading cause of cancer-related deaths, with a poor overall survival of under one year. Metastatic tumors that arise from malignant primary tumors account for the majority of cancer-related deaths for GC. Hypoxia-inducible transcription factors (HIFs), including HIF-2α, and integrin such as ITGβ5 play important roles in tumor metastasis. However, the regulatory relationship and functional significance between HIF-2α and ITGβ5 in GC remain poorly understood. We analyzed TCGA RNA-seq data to identify hypoxia-related biological processes and signaling pathways in GC. Exosome proteomics was used to characterize the protein profiles of extracellular vesicles (EVs) derived from GC cells under hypoxia. Under hypoxic conditions, ITGβ5 expression in GC showed a positive correlation with HIF-2α levels. Clinical analysis confirmed the overexpression of ITGβ5, which was further validated by RT-qPCR, western blot, and flow cytometry. The chromatin immunoprecipitation (ChIP) was performed to confirm the binding of HIF-2α to the promoter of ITGβ5. The role of ITGβ5 in GC cell proliferation, invasion, and migration was investigated through gain- and loss-of-function studies conducted both in vivo and in vitro. Our results showed that HIF-2α directly binds to the promoter of ITGβ5, thereby transcriptionally activating its expression. In vivo and in vitro studies revealed that the overexpression of ITGβ5 significantly enhanced the invasion, migration, and growth of GC. Our study uncovers a novel pathway in which hypoxia-induced activation of HIF-2α promotes the proliferation, invasion, and metastasis of GC by directly upregulating the expression of exosomal ITGβ5. Given these findings, ITGβ5 may serve as a potential prognostic biomarker and therapeutic target for GC.