Accurate assessment of axillary lymph node (ALN) metastasis is essential for developing an effective treatment strategy for breast cancer (BC). Despite advancements in imaging and surgical techniques, a critical need remains for reliable, non-invasive methods to predict axillary response to neoadjuvant therapy (NAT). This study aimed to identify key factors influencing axillary lymph node pathological complete response (pCR) following NAT and to develop a predictive model for axillary pCR (apCR) to support clinical decision-making regarding the necessity of axillary lymph node dissection (ALND).

Clinical data from female patients diagnosed with breast cancer (BC) between January 2019 and December 2024 were retrospectively collected. All patients had biopsy-confirmed metastasis to ipsilateral axillary lymph nodes at initial presentation, received standardized neoadjuvant therapy (NAT), and subsequently underwent ALND. Patients were randomly divided into a training set (n = 354) and a test set (n = 151) in a 7:3 ratio. Based on ALND results, patients were classified into the apCR (axillary pathological complete response) and non-apCR groups, and their clinicopathological and magnetic resonance imaging (MRI) features were compared. Independent predictors of apCR were identified using multivariate logistic regression analysis, and feature selection was performed using the Least Absolute Shrinkage and Selection Operator (LASSO) method. Two predictive models were developed, a Clinical-Pathological-MRI model and a Clinical-Pathological-Delta-MRI model. The predictive performance of both models was evaluated and compared.

A total of 505 patients were enrolled, including 237 patients in the apCR group and 268 in the non-apCR group. The AUC values for the Clinical-Pathological-MRI model were 0.817 in the training set and 0.680 in the test set. For the Clinical-Pathological-Delta-MRI model, the AUC values were 0.844 in the training set and 0.793 in the test set, indicating superior predictive performance. Decision curve analysis (DCA) further demonstrated that the Clinical-Pathological-Delta-MRI model provided greater net clinical benefit compared to the Clinical-Pathological-MRI model in both the training and test sets.

This model may provide valuable support for individualized surgical decision-making and help guide the selective omission of axillary lymph node dissection in appropriate candidates.

Malignant pleural effusion (MPE) is characterized by the accumulation of fluid in the chest cavity, secondary to metastasis from a primary pleural tumor or malignant neoplasms originating from other anatomical sites. MPE is associated with a poor prognosis. Consequently, timely and effective prevention and management of MPE are critical. In Western medicine, the treatment of MPE primarily involves procedures such as surgical puncture for drainage, pleural fixation, chemotherapy, and targeted therapy. In contrast, traditional Chinese medicine (TCM) offers therapeutic modalities including oral decoctions, thoracic perfusion with herbal injections, topical applications of medicinal pastes, and acupoint therapies. The TCM approaches have demonstrated satisfactory clinical outcomes. Advances in the study of TCM for managing MPE in lung tumors are expected to yield a wealth of therapeutic strategies, facilitating the development of more optimized clinical treatments.

Esophageal cancer (EC) remains a significant clinical challenge, characterized by its aggressive nature and poor prognosis. Current therapeutic strategies, including targeted therapies, have limitations due to the complex interplay between tumor heterogeneity and the tumor microenvironment (TME). However, the specific contributions of N6-methyladenosine (m⁶A) methylation to the TME in EC are yet to be fully elucidated.

Through comprehensive bioinformatics analyses, a detailed examination of m⁶A regulators were conducted in EC using datasets from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). Single-cell RNA sequencing (scRNA-seq) and a consensus clustering algorithm was employed to classify m⁶A modification patterns and analyze their relationships with immune cell infiltration and clinical outcomes. Additionally, an m⁶A scoring system was developed based on principal component analysis to assess the prognostic value of identified m⁶A modification patterns.

The findings revealed two distinct m⁶A modification clusters associated with divergent TME characteristics and immune infiltration profiles. Patients exhibiting the immune-inflamed phenotype (m⁶A cluster B) demonstrated significantly improved survival compared to those with the immune-excluded phenotype (m⁶A cluster A). Notably, m⁶A scores correlated positively with immune cell presence and related with adverse prognostic outcomes, indicating their potential as predictive biomarkers for immunotherapy responses. A low m⁶A score indicated a better response to immunotherapy.

This study highlights the critical role of m⁶A methylation in shaping the TME and influencing immune dynamics in EC. The m⁶A score developed herein provides a novel quantitative tool for predicting tumor behavior and treatment efficacy, paving the way for more personalized immunotherapeutic strategies in clinical practice. This scoring system illustrates a strong correlation of EC with TME immune cell composition, suggesting potential as a biomarker for targeted therapeutic strategies for EC.

Parotid gland tumors (PGTs) are the most common salivary gland neoplasms, encompassing diverse benign and malignant pathologies. Accurate preoperative diagnosis is vital for surgical planning, functional outcomes (e.g., facial nerve preservation), and prognosis. While histopathology remains the gold standard, non-invasive imaging, such as ultrasound (US) and MRI, plays a critical role in initial tumor characterization. US is widely used due to its accessibility and cost-effectiveness, but its utility is constrained by acoustic limitations and operator dependence. MRI, with superior soft tissue contrast and multiplanar capabilities, excels in delineating tumor extent and neural involvement but often struggles to differentiate benign from malignant lesions due to overlapping imaging features. The comparisons of diagnostic performance between US and MRI limited, and optimal imaging parameters for specific PGT subtypes remain underinvestigated. The aim of the present study was to review and summarize the clinical presentations and histological types of parotid tumors, whilst also evaluating the diagnostic accuracy of US and MRI, to determine optimal US imaging parameters for pleomorphic adenomas and Warthin tumors. The medical records, including imaging examination results, type of parotidectomy and postoperative pathological findings, of 214 patients with confirmed PGTs were collected from the database of Central Hospital of Wuhan (Wuhan, China). The nature of the tumor was assessed based on imaging findings (US and MRI), with postoperative pathology (hematoxylin and eosin and immunohistochemistry) used as the gold standard. The sensitivity, specificity, accuracy, positive predictive value (PPV) and negative predictive value (NPV) for US and MRI were established. The area under the curve (AUC) was computed to compare the accuracy of US and MRI in identifying the nature of parotid gland tumors. The Youden index was calculated to evaluate the diagnostic power. Data analysis was conducted using SPSS version 29.0, where statistical significance was set at P<0.05 using the χ² test. In the field of PGT diagnosis, the combination of US and MRI technologies was found to significantly enhance diagnostic precision. This integrated approach showed a statistically significant improvement over the use of US alone (P<0.05). Although MRI, as an independent modality, showed higher accuracy compared with that of US, the difference between MRI and US was not statistically significant. The receiver operating characteristic curve analysis indicated that the AUC for MRI in diagnosing benign and malignant parotid gland tumors was 0.899, which was significantly greater compared with that of US (0.702; P<0.001). The combined diagnosis using US and MRI achieved the highest specificity (94.8%), compared with US (52.6%) and MRI (71.9%) alone. For the combined US-MRI approach, the PPV, NPV and Youden index were 84.6, 95.0 and 0.68%. For US and MRI alone, the PPV, NPV and Youden index were 64.7, 94.1 and 0.34%, and 75.8, 95.0 and 0.67%, respectively. To conclude, these data suggest that the amalgamation of MRI and US can provide an efficacious means of diagnosing PGTs, thereby constituting an instrumentation for the preoperative qualitative evaluation of these tumors.

Fundic gland tumors are a rare subtype of gastric tumors with fundic gland differentiation. This group of tumors has a low incidence rate and shows indistinctive cellular atypia, obvious structural atypia, special tissue morphology, and clinical prognosis, thus leading to diagnostic challenges.

We aimed to investigate the clinical and endoscopic characteristics and pathological features of gastric adenocarcinoma of the fundic gland (GA-FG) to provide a better understanding of this disease.

We collected data from patients diagnosed as having GA-FG at Guangdong Provincial People's Hospital between January 2019 and April 2024. The analysis focused on their clinical data, endoscopic characteristics, pathological morphological characteristics, immunohistochemistry results, treatment, and prognosis.

Among the four patients were two men and two women (age range, 52-65 years). The tumors were mainly located in the gastric fundus and gastric body, and the lesions commonly had a superficial bulge. Three patients had an initial diagnosis of oxyntic gland adenoma, which was diagnosed as GA-FG after complete resection. These tumors were negative for MUC5AC, but showed diffuse strong positivity for MUC6 and pepsinogen I, and synaptophysin expression.

GA-FG is a rare gastric tumor with unique morphological features. As it is difficult to diagnose with a biopsy, immunohistochemistry plays an important role in the differential diagnosis. Oxyntic gland adenoma can be regarded as the intramucosal stage of GA-FG. Although all patients were negative for MUC5AC expression, MUC6 and pepsinogen I can help the diagnosis of GA-FG.

Helicobacter pylori is a globally prevalent bacterium associated with several gastrointestinal diseases, including peptic ulcers and gastric cancer. Growing interest has emerged in understanding how H. pylori affects gut microbiota and whether eradication therapies impact microbial balance, potentially influencing disease outcomes, including cancer progression.

A systematic review was conducted across PubMed, Scopus, and Web of Science databases using predefined keywords and Medical Subject Headings (MeSH) terms. Quality assessment was performed using the MINORS and Jadad scales.

A total of 45 studies met the inclusion criteria, which evaluated microbial changes in H. pylori -infected individuals before and after eradication therapies. H. pylori infection resulted in significant alterations in gut and gastric microbiota, with a notable increase in inflammation-associated bacteria, such as Proteobacteria and Streptococcus. In gastric cancer patients, microbial diversity was reduced, with decreased levels of Bifidobacterium and Actinobacteria, and increased levels of Prevotella and Dialister, both associated with pro-inflammatory environments. Eradication therapies generally worsened dysbiosis initially, but probiotic supplementation promoted faster recovery of beneficial bacteria, improving microbial balance and reducing cancer-related dysbiosis.

H. pylori infection disrupts the gut microbiota, with eradication therapies further altering microbial composition. The restoration of microbial diversity is improved by probiotic supplementation. Understanding the long-term impacts of these therapies on gut health is essential for refining treatment strategies, particularly in preventing H. pylori -associated diseases like gastric cancer.

Polycystic ovary syndrome (PCOS) is a prevalent reproductive endocrine disorder characterized by significant clinical heterogeneity. The etiology of PCOS remains elusive, though it is closely linked to genetic, metabolic, endocrine, and environmental determinants. Resveratrol, a natural polyphenol, has garnered considerable interest due to its diverse biological activities. While resveratrol has been shown to ameliorate disorders in glucose, lipid, and endocrine metabolism associated with PCOS, the precise underlying mechanisms remain unclear. This narrative review aims to explore the potential mechanisms through which resveratrol operates, considering the multifaceted pathological pathways of PCOS, thereby offering insights for clinical applications and drug development.

The high morbidity and mortality of liver diseases warrant the development of more effective therapeutic methods. Extracellular vesicles (EVs) are optimal drug delivery vehicles, albeit with insufficient targeting specificity. The aim of this study was to develop modified red blood cell-derived EVs (RBC-EVs) for targeted drug delivery into hepatocytes, and verify their therapeutic efficacy in animal models of acute liver failure (ALF), non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC).

RBC-EVs were extracted and modified with triantennary N-acetyl galactosamine sequences (GalNac-RBC-EVs), then loaded with drugs or oligonucleotides. The GalNac-RBC-EVs uptake by hepatocytes was monitored both in vitro and in vivo. Models of ALF, NAFLD and HCC were established using C57BL/6J mice. RBC-EVs/GalNac-miR-155-ASO was prepared for the treatment of ALF by anchoring GalNac-miR-155-ASO to RBC-EVs. GalNac-RBC-EVs loaded with PJ34 (GalNac-RBC-EVs/PJ34) were used for treating NAFLD. Finally, GalNac-Rab7-siRNA and PJ34 were co-loaded into RBC-EVs (RBC-EVs/GalNac-Rab7-siRNA/PJ34) as a therapeutic agent for HCC. The therapeutic efficacy, biosafety and stability of the modified RBC-EVs were analyzed as per standard protocols.

GalNac-RBC-EVs exhibited higher hepatocyte accumulation via asialoglycoprotein receptor (ASGPR)-mediated uptake both in vivo and in vitro. In ALF, RBC-EVs/GalNac-miR-155-ASO reduced inflammation through suppression of pyroptosis (P<0.0001), apoptosis (P<0.0001), and mitigation of necroptosis (P<0.0001). For NAFLD/HCC treatment, GalNac-RBC-EVs/PJ34 decreased hepatic triglyceride (P<0.0001) and attenuated HCC growth (P<0.001) via PARP-1 inhibition (P<0.0001). Co-delivery of GalNac-Rab7-siRNA enhanced PJ34 efficacy (P<0.0001) by prolonging drug retention. No significant toxicity was observed in vital organs (ALT/AST levels, P>0.05; histopathology scores, P>0.05).

Drug-loaded GalNac-RBC-EVs selectively targeted the hepatocytes, and displayed significant therapeutic efficacy in ALF, NAFLD or HCC without any side effects. Altogether, RBC-EVs modified with GalNac are a promising drug carrier for the effective and precise treatment of various liver diseases.

BACKGROUND This article presents a rare case of pancreatic cancer complicated by a leukemoid reaction, alongside 4 similar cases treated at our hospital between 2016 and 2024. Leukemoid reactions are uncommon paraneoplastic manifestations, and their optimal management remains undefined. Herein, we systematically analyze the clinical characteristics and potential molecular mechanisms involved in the development and progression of tumor-associated leukemoid reactions, and summarize our diagnostic and therapeutic approaches. CASE REPORT We reviewed the records of 5 patients at our hospital who had malignancies complicated by leukemoid reactions. Medical histories, laboratory tests, imaging findings, bone marrow biopsy results, and treatment details were collected and analyzed. We explored the pathogenesis, diagnostic strategies, and treatment modalities for leukemoid reactions. A 52-year-old man with advanced pancreatic adenocarcinoma and a KRAS p.G12D mutation, developed extreme leukocytosis (96.22×10⁹ white blood cells/L) in the context of hepatic metastases. Despite broad-spectrum antimicrobial coverage, cytoreductive therapies, and supportive measures (bilirubin adsorption and plasma exchange, continuous veno-venous hemofiltration), his condition rapidly deteriorated, culminating in multi-organ failure. The 4 additional patients - 1 each with metastatic breast cancer, colon cancer, cholangiocarcinoma, and recurrent pancreatic cancer - exhibited similarly aggressive courses, with only transient stabilization observed in the breast cancer case. CONCLUSIONS Patients with malignancies complicated by leukemoid reaction generally have a poor prognosis. Clinicians should be alert to markedly elevated white blood cell counts, promptly investigate underlying causes, and initiate individualized treatments. Future research should focus on the molecular mechanisms driving the development and progression of leukemoid reactions and therapeutic interventions to enhance patient survival and clinical outcomes.

Many early-stage lung adenocarcinoma patients experience recurrence or metastasis after surgery, and the efficacy of targeted therapies remains suboptimal, significantly impacting the prognosis of these patients. Our study aims to investigate the impact of SCGB3A1 on the prognosis of lung adenocarcinoma patients and its role in immunity. We propose that SCGB3A1 may offer a novel treatment approach for lung adenocarcinoma patients who do not respond well to targeted therapies.

We obtained RNA sequencing data from 539 lung adenocarcinoma samples, 59 normal tissues, and 2 metastatic cancer tissues from The Cancer Genome Atlas database. Using Venn diagrams, we analyzed the expression of SCGB3A1 and other differentially expressed genes (DEGs) in different patient groups. Additionally, we performed another Venn diagram analysis to explore the association between SCGB3A1 and immune-related genes. We investigated the relationship between SCGB3A1 expression and patient clinical-pathological data and prognosis. Furthermore, through GO, KEGG, and GSEA enrichment analyses, we explored the functional roles of SCGB3A1 and its association with immune cell infiltration and immune checkpoint genes. The role of SCGB3A1 in LUAD was investigated by cytological experiments.

The results indicated that SCGB3A1 is associated with both prognosis and immunity. In lung adenocarcinoma, SCGB3A1 may function as a tumor suppressor gene. The high-expression group of SCGB3A1 exhibited a better prognosis and more pronounced immune cell infiltration. Additionally, SCGB3A1 was associated with smoking status and tumor size. A multivariate Cox regression model suggested that SCGB3A1 expression, pathological type, and ethnicity independently impact patient prognosis. Functional enrichment analysis indicated that SCGB3A1 was related to tumor progression, cell proliferation, and immune suppression. Furthermore, ssGSEA analysis revealed that SCGB3A1 expression is associated with immune cell infiltration and tumor-related immune genes. Experimental validation suggested that the overexpression of SCGB3A1 suppressed cell proliferation, migration, and invasion of LUAD.

In summary, this study investigated the association between SCGB3A1 and the prognosis of early-stage lung adenocarcinoma. The findings revealed that SCGB3A1 is related to immune cell infiltration and tumor-related immune gene expression, which may provide insights into the role of SCGB3A1 in immunotherapy. The cytological experiments indicate that SCGB3A1 is a potential therapeutic target for LUAD.