Background Superior vena cava syndrome (SVCS) is a common condition predominantly caused by lung cancer. The presence of symptoms of SVCS, such as elevated intracranial pressure and laryngeal edema, indicates an unfavorable prognosis for lung cancer patients. Superior vena cava (SVC) stenting is the first‐line treatment for SVCS. In this study, we retrospectively analyzed SVCS cases treated with stenting in our center to explore the safety and effectiveness of stenting in the treatment of SVCS. Methods We reviewed 16 patients with SVCS caused by lung cancer who were treated at our center with endovascular stenting between 2016 and 2018. Patient information such as age, sex, type of lung cancer, obstruction condition, complications, survival time, and postoperative treatments are summarized. Results There were no treatment‐related complications in the perioperative period in any of the patients. Examination at postoperative day 2 indicated that the accompanying SVCS symptoms had improved in all patients. The median survival of patients treated along with combined postoperative chemotherapy and antivascular targeted therapy reached seven months (1–18 months). Conclusions SVC stenting is effective as a first‐line treatment modality for patients with SVCS caused by lung cancer. In combination with other treatment modalities, it can significantly alleviate symptoms and reduce complications, and thus it plays an important role in the treatment of patients with SVCS caused by lung cancer.

Hypoxia plays a crucial role in the pathogenesis of various cancers, especially lung adenocarcinoma (LUAD), by altering cancer metabolism to promote escape mechanisms. Anoikis, a specialized form of programmed cell death, is evaded by LUAD cells during tumor progression and metastasis through upregulation of anti-apoptotic proteins. Investigating the impact of hypoxia-anoikis-related genes on prognosis and therapy prediction in LUAD is essential. Gene expression and clinical data from 489 LUAD patients and 49 normal tissues in The Cancer Genome Atlas (TCGA) dataset were used as the training set, while GSE72094, GSE31210, and GSE30219 datasets were used for validation. Weighted Gene Co-Expression Network Analysis (WGCNA) identified genes associated with hypoxia and anoikis. Machine learning models were evaluated using the C-index. Kaplan-Meier survival analysis, immune cell infiltration, tumor mutational burden (TMB), and sensitivity to therapy were assessed based on risk scores. A total of 21 hypoxia-anoikis-related prognostic genes were identified. The Random Survival Forest (RSF) model had the highest C-index. High-risk patients had significantly lower survival rates. Immune analysis showed higher immune infiltration in the low-risk group, with lower immune escape potential in these patients. Risk scores were correlated with sensitivity to targeted therapy and chemotherapy. MCF2 was identified as a key prognostic gene, and its knockdown inhibited LUAD cell proliferation and metastasis. These 21 genes offer insights into LUAD prognosis and therapy response, guiding personalized treatment strategies for LUAD patients.

Purpose: This research intends to investigate the treatment of non-small cell lung cancer (NSCLC) using Toripalimab, focusing on its effectiveness and safety profile. Efficacy refers to the survival prognosis, while safety pertains to the occurrence of adverse events in our study. It also aims to provide reference information for neoadjuvant and postoperative therapies.Methods: Up to March 20, 2024, studies on randomized controlled trials and single-arm trials involving Toripalimab for NSCLC were sourced from the Cochrane Library, Embase, PubMed, and Web of Science databases. Data extraction and analysis were independently conducted by two researchers utilizing Stata 15.0 and R software.Results: A total of 8 studies were analyzed, including 6 single-arm studies and 2 randomized controlled trials (RCTs). Toripalimab treatment in the RCTs showed an overall survival (OS) of [HR=0.67, 95% CI (0.53, 0.85); p=0.71]. The objective response rate (ORR) from single-arm studies was reported as [ES=0.59, 95% CI (0.36, 0.81); p<0.01], and progression-free survival (PFS) was [ES=4.89, 95% CI (2.65, 9.02); p<0.01]. Furthermore, observed adverse effects included Anemia [OR=0.53, 95% CI (0.26, 0.79); p<0.01], Neutropenia [OR=0.43, 95% CI (0.20, 0.68); p<0.01], and Thrombocytopenia [OR=0.28, 95% CI (0.18, 0.43); p<0.01].Conclusions: Toripalimab, being China’s first domestically developed anti-tumor PD-1 antibody drug, shows potential advantages over traditional chemotherapy in possibly prolonging patients’ survival times. However, the limited number of studies included indicates the need for additional single-arm and RCT studies to further validate these findings.Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier (CRD42024519806).

Phyllodes tumo (PT) of the breast are classified into benign, borderline, and malignant types. Malignant phyllodes tumor (MPT) with metastasis, particularly those containing sarcomatous components, have a notably poor prognosis. The most common sites of metastasis are the lungs, although metastases can also occur in the pleura and other areas. Metastatic PT is typically treated according to NCCN guidelines for soft tissue sarcomas. The prognosis for patients is extremely poor, with survival typically not exceeding five years. Therefore, the treatment of metastatic MPT presents significant challenges. A 67-year-old female with a history of PT surgery was hospitalized due to acute chest tightness and shortness of breath. MRI revealed a large mass in the left thoracic region, measuring 7.9 × 10.8 × 11.4 cm. A biopsy conducted prior to hospitalization indicated spindle cell soft tissue sarcoma. Due to critical vital signs, she underwent an emergency thoracotomy. Postoperative analysis confirmed the diagnosis of thoracic metastasis from MPT with sarcomatous components. Genetic analysis of the tumor tissue post-surgery revealed a KDM6A gene mutation. Unfortunately, subsequent imaging showed a recurring mass in the left thoracic space, approximately 8 cm in size. Considering the side effects of NCCN-recommended treatments (doxorubicin and ifosfamide) and the high cost of targeted therapies, the patient and her family chose tislelizumab. After six cycles of treatment, the patient’s progression-free survival reached 15 weeks. Due to unsatisfactory treatment effects, the patient and her family decided to discontinue therapy, and the patient passed away in July 2024. Although the combination of surgery and postoperative immune checkpoint inhibitors remains to be validated, this case provides valuable insights into the management of thoracic metastasis from MPT. It offers potential new options for personalized immunotherapy in metastatic MPT.

Lung adenocarcinoma (LUAD) remains one of the most prevalent and lethal cancers globally, making it critical to understand the mechanisms driving its progression and improve prognosis. Moreover, cuproptosis and mitochondrial dysfunction may be involved in lung cancer. Therefore, the present study aimed to identify mitochondrial genes associated with cuproptosis to develop a prognostic model for patients with LUAD, with the potential to predict survival outcomes and responses to treatment. Bulk RNA‑sequencing data was utilized from The Cancer Genome Atlas and the Gene Expression Omnibus (GEO), and Pearson correlation analysis was employed to identify mitochondrial genes associated with cuproptosis. A prognostic model was constructed using univariate Cox regression combined with least absolute shrinkage and selection operator analysis, and a nomogram was developed to predict survival with clinical relevance. The accuracy of the model was evaluated using two independent GEO datasets. Additionally, the clinical value of the risk score model was assessed using immune infiltration analysis, tumor mutational burden and drug sensitivity predictions. Furthermore, the effects of superoxide dismutase 2 (SOD2) gene knockdown on tumor metastasis and proliferation were experimentally evaluated. A set of 22 mitochondrial genes associated with cuproptosis were identified: Metabolism of cobalamin associated D, SOD2, human immunodeficiency virus‑1 Tat interactive protein 2, cytochrome C somatic, mitochondrial pyruvate carrier 1, adenylate kinase 2, mitochondrial ribosomal protein L44, transforming growth factor β regulator 4, mitochondrial transcription factor A, tetratricopeptide repeat domain 19, coiled‑coil‑helix‑­coiled‑coil‑helix domain containing 4, sideroflexin 1, ATP binding cassette subfamily D member 1, NADH:ubiquinone oxidoreductase complex assembly factor 7, NOP2/Sun RNA methyltransferase 4, NME/NM23 nucleoside diphosphate kinase 6, X‑Prolyl aminopeptidase 3, lipoyltransferase 1, mitochondrial methionyl aminopeptidase type 1D, carbonic anhydrase 5B, kynurenine 3‑monooxygenase and alcohol dehydrogenase iron containing 1. The model was validated as an independent predictor of overall survival, dividing patients into high‑ and low‑risk groups. Immune infiltration analysis revealed that tumors in the low‑risk group displayed more active immune responses and improved immune function. Drug sensitivity analysis suggested that high‑risk patients may be more responsive to specific drug treatments. Finally, knockdown of the SOD2 gene suppressed tumor cell metabolism, proliferation and metastasis. In conclusion, the present study successfully established a prognostic model based on cuproptosis‑related mitochondrial genes and developed a nomogram to predict LUAD prognosis with high accuracy, thereby providing improved tools for treatment decision‑making and enhancing patient outcomes.

Pulmonary Langerhans cell histiocytosis (PLCH) is an uncommon myeloid disorder of the lung characterized by the accumulation of Langerhans-like cells within the pulmonary parenchyma. On imaging, it typically presents as nodular or cystic lesions and is closely associated with cigarette smoking. Although PLCH can occur in both children and adults, it is more frequently observed in younger smokers and is relatively rare in elderly individuals. In most cases, the disease follows a slow and sometimes self-limiting course, and systemic therapy is not routinely required. However, radiologic differentiation from malignant ground-glass nodules may be challenging. The development of PLCH after lung adenocarcinoma surgery is rare. Here, we report the case of a 72-year-old woman with lung adenocarcinoma. Following resection of a right lung nodule, molecular testing identified an EGFR exon 19 deletion, and icotinib was subsequently administered for contralateral ground-glass nodules. During postoperative follow-up, new lesions were detected in the rib adjacent to the surgical field as well as in the lung, raising concern for possible bone metastasis on imaging. Percutaneous biopsy with immunohistochemical analysis demonstrated positivity for CD1a, Langerin, and S-100, while lung adenocarcinoma-associated markers, including CK7, TTF-1, and Napsin A, were negative, supporting a diagnosis of PLCH. The next generation sequencing found BRAF V600E mutation in PLCH lesions. After symptomatic treatment and long-term follow-up, the lesions gradually improved and partially disappeared. Looking back on the previously reported cases, it is not common for PLCH and lung adenocarcinoma to coexist. In published reports, these two conditions generally have different driving gene changes, and their potential biological relationship is still unclear. This case shows that when new lesions are found after lung cancer surgery, besides tumor recurrence, other diagnoses, namely PLCH, should be considered, and the diagnosis should be confirmed by histopathological examination.