To investigate the effect of LINC00641 on the viability and apoptosis of acute myeloid leukemia (AML) cells and its mechanism.

To establish venetoclax-resistant acute myeloid leukemia (AML) cell lines, assess the sensitivity of venetoclax-resistant cell lines to the BCL-2 protein family, and investigate their resistance mechanisms.

To study the effects and mechanisms of juglone on the proliferation and apoptosis of acute myeloid leukemia (AML) cells.

Non-small cell lung cancer (NSCLC), as the predominant histological subtype of lung cancer, accounts for approximately 85% of all lung cancer cases. In recent years, immune checkpoint inhibitors (ICIs), represented by programmed death 1/programmed death ligand 1 (PD-1/PD-L1) inhibitors, have achieved breakthrough advancements in patients with driver gene-negative NSCLC. They have been established as a key component of first-line treatment regimens and have significantly improved clinical outcomes. However, limited clinical evidence has emerged showing the phenomenon of histological transformation from NSCLC to small cell lung cancer (SCLC) in patients experiencing disease progression after ICIs monotherapy or combination therapy. Systematic research data on the clinical characteristics, molecular biological basis, and subsequent treatment strategies for such transformation events are currently lacking. This article reports a case of SCLC transformation occurring in a patient with KRAS-mutated lung adenocarcinoma after 16 months of ICIs combination therapy and provides a systematic review of 22 similar published cases. The study demonstrates that small cell transformation is a critical mechanism of immunotherapy resistance, and transformed patients exhibit poor prognosis. The research emphasizes the importance of dynamic monitoring of neuron-specific enolase (NSE) and standardized repeat biopsies during treatment, providing a basis for clinical practice. This aids in enhancing the recognition and management capabilities for this rare histological transformation, ultimately improving patient outcomes.

The incidence and mortality rates of lung cancer remain high, making it the leading cause of cancer-related deaths. In women, the predominant histological subtype is lung adenocarcinoma, commonly associated with epidermal growth factor receptor (EGFR) mutations, and EGFR-tyrosine kinase inhibitors (EGFR-TKIs) can significantly improve patient prognosis. Metastasis of primary lung cancer to the endometrium is extremely rare and is often misdiagnosed as a primary reproductive system tumor, and its occurrence indicates poor prognosis. This article reports a case of an advanced lung adenocarcinoma patient with EGFR mutation, who developed abnormal vaginal bleeding after EGFR-TKIs treatment failure, and biopsy confirmed endometrial metastasis. A review of similar cases is also presented.
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Lung cancer remains the leading cause of cancer-related incidence and mortality worldwide. Among its histological subtypes, non-small cell lung cancer (NSCLC) accounts for the majority of cases, representing the predominant pathological type. Notably, in the elderly population, NSCLC continues to be a major contributor to cancer-related deaths. With the global ageing population, immunosenescence has emerged as a key factor influencing the occurrence, progression, and the efficacy of immunotherapy of NSCLC. Immunosenescence refers to the age-related decline in immune system function, which manifests as alterations in both the quantity and functionality of immune cells. These include thymic involution, T cell exhaustion, epigenetic modifications, weakened immune responses, and a chronic low-grade inflammatory state. This review comprehensively analyzes the role of immunosenescence in elderly patients with advanced NSCLC and proposes potential therapeutic strategies to intervene in the immunosenescence process. By targeting immunosenescence, these strategies aim to inhibit the progression of NSCLC and improve the effectiveness of immunotherapy.
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Lung cancer, particularly non-small cell lung cancer (NSCLC), is a leading cause of cancer-related mortality worldwide. In recent years, metabolomics has emerged as a key systems biology approach for analyzing small-molecule metabolites in cells, tissues and organisms. It provides new strategies for early diagnosis and metabolic profiling. Additionally, metabolomics plays a crucial role in studying resistance mechanisms in lung cancer. Tumor cell metabolic reprogramming is a key driving factor in the initiation and progression of lung cancer. Metabolomics studies have revealed how lung cancer cells regulate critical pathways such as energy metabolism, lipid metabolism, and amino acid metabolism to adapt to the demands of rapid proliferation and invasive metastasis. This review summarizes the latest advances in metabolomics research in lung cancer, focusing on the characteristics of metabolic reprogramming, the identification of potential metabolic biomarkers, and the prospects of metabolomics in early diagnosis and the elucidation of resistance mechanisms in lung cancer.
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Small cell lung cancer (SCLC), a highly aggressive subtype of lung cancer that originates from pulmonary neuroendocrine cells, accounts for 10% to 15% of all lung cancers. It is characterized by a high rate of early metastasis and extremely poor prognosis, often accompanied by challenges such as drug resistance and recurrence. Related researches indicates that the Notch signaling pathway plays a crucial role in the occurrence and development of SCLC by regulating processes such as cell proliferation, differentiation, and apoptosis. In SCLC, abnormal Notch signaling may promote tumor malignancy and the occurrence of drug resistance. Additionally, the Notch pathway is involved in the epithelial-mesenchymal transition of SCLC and influences immune escape mechanisms through interactions with the tumor immune microenvironment. This article reviews the molecular mechanisms of Notch signaling in SCLC, including the roles of its receptors and ligands, signal transduction processes, and its role in tumorigenesis. It also discusses the research progress of Notch signaling as a potential therapeutic target and looks forward to future research directions in this field.
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Lung cancer remains one of the most prevalent and deadly malignancies worldwide, with persistently low five-year survival rates. This poor prognosis is primarily attributed to challenges such as difficulties in early diagnosis, high tumor heterogeneity, and strong therapeutic resistance. Although recent advances in targeted therapies and immune checkpoint inhibitors have significantly improved the prognosis of some patients, the majority still encounter primary or secondary resistance. Galectin-3, a multifunctional glycan-binding protein, is constitutively expressed in pulmonary tissues. Its expression encompasses bronchial and alveolar epithelial cells, the pulmonary vasculature, and resident immune cells. Galectin-3 plays a central role in lung cancer progression by regulating tumor cell proliferation, immune evasion, and angiogenesis. The complex immunosuppressive mechanisms within the tumor microenvironment not only facilitate tumor growth and metastasis but also partially limit the efficacy of cancer immunotherapies. Overcoming these barriers requires the exploration of novel regulatory targets to break through therapeutic bottlenecks. This review systematically elucidates the mechanisms by which galectin-3 interacts with immune cells (e.g., T cells, macrophages) in the tumor microenvironment and evaluates its potential as a therapeutic target, including inhibitor development and combination immunotherapy strategies. The findings aim to provide a theoretical foundation for advancing galectin-3 as a novel therapeutic target in lung cancer and offer new perspectives for overcoming current immunotherapy resistance.
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Objective: To investigate the clinicopathological features, genetic characteristics, and differential diagnosis of glomangiomatosis with uncertain malignant potential. Methods: Two cases of glomangiomatosis with uncertain malignant potential were collected at Henan Provincial People's Hospital from 2013 and 2023. Immunohistochemistry and next generation sequencing (DNA-seq) were used to detect the related protein and gene variation. Patients were followed up. Results: Case 1 was male, 34 years old; and case 2 was female, 28 years old. Both had tumor recurrence in the original site. There were multiple nodules at right calf and ankle, involving superficial subcutaneous tissue and deep interfascicular muscles; some nodules were borderless and painful. Microscopically, the tumor was nodular with fibrous pseudocapsule, some had indistinct borders and diffuse infiltration to the surrounding adipose tissue. The tumor cells were round to ovoid with inconspicuous nucleoli, partly surrounding small irregularly dilated thin-walled blood vessels. The recurrent tumors showed epithelioid morphology in some of the tumor cells, with eosinophilic cytoplasm, some apparent nucleoli, mild to moderate nuclear atypia, and brisk mitotic figures. Focally, perimuscular cell differentiation was noted. The small lesion showed intravascular tumor thrombus. NGS revealed BRAF V600E mutation in case 1, and BRAF V600E mutation combined with PDGFRB gene amplification in case 2. Conclusions: Glomangiomatosis with uncertain malignant potential is a rare variant of glomus tumor. It has a unique growth pattern morphologically, BRAF V600E mutation, and invasive biological behavior.

Objective: To investigate the clinicopathological features of SMARCA4-deficient uterine sarcoma. Methods: Five cases of SMARCA4-deficient uterine sarcoma at the Department of Pathology, the First Affiliated Hospital of Nanjing Medical University from 2018 to 2024 were collected. The morphological and immunohistochemical features were observed and analyzed. A follow-up study was also carried out. Results: Five female patients, aged 24, 54, 56, 61, and 41 years, respectively, presented with vaginal bleeding or abdominal pain. All patients had imaging findings of intracavitary lesion in the uterus, with tumor sizes ranging from 3.0 cm to 8.8 cm. The patients were followed up for 2 to 14 months. Case 1 died 9 months after surgery, whereas the remaining four patients were still alive. Histologically, the tumor cells exhibited a diffuse growth pattern, with an infiltration depth involving more than half of the myometrium. Portions of the interstitium appeared sclerosed. Benign endometrial glandular structures were observed in a leaf-like or fissured pattern, resembling those of uterine adenosarcoma. The tumor cells were large epithelioid with abundant or faintly eosinophilic cytoplasm, and the nuclei were moderately to markedly atypia with prominent nucleoli and brisk mitosis. Rhabdoid cells were seen. Some areas showed small round blue cells, with occasional spindle cells and myxoid stroma. Additionally, widespread or focal lymphovascular space invasion was observed within the myometrium. All five cases exhibited absence of SMARCA4 (BRG1) expression and retained SMARCB1 (INI1). Claudin4 expression was negative. There was no deficient expression of mismatch repair proteins MLH1, PMS2, MSH2 and MSH6. p53 showed wild-type expression. Ki-67 index ranged from 30% to 60%. CKpan, CK7, ER, PR, and PAX8 were negative. Conclusions: SMARCA4-deficient uterine sarcoma is rare, highly aggressive, and has a poor prognosis. The tumor exhibits a broad morphological spectrum, with rhabdoid cells and adenosarcoma-like structures serving as important diagnostic clues. The absence of BRG1 expression lends support to a definitive diagnosis.

Objective: To investigate the clinicopathological characteristics of well-differentiated papillary mesothelial tumor (WDPMT). Methods: Sixteen cases of resected WDPMTs diagnosed at the Affiliated Hospital of Qingdao University, Qingdao, China from 2017 to 2024 were collected and the clinicopathological features were retrospectively analyzed. Results: There were 7 males amd 9 females, with a mean age of 53.8±14.8 years (range, 25-83 years). Tumor size ranged from 3 to 12 mm in maximum diameter. Of the 16 cases, 15 involved the peritoneum and 1 involved the pleura, one of which occurred on the surface of ovary. All cases were incidentally identified during unrelated surgical procedures. Histologically, tumors exhibited arborizing papillary growth patterns and frequently displayed hierarchically branching papilla. Tumor cells showed cuboidal to flattened cell morphology with minimal nuclear atypia. Mitotic figures were not noted in all cases. Entrapped gland-like tumor cell clusters were found in the stroma of tumor papilla in 1 of the 16 cases. Immunohistochemically, the tumor cells expressed mesothelial markers (Calretinin, D2-40, and CK5/6) in all cases, and BAP1 and MTAP were immunoreactive in all tested cases. Fluorescence in situ hybridization revealed no CDKN2A deletions. Conclusions: WDPMT predominantly occurs in the peritoneum and typically demonstrates indolent biological behaviors. It often shows overlapping features with mesothelioma in situ and epithelioid mesothelioma. The hierarchical branching papillae is its diagnostic hallmark, while routine immunohistochemical evaluation of BAP1 and MTAP is also recommended for differential diagnosis of these tumors.