Objective G protein-coupled estrogen receptor 1 (GPER1) has been reported to exert tumor-suppressive effects in various malignancies. However, the mechanism by which GPER1 modulates macrophage M2 polarization via the myelocytomatosis oncogene (MYC) signaling pathway and its impact on gastric cancer (GC) progression remains poorly understood. This study aims to explore the role of the GPER1-MYC-interleukin 10 (IL-10) axis in GC. Methods Bioinformatic analyses were conducted to assess GPER1 expression levels and associated signaling pathways. AGS and HGC-27 gastric cancer cell lines with stable GPER1 overexpression or knockdown were generated, using normally cultured cells as controls. Cell proliferation, migration, and invasion were evaluated using the Cell Counting Kit-8 (CCK-8), wound healing, and TranswellTM assays, respectively. Western blotting was performed to examine MYC pathway activation, and the MYC-specific inhibitor 10058-F4 was used for mechanistic validation. A TranswellTM co-culture system was established to simulate tumor-macrophage interactions. Flow cytometry was used to quantify the proportion of M2 macrophages, and IL-10 secretion was measured via ELISA. Results GPER1 expression was significantly downregulated in GC tissues and showed a negative correlation with MYC signaling activity. Knockdown of GPER1 promoted malignant phenotypes in gastric cancer cells, whereas GPER1 overexpression exerted suppressive effects. Mechanistically, GPER1 inhibited M2 macrophage polarization and reduced GC cell proliferation, invasion, and migration by downregulating IL-10 expression via MYC suppression. Notably, the MYC inhibitor reversed the tumor-promoting effects induced by GPER1 knockdown and enhanced the antitumor effects of GPER1 overexpression. Conclusion GPER1 modulates macrophage M2 polarization through the MYC-IL-10 axis, thereby affecting gastric cancer progression. These findings indicate GPER1 as a potential therapeutic target for gastric cancer intervention.

To clarify the prognostic significance of 1q21 amplification in multiple myeloma (MM), and explore the efficacy and prognosis of ixazomib in the treatment of MM patients with 1q21 amplification.

To investigate the bone marrow and peripheral blood cytological characteristics and prognosis in acute myeloid leukemia (AML) with FLT3-ITD mutation.

To explore the expression level of m6A methyltransferase ZC3H13 gene in primary acute myeloid leukemia (AML) and its relationship with clinical features and prognosis.

To investigate the molecular characteristics of low-risk acute myeloid leukemia (AML) at recurrence, and analyze the factors affecting retreatment efficacy and prognosis.

Non-small cell lung cancer (NSCLC), the predominant histological subtype of lung cancer, mandates precise screening and accurate prognostic assessment to guide therapeutic strategies and improve patient survival. The initiation and progression of NSCLC are intimately linked to inflammatory responses. Interleukin-6 (IL-6), a pivotal inflammatory mediator, critically modulates the tumor microenvironment, immune evasion, tumor progression, and therapy resistance in NSCLC. Recent evidence indicates that IL-6 not only participates in the biological behavior of NSCLC but also holds promise as a potential biomarker for early detection and prognostication. This review summarizes the role of IL-6 in NSCLC screening, treatment-related adverse events, and its utility in the management of NSCLC-associated comorbidities.
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Lung cancer remains a life-threatening malignancy with complex pathogenesis. This paper provides a systematic review of autophagy and ferroptosis-related signaling pathways, key regulatory factors, and their associated mechanisms, including the nuclear receptor coactivator 4 (NCOA4)-mediated ferritin autophagy-ferroptosis axis, mitochondrial autophagy, lipid droplet autophagy, circadian autophagy, chaperone-mediated autophagy, etc.. The review elucidates the roles of the tumor microenvironment and non-coding RNAs in autophagy-ferroptosis processes in lung cancer. Furthermore, it explores the potential of modern drugs and active components from traditional Chinese medicine to improve lung cancer outcomes by targeting autophagy and ferroptosis, proposing that targeting their interactive pathways could offer novel therapeutic strategies for lung cancer.
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Lung cancer is one of the most prevalent and lethal malignant tumors worldwide, with lung adenocarcinoma (LUAD) being a major subtype. In recent years, research has revealed that the tumor microenvironment (TME) plays a crucial role in the development and progression of LUAD. Notably, the role of neutrophils has increasingly garnered attention. Studies have shown that neutrophils can differentiate into various phenotypes within the TME, exhibiting multiple pro-tumorigenic functions. Additionally, neutrophils can secrete neutrophil extracellular traps (NETs) in response to certain stimuli. Although NETs possess anti-tumor characteristics, an increasing number of studies have uncovered their multifaceted pro-tumor functions. This review describes the role of neutrophils in the initiation, development, and metastasis of LUAD, focusing on immunoregulation, cellular metabolism, genetics, and various molecular mechanisms.
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Tyrosine kinase inhibitors (TKIs) resistance poses a significant challenge in the targeted therapy of lung adenocarcinoma (LUAD), highlighting the need to identify key molecular markers associated with both drug resistance and prognosis to guide precision treatment. This study aimed to elucidate the molecular mechanisms underlying TKIs resistance in LUAD, identify core differentially expressed genes (DEGs), clarify the relationships between different gene clusters and patient survival/drug response, and construct and validate a prognostic risk model for LUAD, thereby providing a foundation for precision therapy and prognostic assessment.

Objective: To investigate the clinicopathological features, immunophenotype, molecular genetic characteristics, and prognosis of clear cell meningioma (CCM). Methods: Seventeen cases with diagnosed of CCM from four hospitals [Xuanwu Hospital (6 cases), Sanbo Brain Hospital (3 cases), Beijing Children's Hospital (4 cases) Affiliated with Capital Medical University; Provincial Hospital Affiliated to Shandong First Medical University (4 cases)], from August 2017 to April 2025, were analyzed. All specimens of CCM cases were H&E stained, followed by immunohistochemistry (IHC), next-generation sequencing (NGS), and DNA methylation profiling. Clinical follow-up and prognostic analysis were performed. Results: The cohort included six males and eleven females, with a median age of 11 (6, 44) years; 10 were pediatric patients, 7 were adult patients. None had neurofibromatosis type 2. Tumor locations included spinal canal (n=5), cerebellopontine angle (n=4), middle/posterior fossa (n=4), petroclival region (n=3), and jugular foramen (n=1). Histologically, tumors showed sheets of polygonal cells with clear glycogen-rich cytoplasm, round/oval nuclei with inconspicuous nucleoli, prominent perivascular and interstitial hyalinized collagen proliferation, and scattered lymphoplasmacytic infiltrates. No other meningioma subtypes were identified (17/17). IHC showed variable expression of EMA, vimentin, SSTR2, and PR, with universal loss of SMARCE1 nuclear expression. The median Ki-67 index was 6%. NGS revealed no NF2 alterations (0/10), while SMARCE1 mutations were detected in 9/10 of cases, including: 2 sites with splice-site mutations, 2 sites with nonsense mutations and 3 sites with frameshift mutations. DNA methylation unsupervised clustering demonstrated distinct profiles separating CCMs (8/33) from other meningiomas (25/33). Among 14 patients with follow-up (median 32 months, range 2-145 months), recurrence occurred in 6 cases and death in 1 case; all recurrence/death cases were pediatric patients. CCM patients had significantly higher recurrence/progression risk compared with WHO grades 1 and 2 meningiomas (HR=3.863, 95%CI: 1.435-10.401,P=0.02), with earlier recurrence. High Ki-67 index (≥10%) was associated with increased risk of recurrence (P<0.01). Conclusions: CCMs exhibit unique age distribution, anatomical predilection, histopathological changes, immunophenotype (SMARCE1 loss), and molecular profile (SMARCE1 mutations, distinct methylation signature). They demonstrate aggressive behavior, particularly in pediatric patients and cases with high proliferative activity, warranting close clinical surveillance and consideration of adjuvant therapy.

Objective: To investigate the clinical, radiologic, pathological and molecular genetic features of polymorphous low-grade neuroepithelial tumor of the young (PLNTY). Methods: A retrospective analysis was performed on fourteen PLNTY cases, diagnosed at the Department of Pathology, Xuanwu Hospital, Capital Medical University, from August 2018 to December 2024. The clinical, radiologic, prognostic, histopathological, molecular genetic features, and DNA methylation clustering were analyzed. Results: Among the 14 patients (10 males, 4 females), the age range was 8-34 years, with a median age of 21 (14, 29) years. The patient's major, initial clinical symptom was epilepsy (13/14). Among 9 MRI exanimated cases, 4 showed cystic-solid abnormal signals, and 5 appeared as solid masses. Most were hypointense on T1 and hyperintense on T2. Five cases had enhancement, with no obvious diffusion restriction on DWI. Among 5 CT examined cases, 4 showed high density, and 1 showed low density. The characteristic histopathologic features of the tumor cells were oligodendroglioma-like, spindle, pleomorphic and associated with foci of calcifications. GFAP and Olig2 were expressed in tumor cells in all 14 cases (14/14). Neuronal markers (NeuN, NF) were negative in 13/13 cases. CD34 showed diffuse strong positivity in all cases (14/14). BRAF V600E was positive in 8/11 cases. Thirteen cases (13/13) harbored mitogen-activated protein kinase (MAPK) pathway alterations, including BRAF (10/13) and FGFR2/3 (3/13) gene mutations. In 7 PLNTY cases, t-SNE cluster analysis of DNA methylation profiles showed clustering with ganglioglioma, PLNTY, and pilocytic astrocytoma. Until November 2025, 13 patients have been seizure-free postoperatively, and all 14 patients showed no tumor progression or recurrence. Conclusions: PLNTY usually occurs in adolescents and is associated with epilepsy. Its diagnosis necessitates a combination of clinical, histopathological, and molecular genetic alterations. In molecular level, PLNTY exhibits alterations in the MAPK pathway; while its DNA methylation profile demonstrates diversity. Most patients achieved seizure-free outcomes postoperatively, indicating a favorable prognosis.

Objective: To investigate the clinicopathological characteristics of pediatric Ewing sarcoma in the rare sites. Methods: Seven surgical resection specimens and one consultation case diagnosed at Shanghai Children's Medical Center (4 cases), Shanghai Jiaotong University, Shanghai; Zhejiang Children's Hospital (2 cases), Hangzhou and Jiangxi Children's Hospital (2 cases), Nanchang, China from January 2019 to June 2024 were collected. The tissues were subject to histological examination and immunohistochemistry using EnVision system. The fluorescence in situ hybridizations (FISH) for EWSR1::FLI1 gene fusion and EWSR1 gene-breakapart were performed. The paraffin sections were used for next-generation sequencing (NGS). Results: There were 8 pediatric patients (4 boys and 4 girls). Their ages ranged from 7 to 14 years, with a median age of 12.5 (10.0, 13.5) years. The tumors were located in the right submandibular gland (1 case), tail of the pancreas (1 case), prostate (1 case), small intestine (1 case), nasal vestibule (1 case), adrenal gland (1 case), and right kidney (2 cases). Histologically, the tumors showed relatively uniform small round cells with an invasive growth pattern. The adamantinoma-like Ewing sarcoma occurring in the right submandibular gland had obvious characteristics of epithelial differentiation. Immunohistochemistry showed diffuse positivity for CD99, NKX2.2 in most tumors, partial or diffuse positive for epithelial and neuroendocrine markers in some cases, as well as complete negativity for desmin in all tumors. Molecular genetic study showed EWSR1 gene translocation and FUS::FLI1 gene fusion using FISH and NGS. All cases underwent chemotherapy or adjuvant radiotherapy. The follow-up for 10 to 44 months found that two patients were dead, one had recurrence and the others were free of disease. Conclusions: Extraskeletal Ewing sarcoma is rare. Careful histologic evaluation supplemented by immunophenotyping and molecular studies facilitates its diagnosis and differential diagnosis.

Objective: To investigate the clinicopathological and molecular genetic characteristics of uterine leiomyosarcoma. Methods: A retrospective study was performed on twenty-four patients diagnosed with uterine leiomyosarcoma, at Peking University, Third Hospital, from January 2023 to July 2024. The study aimed to analyze the clinicopathological characteristics of uterine leiomyosarcoma using immunohistochemistry and next generation sequence to detect the molecular genetic alterations. Results: Among the twenty-four cases, patient's age ranged from 29 to 74 years, with a median age of 45.5 (37.5, 49.3) years. Tumor size ranged from 6 to 20 cm, with an average size of 11 cm. Before surgery, sixteen patients had received hormone therapy, traditional Chinese medicine, health supplements, and/or oxytocin during surgery. Among these sixteen cases, eight cases showed morphological changes of the tumor cells, with the nature of necrosis being difficult to characterize, posing diagnostic challenges. Immunohistochemical analysis revealed positive expression of smooth muscle markers in all 24 cases. A mutant p53 expression pattern was observed in 14 cases, while loss of Rb expression was noted in 17 cases. Loss of ATRX and PTEN expression was detected in 13 and 11 cases, respectively.All twenty-four cases demonstrated microsatellite stability. Twenty-three cases showed a low tumor mutational burden (TMB), while one case showed high TMB. All cases showed variations of copy number and gene mutations involving multiple genes. The most common molecular genetic aberrations were loss of copy number or mutation in TP53 and RB1. Simultaneous genetic aberrations in both TP53 and RB1 were identified in fifteen cases. Furthermore, eleven cases showed copy number loss of BRCA2 and one case showed a missense mutation of BRCA2. Twenty-one cases revealed frequent copy number variations in homologous recombination repair-related genes, including FANCA, FANCM, RAD51B, BARD1, FANCE, ATM, CHEK2 etc. Thirteen cases showed loss of ATRX protein expression. Conclusions: Uterine leiomyosarcoma is characterized by multiple copy number variations and gene mutations, most frequently involving TP53 and RB1. Additional common molecular features include copy number variations of homologous recombination repair-related genes, ATRX protein expression loss, low tumor mutational burden, and microsatellite stability. Secondary morphological changes in uterine leiomyosarcomas associated with hormone therapy pose significant diagnostic challenges. Next generation sequencing can provide valuable evidence for the diagnosis of morphologically challenging cases of leiomyosarcoma in clinical practice.